WEIGHT GAIN A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Weight Gain: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84239-6 1. Weight Gain-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on weight gain. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON WEIGHT GAIN........................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Weight Gain................................................................................ 11 E-Journals: PubMed Central ....................................................................................................... 69 The National Library of Medicine: PubMed ................................................................................ 71 CHAPTER 2. NUTRITION AND WEIGHT GAIN ............................................................................... 117 Overview.................................................................................................................................... 117 Finding Nutrition Studies on Weight Gain............................................................................... 117 Federal Resources on Nutrition ................................................................................................. 120 Additional Web Resources ......................................................................................................... 120 CHAPTER 3. ALTERNATIVE MEDICINE AND WEIGHT GAIN ........................................................ 125 Overview.................................................................................................................................... 125 National Center for Complementary and Alternative Medicine................................................ 125 Additional Web Resources ......................................................................................................... 130 General References ..................................................................................................................... 134 CHAPTER 4. DISSERTATIONS ON WEIGHT GAIN .......................................................................... 135 Overview.................................................................................................................................... 135 Dissertations on Weight Gain.................................................................................................... 135 Keeping Current ........................................................................................................................ 136 CHAPTER 5. CLINICAL TRIALS AND WEIGHT GAIN ..................................................................... 137 Overview.................................................................................................................................... 137 Recent Trials on Weight Gain.................................................................................................... 137 Keeping Current on Clinical Trials ........................................................................................... 140 CHAPTER 6. PATENTS ON WEIGHT GAIN ..................................................................................... 143 Overview.................................................................................................................................... 143 Patents on Weight Gain............................................................................................................. 143 Patent Applications on Weight Gain ......................................................................................... 170 Keeping Current ........................................................................................................................ 194 CHAPTER 7. BOOKS ON WEIGHT GAIN ......................................................................................... 197 Overview.................................................................................................................................... 197 Book Summaries: Federal Agencies............................................................................................ 197 Book Summaries: Online Booksellers......................................................................................... 205 The National Library of Medicine Book Index ........................................................................... 207 Chapters on Weight Gain........................................................................................................... 207 CHAPTER 8. MULTIMEDIA ON WEIGHT GAIN .............................................................................. 221 Overview.................................................................................................................................... 221 Video Recordings ....................................................................................................................... 221 CHAPTER 9. PERIODICALS AND NEWS ON WEIGHT GAIN ........................................................... 225 Overview.................................................................................................................................... 225 News Services and Press Releases.............................................................................................. 225 Newsletters on Weight Gain ...................................................................................................... 227 Newsletter Articles .................................................................................................................... 228 Academic Periodicals covering Weight Gain ............................................................................. 230 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 231 Overview.................................................................................................................................... 231 U.S. Pharmacopeia..................................................................................................................... 231 Commercial Databases ............................................................................................................... 232 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 235 Overview.................................................................................................................................... 235
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NIH Guidelines.......................................................................................................................... 235 NIH Databases........................................................................................................................... 237 Other Commercial Databases..................................................................................................... 240 APPENDIX B. PATIENT RESOURCES ............................................................................................... 241 Overview.................................................................................................................................... 241 Patient Guideline Sources.......................................................................................................... 241 Finding Associations.................................................................................................................. 258 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 261 Overview.................................................................................................................................... 261 Preparation................................................................................................................................. 261 Finding a Local Medical Library................................................................................................ 261 Medical Libraries in the U.S. and Canada ................................................................................. 261 ONLINE GLOSSARIES................................................................................................................ 267 Online Dictionary Directories ................................................................................................... 269 WEIGHT GAIN DICTIONARY.................................................................................................. 271 INDEX .............................................................................................................................................. 365
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with weight gain is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about weight gain, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to weight gain, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on weight gain. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to weight gain, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on weight gain. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON WEIGHT GAIN Overview In this chapter, we will show you how to locate peer-reviewed references and studies on weight gain.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and weight gain, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “weight gain” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Breastfeeding and Weight Gain Source: Heart and Soul. 8(6): 58. August 2001. Summary: A Cornell University study of more than 2,000 new mothers found that women who begin pregnancy with an average weight but who gain more than 35 pounds before giving birth are 74 percent more likely to have difficulty breastfeeding. The study identifies several associations between weight gain and breastfeeding. The areolae (the dark area around the nipples) are often much larger on full-breasted women, making it difficult for infants to compress breast tissue to get an adequate supply of milk. Obese women may also have trouble finding comfortable positions for nursing an infant. Women of average weight receive progesterone from the placenta. After delivery, the placenta is expelled, signaling the body to start producing milk. Since
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fat is also a source of progesterone, obese women continue to produce progesterone after expelling the placenta, potentially slowing down milk production. •
Infant Weight Gain and Childhood Overweight Source: Healthy Weight Journal. 16(4):50. July/August 2002. Summary: A study conducted by the National Collaborative Perinatal Project found that infants who experience rapid weight gain during the first 4 months of life are more likely to be overweight at age 7 years. The prospective study of 19,397 children from birth to age 7 included both Black and White children in 12 locations around the country. The researchers found a 30 percent increase in overweight status at age 7 for each 100 grams of weight increase in the first 4 months of life. These findings were independent of birth weight and weight at 1 year. The authors suggest that early infancy is linked to obesity and propose that the first 4 months of life may be a time when energy balance regulation related to later obesity develops.
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Weight Gain After Kidney Transplantation. (editorial) Source: American Journal of Kidney Diseases. 38(2): 409-410. August 2001. Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Website: www.harcourthealth.com. Summary: Cardiovascular disease is now the leading cause of long term morbidity and mortality in kidney transplant recipients. Some of the immunosuppressive drugs used to prevent renal allograft (the transplanted kidney) rejection play a key role by causing or exacerbating (making worse) hypertension (high blood pressure), hyperlipidemia (high levels of fats in the blood), and glucose intolerance. These cardiovascular risk factors are compounded by the increase in body weight that occurs in the vast majority of patients after kidney transplantation. This article serves as a commentary on a related research article (Clunk et al, 2001) on weight gain after kidney transplantation. The research study identifies subgroups of patients who are at risk for posttransplant weight gain and who should be targets for aggressive intervention measures (including steroid sparing immunosuppressive regimens) designed to prevent it. The commentary author laments the fact that the researchers did not correlate posttransplant weight gain with outcomes such as acute rejection or graft survival. The emerging profile of the patient at risk for posttransplant weight gain (i.e., the poor, young, African American female) is strikingly similar to the profile of patients at high risk for acute rejection and graft loss. The commentary author also notes that further studies are needed to explore the relationships between posttransplant weight gain, obesity, and rejection. 12 references.
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Late Night Eating and Weight Gain Source: Running and Fitnews. 19(3):3. March 2001. Contact: The American Running Association. 4405 East West Highway, Number 405, Bethesda, MD 20814, 800/776-2732. Summary: Does eating most of one's calories at night cause weight gain? The author of this column replies that consuming calories in excess of total energy requirements causes weight gain. If an individual does not eat more than his or her daily needs throughout the day and evening, then eating a greater percentage of those total calories at night will not cause weight gain in itself. Studies show, however, that people who do not eat regularly throughout the day may have a lower metabolic rate and may tend to
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binge at night, due to the effects of fasting. Skipping regular meals may create eating habits that not only make it hard to consume enough fruits and vegetables but also may result in consuming more calories than the body is able to use. Eating regular meals and nutritious snacks throughout the day ultimately makes better sense for health and fitness. •
Fertility Events Link to Women's Weight Gain Source: Healthy Weight Journal. 115(2):18-19. March/April 2001. Summary: Excess weight gain in a woman's life occurs at the beginning of menstruation, with pregnancy, and at menopause, according to studies presented at the annual meeting of the North American Association for the Study of Obesity (NAASO). Studies at Tufts University show that early menstruation may be an intermediary to later obesity and can also contribute independently to an increased risk of later obesity. Weight retention after pregnancy, a risk factor for obesity, is a greater risk for AfricanAmerican women than Caucasians. A National Institutes of Health (NIH) funded study, the Women's Healthy Lifestyle Project, shows that postmenopausal women have higher levels of body fat and central adiposity than other women of the same age. This 5- year randomized clinical trial of 535 initially premenopausal women showed that after 4.5 years, women in the control group gained an average of 5.2 pounds. In the intervention group, which made lifestyle changes, twice as many women were at or below their original weight.
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Thirst, Interdialytic Weight Gain, and Thirst-Interventions in Hemodialysis Patients: A Literature Review Source: Nephrology Nursing Journal. 28(6): 601-613. December 2001. Contact: Available from American Nephrology Nurses' Association. East Holly Avenue, Box 56, Pitman, NJ 08071-0056. (856) 256-2320. Fax (856) 589-7463. Website: www.annanurse.org. Summary: Noncompliance is a common problem in patients on hemodialysis. Noncompliance is found in all aspects, but adhering to the fluid restriction is the most difficult aspect for most patients. This article reports on a literature search completed for the period of 1980 to 1999 that identified studies on the prevalence of thirst in hemodialysis (HD) patients and the relationship between thirst and interdialytic weight gain, as well as intervention studies in which thirst was used as an outcome variable. Twenty-three studies fulfilled the selection criteria and were included in the analysis. The prevalence of thirst varied between 6 and 95 percent across studies. In most studies, more thirst was related to more weight gain. However, the studies were difficult to compare due to methodological differences. Three types of interventions were found: technical interventions in the dialysis mechanisms (increasing the frequency of dialysis sessions and varying the concentration of sodium in the dialysate), pharmaceutical (drug) interventions (ACE inhibitors), and a dietetic intervention. The author stresses that almost no conclusions could be drawn with regard to the effectiveness of these interventions due to methodological differences and weaknesses and due to the small sample sizes. 1 figure. 4 tables. 34 references.
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Weight Gain Associated With Improved Glycemic Control in Population-Based Sample of Subjects With Type I Diabetes Source: Diabetes Care. 13(11): 1106-1109. November 1990.
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Summary: Previous studies have suggested that weight gain is an identifiable risk associated with efforts to lower blood glucose with intensive insulin therapy in patients with insulin-dependent diabetes mellitus (IDDM). Four hundred and five adults with IDDM, who were diagnosed before age 30, were studied from 1980-1982 and in a followup examination from 1984-1986. Weight gain over the 4-year interval averaged 1.8 kilograms (kg). Weight gain was significantly associated with improvements in glycosylated hemoglobin levels; the quartile of subjects with the greatest improvements in glycemic control gained 3.4 kg, whereas the quartile of subjects with the smallest improvements in glycemic control lost 0.6 kg. Weight gain was also correlated with increases in the number of shots of insulin per day and change in the treatment regimen from one type of insulin to a combination of short-and long-acting insulins. These results suggest that weight gain may be an adverse consequence of improved glycemic control. (AA-M). 1 figure. 1 table. 9 references. •
Variables Affecting Weight Gain in Renal Transplant Recipients Source: American Journal of Kidney Diseases. 38(2): 349-353. August 2001. Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Website: www.harcourthealth.com. Summary: Previous studies of renal (kidney) transplant recipients have suggested that weight gain after transplantation is relatively common, especially among certain populations. This article reports on a retrospective study of 977 renal transplant recipients at the University of Alabama at Birmingham that was conducted to identify patterns of weight change (as mean percentage of body weight at transplantation) attributed to race, sex, income, age at transplantation, pretransplantation time on dialysis, incidence of diabetes, rejection episode(s), or obesity at transplantation. Patients were evaluated at 3, 6, 9, and 12 months posttransplantation and at 2 and 3 years, when available. Analyses at 1 year showed that blacks achieved a greater weight change than whites, women had greater gains than men, and low income patients had greater mean gains versus medium and high income patients. Advancing age and weight gain were inversely correlated (when age went up, weight gain was less). Having one or more rejection episodes indicated less weight gain than having no rejection episode. Incidence of diabetes or time on dialysis was not a significant predictor of weight gain. The authors summarize that black race, female sex, low income, younger age, and no incidence of rejection episodes were significantly associated with weight gain at 1 year in the multivariate analysis. 2 figures. 3 tables. 21 references.
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Infant Feeding, Early Weight Gain, and Risk of Type 1 Diabetes Source: Diabetes Care. 22(12): 1961-1965. December 1999. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article describes a case control study that evaluated whether the increased risk of type 1 diabetes conferred by an early introduction of cow's milk supplements can be mediated by accelerated growth in formula fed infants. All Finnish children 14 years old or younger who were diagnosed with type 1 diabetes between September 1986 and April 1989 were invited to participate in the study. Birth date and gender matched control children were randomly selected from the Finnish Population Registry. At least three weight measurements from the first year of life were obtained for 435 full term subjects who had diabetes and 386 control subjects from well baby
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clinics and school health care units. The proportion of children who received formula feeding by the age of 3 months was 33 percent in the children who had diabetes and 25 percent in the control subjects. Neither the total duration of breastfeeding nor the age at introduction of solid foods differed between the children who had diabetes and control subjects. Increase in body weight was greater in the girls who had diabetes than in the control girls, and the difference increased from 111 grams at 1 month of age to 286 grams at 7 months. For boys, the difference in weight between the boys who had diabetes and the control subjects remained stable during infancy. Increased weight was associated on average with a 1.5-fold risk of type 1 diabetes. Early introduction of formula feeding was also associated with an increased risk of type 1 diabetes after adjustment for the individual weight gain curve. No evidence for interaction was observed. The article concludes that the findings indicate that an early exposure to cow's milk formula feeding and rapid growth in infancy are independent risk factors of childhood type 1 diabetes. 1 appendix. 3 figures. 1 table. 19 references. (AA-M). •
Effect of Excessive Weight Gain with Intensive Therapy of Type 1 Diabetes on Lipid Levels and Blood Pressure: Results from the DCCT Source: JAMA. Journal of the American Medical Association. 280(2): 140-146. July 8, 1998. Summary: This article describes a randomized controlled trial that determined the effect of weight gain in intensive treatment of type 1 diabetes on lipid levels and blood pressure. Participants were 1,168 people with type 1 diabetes who were enrolled in the Diabetes Control and Complications Trial and were 18 years or older at baseline. A total of 586 participants received intensive diabetes treatment and 582 received conventional diabetes treatment. The mean followup period was 6.5 years. Outcome measures were plasma lipid levels and blood pressure in each treatment group as categorized by quartile of weight gain. Results indicate that with intensive treatment, participants in the fourth quartile of weight gain had the highest body mass index (BMI), blood pressure, and levels of triglyceride, total cholesterol, low density lipoprotein cholesterol (LDL-C), and apolipoprotein B, compared with the other weight gain quartiles. The greatest difference was seen in comparison to the first quartile. In addition, the fourth quartile group had a higher waist-to-hip ratio; more cholesterol in the very low density lipoprotein, intermediate dense lipoprotein, and dense LDL fractions; and lower highdensity lipoprotein cholesterol and apolipoprotein A-I levels than the first quartile. Baseline characteristics did not differ between the first and fourth quartiles of weight gain with intensive therapy, except for a higher hemoglobin A1c in the fourth quartile. Weight gain with conventional therapy resulted in smaller increases in BMI, lipids, and systolic blood pressure. The article concludes that changes in lipid levels and blood pressure that occur with excessive weight gain with intensive therapy are similar to those seen in the insulin resistance syndrome and may in time increase the risk of coronary artery disease in this subset of subjects. 3 figures. 5 tables. 27 references. (AAM).
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Improved Glycemic Control Reduces the Impact of Weight Gain on Cardiovascular Risk Factors in Type 1 Diabetes: The Epidemiology of Diabetes Complications Study Source: Diabetes Care. 22(7): 1084-1091. July 1999. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472.
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Summary: This article describes a study that assessed the prevalence and incidence of overweight in type 1 diabetes, identified factors associated with weight gain and improved glycemic control, and examined relationships among weight gain, glycemic control, and cardiovascular risk factors. The prevalence and incidence of overweight in the 441 subjects participating in the Pittsburgh Epidemiology of Diabetes Complications were compared with those of the general population. Factors associated with weight gain and improved glycemic control were identified, and relationships among weight gain, glycemic control, and cardiovascular risk factors were examined for a mean duration of 6.9 plus or minus 2.2 years. The study found that, at baseline, the prevalence of overweight for men and women was 10.4 percent and 11.4 percent, respectively, and was lower than the age and sex specific estimate for the general population. The incidence of overweight was comparable in men and women and did not differ from that of the general population. Weight gain correlated with improvements in glycosylated hemoglobin (HbA1c). Patients with the highest baseline HbA1c levels gained the most weight and had the greatest improvement in glycemic control. Weight gain favorably influenced the lipid profile in the setting of improved glycemic control but adversely influenced the lipid profile in the absence of improved glycemic control. Weight change was directly associated with change in blood pressure, but the incidence of hypertension was more strongly influenced by the development of nephropathy. The article concludes that despite the overall increase in obesity in the general population, the prevalence of overweight in type 1 diabetes remains lower than in the general population, and the incidence of overweight in type 1 diabetes does not differ from that of the general population. 3 figures. 4 tables. 28 references. (AA-M). •
Weight Gain as a Risk Factor for Clinical Diabetes Mellitus in Women Source: Annals of Internal Medicine. 122(7): 481-486. April 1, 1995. 1995. Summary: This article describes a study undertaken to examine the relation between adult weight change and the risk for clinical diabetes mellitus among middle aged women. A 15 year prospective cohort study followed 114,281 female registered nurses aged 30 to 55 years, who did not have diagnosed diabetes mellitus, coronary heart disease, stroke, or cancer at baseline. During 1.49 million person-years of followup, 2,204 cases of diabetes were diagnosed. After adjustment for age, body mass index was the dominant predictor of risk for diabetes. The authors conclude that the excess risk for diabetes with even modest and typical adult weight gain is substantial. They note that women who lost more than 5.0 kg reduced their risk for diabetes mellitus by 50 percent or more. These results were independent of family history of diabetes. Their findings support the importance of maintaining a constant body weight throughout adult life. 5 tables. 20 references. (AA-M).
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Weight Gain and Heart Disease in Type 1 Source: Diabetes Forecast. 53(6): 105. June 2000. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article presents the results of a study that investigated the relationship between weight gain and heart disease in type 1 diabetes. The 6 year study of 1,168 adults who had type 1 diabetes separated participants into an intensive insulin treatment group and a conventional treatment group. At follow up, participants were further separated into a group whose weight remained the stable, a group whose weight gain was approximately 10 pounds, a group whose weight gain was approximately 20
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pounds, and a group whose weight gain was approximately 40 pounds. The study found that people in the intensive treatment group that gained the most weight had significantly higher levels of triglycerides, total cholesterol, and low density lipoprotein cholesterol than those in the other intensive treatment groups. Mean blood pressure was also slightly higher in the intensive treatment group who gained the most weight. However, the benefits of tight blood glucose control were evident. For example, there were fewer cardiovascular events in the intensive therapy group. The researchers concluded that the changes in lipid levels and blood pressure that occur with excessive weight gain may increase the risk of coronary artery disease in people who have type 1 diabetes. •
Season of Weight Gain Source: Diabetes Forecast. 55(11): 82-83. November 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reminds readers with diabetes of some strategies to help avoid the typical weight gain that accompanies holiday celebrations through the fall and winter seasons (Thanksgiving through New Year's). The author stresses that the best idea is to come up with a plan of action to ease the temptation to overeat at parties and other festivities. The author outlines tips to keep weight in check during the holiday season, including mall walking (extra exercise), pacing oneself (eat in moderation and chew food slowly and thoroughly), opt for low calorie alternatives (modify recipes), and avoid stress (more recommendations for exercise). The author also mentions the importance of a workout buddy or other folks whose help can be enlisted to help keep the holidays healthy and happy.
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Weight Gain in Women With Gestational Diabetes Source: Obstetrics and Gynecology. 81(4): 523-528. April 1993. Summary: This article reports on a study to evaluate weight gain during pregnancy in women with gestational diabetes (GDM) and to determine whether there was a stronger or weaker correlation of maternal weight gain with neonatal birth weight in women with gestational diabetes as compared with a control group. At delivery, 78 women with GDM and 312 control subjects were evaluated and classified according to pregravid weight for height. Weight gain during pregnancy and neonatal birth weight in the women with GDM and in the control group were compared. A weight gain curve for each patient was generated to assess the rate of weight gain during early, middle, and late gestation. Weight gain was 2.5 kg less in the women with GDM as compared with the controls. When adjusted for pregravid weight, maternal age, and gestational age at delivery, only underweight women with GDM persisted in having significantly less weight gain as compared with the control subjects. There were no significant differences in infant birth weight between any gestational diabetes and control weight categories. The rate of weight gain was decreased in overweight women with GDM versus control subjects in late pregnancy. There was a significant correlation between maternal weight gain and birth weight in underweight and average weight control women, but not in overweight controls or in any patients with GDM. The authors conclude that weight gain in women with GDM is less than in control patients, primarily because of greater pregravid weight, and does not correlate with neonatal birth weight. 3 tables. 15 references. (AA-M).
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Longitudinal Study of the Effects of a Gluten-Free Diet on Glycemic Control and Weight Gain in Subjects with Type 1 Diabetes and Celiac Disease Source: Diabetes Care. 25(7): 1117-1122. July 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to describe the longitudinal growth characteristics and glycemic control in children with type 1 diabetes diagnosed with celiac disease and started on a gluten-free diet (GFD). Data on growth and glycemic control for 11 case subjects diagnosed with celiac disease (cd positive group) and started on a GFD were collected prospectively, and two control subjects without celiac disease matched for age, sex, and duration of diabetes (cd negative group) were selected for comparison. In children with type 1 diabetes, untreated celiac disease resulted in lower BMI (body mass index) and lower HbA1c (glycosylated hemoglobin, a measure of blood glucose levels over time). Recovery of BMI with a GFD was associated with further improvement in HbA1c, as compared with pre-GFD, with no expected deterioration in glycemic control during puberty. The authors conclude that these apparent clinical benefits need to be confirmed by larger studies. 2 figures. 2 tables. 33 references.
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Another Skirmish in the Battle of the Bulge: Fighting Weight Gain with the Dialysis Machine Isn't the Answer Source: Renalife. 8(2): 6, 12. 1993. Summary: This brief article, written for people who use self-care hemodialysis, describes the differences between dry weight and water weight and explores the problem of patients fighting weight gain with the dialysis machine. When a patient comes off the dialysis machine at his or her true dry weight, there should be enough fluid in the body after the treatment to keep the blood pressure stable. However, if the patient had actually gained more body weight, and was still bringing himself down to the old dry weight at the end of the treatment, he would be dehydrating himself. The result would be extra fatigue and problems with low blood pressure.
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Modest Weight Gain and the Development of Diabetes: Another Perspective (editorial) Source: Annals of Internal Medicine. 122(7): 548-549. April 1, 1995. 1995. Summary: This editorial comments on an article by Colditz and colleagues that quantified the relations between change in adult weight and the risk for noninsulindependent diabetes (NIDDM). Colditz et al. noted that weight gain after 18 years was strongly related to risk, as was weight gain during middle age. The author of this commentary contrasts these findings with the recommendations of the U.S. Department of Agriculture that suggest that a weight gain of 7 kg for persons 35 years and older is desirable. The author also discusses possible limitations of the Colditz study, including the lack of data regarding physical activity and the limited racial constitution of the study population (98 percent white). 19 references.
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A College Nutrition Science Course as an Intervention to Prevent Weight Gain in Female College Freshme Source: JNE. 33(2): 95-101. March/April 2001.
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Summary: This study explored whether a one-semester college course on nutrition that stresses fundamental principles of human physiology, genetics, and energy metabolism helps prevent weight gain during the first 16 months of college life. Researchers conducted a randomized control trial from January 1997 to May 1998 using 40 female freshman volunteers (21 students took the college course and 19 did not). Body weight, nutrient intakes, and knowledge were measured at baseline, the end of the intervention (4 months from baseline), and 1 year later (16 months from baseline). Students with a higher body mass index (BMI) in the intervention group, whose BMI was higher than 24, reported lower fat, protein, and carbohydrate intakes compared with the higher BMI students in the control group. Dietary changes reported by higher BMI intervention students were associated with the maintenance of baseline body weight for 1 year in contrast with the higher BMI control students who gained an average of 9.2 kilograms. The findings suggest that nutrition education emphasizing human physiology and energy metabolism is an effective strategy to prevent weight gain in at-risk college students. •
Lack of Effect of Long-Term Use of Angiotensin-Converting Enzyme Inhibitors by Hemodialysis Patients on Thirst and Fluid Weight Gain Source: Renal Failure. 24(4): 461-466. 2002. Contact: Available from Marcel Dekker Journals. P.O. Box 5017, Monticello, NY 127015176. (212) 696-9000. Summary: Volume overload is a chronic, troublesome problem in many patients on hemodialysis. These patients suffer from hyperdipsia (excessive thirst) with inability to excrete water. ACE inhibitors have been shown to decrease thirst and interdialytic weight gain in 2 to 4 weeks of usage. This article reports on a study that investigated the effect of long term use of ACE inhibitors. The authors compared hemodialysis patients on ACE inhibitors (n = 7) for more than 6 months to patients not on the drugs (n = 51). Almost one third of patients in each group had an interdialytic weight gain greater than 5 percent of dry weight. No significant difference was found between the two groups with regard to interdialytic weight gain, thirst and mouth dryness scores, and interdialytic mean blood pressure change. There was no demonstrable effect of ACE inhibitors on weight gain or thirst. The authors conclude that long term ACE inhibitor use may not continue to suppress inappropriate thirst and fluid intake after 6 months in hemodialysis patients. 1 figure. 2 tables. 16 references.
Federally Funded Research on Weight Gain The U.S. Government supports a variety of research studies relating to weight gain. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions.
2
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to weight gain. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore weight gain. The following is typical of the type of information found when searching the CRISP database for weight gain: •
Project Title: A CAFETERIA-BASED STUDY OF WEIGHT GAIN PREVENTION Principal Investigator & Institution: Lowe, Michael R.; Psychology; Drexel University 3201 Arch Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2005 Summary: (provided by applicant): Obesity is a risk factor for a number of adverse medical and psychosocial outcomes. Solving the obesity problem will require a much greater emphasis on prevention. Treatment research indicates that interventions focusing directly on the food environment (structured meals and control of food stimuli) have considerable promise for weight control. Prevention research has found little support for trying to modify characteristics (e.g., knowledge, beliefs, skills) of individuals, perhaps because this approach does little to modify the food environment. The proposed research would be implemented in a workplace cafeteria where employees eat year-round and where the nutritional composition of the food can be modified. The influence of two promising interventions on food intake, weight change, and related outcomes will be investigated. The first intervention consists of a training program aimed at reducing the energy density of participants' diets inside and outside of the cafeteria. The second intervention consists of financial incentives to encourage the consumption of cafeteria foods lower in energy density. Participants will be 195 Caucasian and African-American men and women between the ages of 21 and 65. They will have a BMI of 23-35 and will have characteristics associated with an increased risk of weight gain. Selection and intake of lunch foods will be measured with digital photography and cashiers' computerized records of food purchases. Cafeteria patrons will be randomly assigned to 1) a measurement-only condition; 2) an intervention designed to teach participants how to reduce the energy density of their diets; or 3) the reduced energy density intervention plus financial incentives for choosing cafeteria foods low in energy density. The potential moderating influence of individual differences characteristics on outcome will also be evaluated. Outcome measures will be administered repeatedly during the intervention and at 9- and 18-month follow-ups. The assessments will include measures of anthropomorphic and blood lipid variables, nutritional intake (both in and out of the cafeteria), physical activity, overeating, eating self-efficacy, and weight-related quality of life. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ACTIVITY AND OBESITY IN US BLACK & NIGERIAN WOMEN Principal Investigator & Institution: Luke, Amy H.; Assistant Professor; Prev Medicine and Epidemiology; Loyola University Medical Center Lewis Towers, 13Th Fl Chicago, Il 60611 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 31-AUG-2005 Summary: (Abstract from applicant's abstract): The prevalence of obesity has increased in virtually every sub-population in the United States over the past few decades.
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Although obesity and its implications for health are well described, the associated epidemiologic determinants have not been defined for either individuals or populations. Obesity is a complex disorder with multiple etiologies; nonetheless, the underlying process must be a result of excessive energy intake relative to energy expenditure. The importance of the components of the energy budget, i.e., total daily energy expenditure (TDEE), resting metabolic rate (RMR), physical activity (i.e., non-resting EE), and energy intake (EI), is not well understood, however. To date, methodological constraints have made it difficult to unravel the epidemiologic determinants of obesity. Simply put, there are no sensitive measures of TDEE, physical activity or EI presently being used in epidemiologic studies. Doubly labeled water (DLW) does provide a valid and reliable method of measuring TDEE in free-living individuals. Obesity and its sequelae are very prevalent among African-American women, but infrequent among the genetically related population in Nigeria. This natural contrast provides a unique opportunity to study the evolution of obesity risk. We will examine the relationships between the energy budget and weight gain at the individual level in each of these populations, and then compare the patterns across groups. We will also determine the relationship between the various components of the energy budget and associated secondary risk factors for cardiovascular disease. This study will test the following primary hypothesis: low physical activity levels, (i.e., non-resting EE) place women at risk for weight gain and increase in body fat. To test this hypothesis, we will use DLW and RMR measurements to determine the energy budget in population-based samples of 200 African-American and 200 Nigerian women. The relationship between non-resting EE and RMR and weight gain will then be examined in a 3-year prospective study. We will also obtain complementary anthropometrics and physiologic data using routine methods such as questionnaires and blood tests. The proposed study will not use an ecologic design, since conclusions will be based relationships defined among individuals, not the comparison of group means. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ALTERATIONS OF CIRCADIAN TIMING IN SLEEP AND AGING Principal Investigator & Institution: Van Cauter, Eve Y.; Professor; Medicine; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2003; Project Start 01-SEP-1994; Project End 31-MAR-2008 Summary: (provided by applicant): Chronic sleep disturbance is reported by nearly 50% of older adults. Sleep loss also occurs at all ages due to bedtime curtailment, an increasingly prevalent condition. Recent data have revealed the role of sleep duration and quality in metabolic and endocrine function and have indicated that chronic sleep loss may accelerate the development or increase the severity of age-related diseases such as obesity and diabetes. Despite its high prevalence, chronic sleep loss has been understudied. The present Project focuses on the interaction of chronic partial sleep loss and aging. A multi-disciplinary approach combining epidemiology, clinical research (in older insomniacs, middle-aged subjects at risk for obesity and healthy adults of all ages), in vivo studies in laboratory rodents and molecular and genetic analyses will be used to: 1. Delineate the impact of age on sleep regulation during adaptation to and recovery from chronic partial sleep loss; 2. Test the hypothesis that chronic partial sleep loss has adverse effects on biomarkers of aging and increases the risk of obesity and diabetes; 3. Test the hypothesis that paying a sleep debt and/or improving sleep quality has beneficial health and neurobehavioral effects at all stages of adulthood; 4. Determine the influence of the circadian clock on the response to chronic sleep loss; 5. Explore the mechanisms linking chronic sleep loss and metabolic aging; 6. Define the determinants
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of individual differences in sleep capacity and vulnerability to sleep loss in young adulthood, midlife and late life. Project 6 will determine the role of sleep in weight gain in mid life. Project 7 will examine whether exercise is an effective countermeasure for sleep loss in older insomniacs. Project 8 will delineate the role of sleep duration in metabolic aging and weight gain. Project 9 will determine the impact of a sleep debt and individual sleep capacity in young, middle-aged and older men and women. Project 10 will use rat models to define the impact of age on physiologic adaptation to and recovery from sleep restriction. Project 11 will utilize a genetic model of chronic sleep loss with age-related obesity, the Clock mouse, to explore mechanisms linking circadian function, sleep and metabolism. Core 9001 (Methods and Analysis) will provide monitoring equipment for humans and rodents, methods for quantifying output variables and biostatistical support. Core 9002 (Laboratory) will assay blood, saliva and urine constituents for Projects 7, 8 & 9. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANALYSIS OF SEX HORMONES AND LIPOPROTEINS IN YOUNG MALES Principal Investigator & Institution: Barton, Bruce A.; Senior Statistician and Vice President; Maryland Medical Research Institute, Inc 600 Wyndhurst Ave Baltimore, Md 21210 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2004 Summary: (Provided by Applicant) This application requests support for secondary analysis of the Sex Hormones and Lipoproteins in Adolescent Males Study (HD/HL18281), a 3-year (1984-1987) study of lipids, blood pressure, weight, fat patterning, and sex steroid hormones (SSH) in adolescent males. A total of 664 black and white males, ages 10-15, were enrolled into a study designed as a series of repeated data collections over 2 years within age cohorts. Cross-sectional analyses have been used to explain differences during adolescence in SSH and SSH-lipid relationships between black and white boys and between boys with and without a family history of CHD. When the data were originally collected for this study, theoretical models of flexible longitudinal analytic techniques had been developed, but were not available for computer use. These techniques, now supported by software, allow a more powerful and complete analysis of these data. The primary aim of these analyses is to explicate the contribution of changes in SSH and fat patterning to changes in plasma concentrations of high (HDL-C) and low (LDL-C) density lipoprotein cholesterol, triglycerides (TG), and apolipoproteins (apo) Al, All, and B occurring during puberty in males. SSH assayed included estradiol (E2) and free testosterone (T). We will test the following hypotheses: (1) increasing free T predicts/leads to decreases in HDL-C and increases in LDL-C, apo B, and the LDL-C/HDL-C ratio in adolescent males; (2) increasing E2 predicts decreases in apo B, LDL-C and the LDL-C/HDL- C ratio, but the resultant effects will vary with adiposity and fat patterning; (3) rapid weight gain predicts increased central adiposity, defined as the ratio of truncal skinfolds to total skinfolds, and with greater decreases in HDL-C and increases in triglycerides, apo B, LDL-C and the LDL- C/HDL-C ratio. Rapid weight gain predicts increased E2, but the atherogenic effects of increased central adiposity on lipids are greater than the antiatherogenic effects of E2. These analyses will provide a better understanding of metabolic factors underlying obesity-hormone-lipoprotein relationships. Given the welldocumented increase in obesity in American youth, these analyses are especially pertinent and address important public health issues. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ANGIOTENSIN, LEPTIN, AND THE SYMPATHETIC NERVOUS SYSTEM Principal Investigator & Institution: Cassis, Lisa A.; Professor; Pharmacol & Exper Therapeutics; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2001; Project Start 14-AUG-1998; Project End 31-JUL-2003 Summary: (Adapted from the application): Angiotensin II (Ang II), a peptide integral to the central control of blood pressure, regulates sympathetic neurotransmission. The pathophysiological relevance of Ang II/sympathetic interactions has been examined in hypertension and congestive heart failure; however, the relevance of this interaction at noncardiovascular organs innervated by the sympathetic nervous system has not been examined. Preliminary studies demonstrate that chronic infusion of Ang II to rats resulted in a dose-dependent elimination of weight gain and reduction in body weight through pressor-independent mechanisms. The working hypothesis of the proposed studies is that Ang II regulates body weight by activating the sympathetic nervous system, lipids, reducing food intake and altering secretion of adipose-derived leptin. All of the proposed studies will be performed in a rat model of chronic Ang II infusion. The first hypothesis is that Ang II regulates energy expenditure by activating the sympathetic nervous system. Several different approaches will be used to determine the role of the sympathetic nervous system in the effect of Ang II. First the time course for alterations in norepinephrine (NE) turnover and kinetic parameters of the ligand biding site of the NE transporter will be determined in white and brown adipose tissue. Examination of the time course form alterations in release of NE from slices of white and brown adipose tissue and the in vitro effect of Ang II to increase evoked NE release will be examined. The effect of beta blockade on Ang II-regulation of body weight will be examined. To determine if Ang II increases energy expenditure by altering secretion of leptin protein, the time course for alterations in plasma leptin will be determined. Administration of Ang II to ob/ob mice lacking functional leptin will be examined to determine the role of leptin in Ang II-regulation of body weight. The effect of Ang II to mobilize lipids from brown and white adipose tissue will be determined. The role of AT1 receptor in Ang II-disposition of adipose tissue in response to Ang II infusion will be examined. In Hypothesis 2, the role of alterations in food intake in the weightreducing effects of Ang II will be determined. The physiologic/ pathophysiologic significance of Ang II-regulation of body weight is related to disease states whereby plasma Ang II concentrations are elevated (congestive heart failure) or decreased (obesity), contributing to the dysregulation of body weight. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BEHAVIORAL TREATMENT OF EATING PROBLEMS IN CF TODDLERS Principal Investigator & Institution: Powers, Scott W.; Associate Professor; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2001; Project Start 25-JUN-1998; Project End 31-MAY-2003 Summary: Optimal nutritional management for children with cystic fibrosis (CF) is critical for growth, quality of life, and long-term health outcomes. Diagnosis of CF typically occurs between age 6 and 18 months, and one of the first treatment priorities is to get the toddler with CF to eat 50 percent more than an average toddler typically eats. Research is needed to better understand how toddlers with CF (ages 12-36 months) and their families are meeting this biobehavioral challenge because parent-child mealtime interactions learned at this developmental period set the stage for appropriate eating
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behavior in the future and most older children with CF are not meeting the CF nutritional goals. Two studies will be conducted. Study 1 will identify the mealtime behaviors of toddlers with CF and their parents and compare these behaviors with agematched, non-chronically ill toddlers and their parents. Study 2 will use the information from Study 1 to develop and test the efficacy of an empirically- derived behavioral parent-training intervention designed to prevent and/or treat eating behavior problems and enhance growth and development in this population. A prospective, cross- sectional design comparing 30 toddlers with CF and 30 non-chronically ill toddlers will be used in Study 1. A randomized clinical trial design comparing 20 toddlers with CF randomly assigned to a behavioral parent-training intervention (n=10) or an enhanced standard medical care intervention (n=10) will be used in Study 2. For both studies, data will be obtained on child and parent mealtime behaviors, mealtime duration, calorie intake, parent perceptions of mealtimes, and weight. For Study 1 it is hypothesized that toddlers with CF and their families will exhibit more mealtime behavior problems than non-chronically ill toddlers and their families. Data from Study 1 will describe the specific eating problems exhibited by toddlers with CF. For Study 2 it is hypothesized that the behavioral intervention will result in significantly more improvement on behavioral variables such as toddler and parent mealtime behavior, greater calorie intake, and weight gain than the enhanced standard medical care intervention. The long-term objective of this programmatic research plan is to prevent and/or treat the early development of eating behavior problems for children with CF, and therefore decrease the morbidity and mortality associated with malnutrition in CF. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BETA 1 AND BETA 3 ADRENORECEPTORS Principal Investigator & Institution: Granneman, James G.; Psychiatry & Behav Neuroscis; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2001; Project Start 01-DEC-1993; Project End 31-MAR-2004 Summary: The beta3 adrenergic receptor (AR) has been proposed to be a therapeutic target for the treatment of obesity and adult-onset diabetes, and recent work has identified a polymorphism in the human beta3-AR gene that is associated with excess weight gain and insulin resistance. Beta3-AR are expressed almost exclusively in adipocytes where they are co-expressed with beta1-AR. The tissue-specific pattern of beta3-AR gene expression and its co-existence in adipose tissue with beta1-AR has raised several fundamental questions. First, the coexpression of beta1-and beta3-AR in fat cells implies that the beta3-AR subtypes serve different signaling functions in adipocytes, and recent evidence indicates that beta1- and beta3-AR have unique signaling properties and that these receptors activate distinct pathways in adipocytes. The organization of beta1- and beta3-AR signaling in adipocytes will be further characterized and specific hypotheses regarding the biochemical and cellular basis of that organization will be tested. Second, beta1- and beta3-AR exhibit several unique pharmacological and biochemical properties that are amenable to molecular analysis. A panel of epitope- tagged, mutated and chimeric receptors have been created that will allow validation of observations made in adipocyte and further dissection of the molecular bases of beta3-AR subtype-specific signaling properties. These analyses will include examination of the molecular pharmacology of aryloxypropranolamine and phenethanolamine agonists, compounds being developed as selective beta3-AR agonists. An understanding of how these compounds differentially interact with the beta 3-AR subtypes, and the impact of that interaction on receptor signaling is key to understanding their biological actions. Specific aims are: Aim 1. To investigate the
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biochemical organization of beta3-AR signaling in adipocytes. Aim 2. To further characterize the differential signaling properties of beta1- beta3-AR and to examine the cellular and molecular basis. Specific Aim 3. To examine the molecular pharmacology of beta3-AR-selective agonists. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIOCHEMICAL MECHANISMS OF IN VIVO INSULIN RESISTANCE Principal Investigator & Institution: Rossetti, Luciano; Professor; Medicine; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2001; Project Start 01-AUG-1994; Project End 31-JUL-2004 Summary: In this project, we propose to continue our investigation of the biochemical and molecular mechanism(s) by which "insulin resistance" is acquired. Our long-term focus has been on the potential link between nutrient excess and impairment of insulin action. In this regard, we have recently shown that increased nutrient (eg, carbohydrate and lipid) availability results in insulin resistance and in increased leptin gene expression via increased flux of carbons into the hexosamine biosynthetic pathway. We propose herein that a close loop feed-back regulation is normally operating between nutrients and their metabolic outcomes. Thus, nutrient excess is sensed via the hexosamine biosynthetic pathway and generates signals leading to decreased insulin action on glucose uptake and to increased leptin gene expression. They also favor increased storage into lipid via increased tissue levels of Malonyl-CoA and Long ChainCoA and ultimately increased adiposity and weight gain. However, the concomitant induction of leptin expression attempts to counteract this drive by antagonizing the effects of nutrients on Malonyl-CoA and triglyceride storage, on the hexosamine pathway and perhaps via direct effects on insulin signaling. Any disruption of this physiological response (due to either impaired stimulation of leptin expression by nutrients or to decreased effectiveness of leptin action on target tissues) is likely to lead to increased adiposity and more insulin resistance. Based on preliminary results and on this overall hypothesis we wish to pursue the following specific aims: 1. How do nutrients regulate insulin action? We will focus on the interaction between increased lipid availability and skeletal muscle insulin signaling and action. We hypothesize that the susceptibility to develop insulin resistance in response to excessive nutrient exposure is modulated by the skeletal muscle ability to utilize fructose-6-phosphate in the glycolytic pathway. 2. How does leptin modulate hepatic and muscle glucose/lipid metabolism and insulin action? We will examine whether specific hypothalamic targets of leptin play distinct roles in mediating its complex metabolic effects. 3. Is leptin synthesis and/or action modulated following prolonged stimulation? We will generate short-term models of relative hyperleptinemia and will test the hypothesis that the "protective" effect of leptin against nutrient excess wanes if the leptin signal/transduction system is chronically over-stimulated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BIRTH/CHILDHOOD CANCER RISK
WEIGHT
AND
PREGNANCY--BREAST
Principal Investigator & Institution: Nevanlinna, Heli; Georgetown University Washington, Dc 20057 Timing: Fiscal Year 2003; Project Start 22-SEP-2003; Project End 31-AUG-2008 Summary: The breast is suggested to be most sensitive to hormonal and dietary exposures during fetal life, puberty and pregnancy; i.e., when it is growing extensively.
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It has been shown that high birthweight and excessive pregnancy weight gain increase sporadic breast cancer risk. High body weight during childhood paradoxically reduces sporadic breast cancer risk. We hypothesize that familial breast cancer risk is also affected by birthweight, weight during childhood and early puberty, and pregnancy weight gain. The 525 breast cancer families included in this study have been identified and collected as a part of ongoing hereditary breast cancer research programs at the Helsinki University Central Hospital, Tampere University Hospital and Oulu University Hospital. All patients participating in the studies of inherited breast cancer have signed an informed consent giving also permission for a later contact concerning this research. Questionnaires will be mailed to 836 cases and information on birth weight, body size during childhood and pregnancy weight gain as well as reproductive history and lifestyle including current diet will be obtained. Cases will also be requested to forward a questionnaire to their close female family members (sisters or cousins) who have not developed breast cancer. These women will serve as controls. Another control group consists of 1,672 women diagnosed with sporadic breast cancer; i.e., they have no family history of breast cancer. Data for BRCA1- and BRCA2- mutation carriers, and member of all other families who are not carriers of either of these mutations will be analysed separately. The results will determine whether body weight at specific developmental periods alters penetrance of breast cancer in women at high familial risk. If any associations are found, novel dietary-based intervention strategies may be developed and implemented to prevent women at high familial risk from developing breast cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BREAST CANCER RISK REDUCTION IN AFRICAN AMERICAN WOMEN Principal Investigator & Institution: Fitzgibbon, Marian L.; Professor; Psychiatry and Behavioral Scis; Northwestern University Office of Sponsored Programs Chicago, Il 60611 Timing: Fiscal Year 2001; Project Start 10-JAN-2001; Project End 31-DEC-2002 Summary: (adapted from Investigator's abstract) Breast cancer is the leading cause of cancer death in African-American (AA) women. Breast cancer incidence is lower among AA than white women, however mortality rates are higher. Higher body mass index (BMI), lower adherence to recommended early detection behaviors, and lower socioeconomic status (SES) may contribute to these higher mortality rates. AA women are at great risk for obesity with more than 36 percent meeting the criterion for obesity (BMI 30 kg/m2). Weight gain and abdominal adiposity during adult life, especially excess weight in the years preceding diagnosis are increasingly recognized as important risk factors for breast cancer in postmenopausal women. Thus, reversal or prevention of weight gain could have a striking impact on mortality in AA women. Rates of breast screening at recommended intervals is substantially lower among AA than white women. In addition, AA women are more likely to live in poverty and have less access to medical care compared to white women, both of which have been shown to influence preventive health care behaviors and the stage of breast cancer at diagnosis. No study to date has simultaneously addressed both weight and breast health in an integrated intervention among low SES AA women. The proposed R21 pilot study was submitted in response to an RFA entitled "Exploratory grants in behavioral cancer control." The specific aims are to test the feasibility of a 20-week integrated intervention: 1) with 60 overweight low socioeconomic status AA women; 2) to produce a 7 percent weight loss through a reduction in dietary fat and increase fruit/vegetable consumption and physical activity and 3) to improve breast health practices (i.e., mammography, CBE,
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BSE). Results will be applied to the design of a larger intervention trial with intermediate biological endpoints. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CENTRAL OOBESITY SYNDROME IN A SUBSET OF TYPE 1 DIABETES Principal Investigator & Institution: Brunzell, John D.; Prpfessor of Medicine; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 01-SEP-1976; Project End 31-MAR-2007 Summary: (provided by applicant): Project 2 started as an ancillary study of lipoprotein metabolism to the NIH sponsored clinical trial of intensive diabetes therapy in type 1 diabetics to prevent microvascular disease called the Diabetes Control and Complication Trial (DCCT). The Epidemiology of Diabetes Intervention and Complications (EDIC) is a ten year non-interventional follow-up of DCCT to evaluate the natural history of macrovascular and nephropathy complications in type 1 diabetes. In DCCT, we found that atherogenic small dense LDL were increased with hyperglycemia, microalbuminuria and were increased in that subset of subjects who gained excess weight as a complication of intensive diabetes therapy during DCCT. Those who gained weight with intensive diabetes therapy were centrally obese, insulin resistant, hypertensive, dyslipidemic and had type 2 diabetic parents. This suggests they had inherited the metabolic-central obesity syndrome in addition to type 1 diabetes. This new proposal will use the phenotypes of 1) excessive weight gain with intensive diabetes therapy and 2) the presence of small dense LDL particles as markers of the central obesity-insulin resistance metabolic syndrome that occurred in this subset of type 1 subjects during intensive diabetes therapy. These markers of the central obesity syndrome will be used to predict the occurrence of cardiovascular events and the development or progression of microalbuminuria during the course of EDIC. Candidate genes for development of the central obesity syndrome and for the interaction of excess weight gain with the development of hypertension will be examined. Intraabdominal fat by CT scan and postheparin plasma hepatic lipase will be measured to further develop the phenotype associated with the excessive weight gain with intensive therapy and with development of nephropathy in the Seattle cohort and three Minnesota cohorts of EDIC. The development of the central obesity syndrome with intensive diabetes therapy in type 1 diabetic patients may predispose them to increased risk of cardiovascular disease and nephropathy. If so, modifications of clinical therapy will need to be made in this subset of individuals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CHILDHOOD PHARMACOGENETICS
ABSENCE
EPILEPSY
RX,
PK-PD-
Principal Investigator & Institution: Glauser, Tracy A.; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-MAY-2008 Summary: (provided by the applicant): The optimal treatment for Childhood Absence Epilepsy (CAE), a common pediatric epilepsy syndrome affecting 10-15% of all children with epilepsy, and the basis for the inter-individual variation in response to therapy, has not been defined. Commonly misperceived as a benign epilepsy syndrome, patients with CAE demonstrate variable response to therapy, exhibit cognitive deficits, and demonstrate long-term psychosocial difficulties. The objectives of this proposal are: 1) to
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identify the anti-epileptic drug (AED) that produces and sustains the highest rate of seizure control coupled with the lowest incidence of treatment limiting toxicity for children with CAE, and 2) to determine the pharmacogenetic and non-heritable factors underlying the inter-individual variation in AED efficacy and toxicity. A randomized, double-blind comparative trial of Ethosuximide (ETX), lamotrigi_ (LTG) and valproate (VPA) as initial monotherapy will be performed in children with CAE utilizing freedom from failure rate as the primary endpoint. Twenty sites in the U.S. will enroll 473 children, 2- 13 years of age, over a 3-year period. Treatment success will be defined as a composite of seizure control and short and long-term tolerability. Each AED's impact on cognition (especially attention), behavior, and quality of life will be studied. Each patient's epilepsy syndrome will be extensively phenotyped with video EEGs. Individual systemic drug exposures, determined using a population pharmacokinetic (pK) approach, will define the impact of interpatient variability in drug disposition on AED efficacy and toxicity, and will be utilized in pharmacogenetic (pG) correlative studies of select drug metabolizing enzymes. The role of polymorphic variation in the genes coding for the alpha1G, alpha1H, alpha1I subunits of the T type calcium channels in response to therapy will be investigated. Factors potentially predictive for the most common treatment limitations of each AED will be studied, including the pG, pK and clinical profiles of patients developing LTG associated rash, VPA induced weight gain or evidence of impaired neurocognitive skills (potential limitation of all AEDs). This study will determine the AED that provides for the greatest likelihood of seizure control coupled with the best short and long term tolerability. By comprehensively defining the phenotypic spectrum of absence seizures along with pG and non-heritable factors that underlie interpatient variability in AED response, this proposal will form the foundation of a pharmacologically rational approach to syndrome based AED therapy. Knowledge gained by this study will lead to individualized treatment for children with CAE that may in part be generalizable to other pediatric and adult seizure disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: APPROACHES
CLINICAL
TRIALS
IN
SCHIZOPHRENIA--MOLECULAR
Principal Investigator & Institution: Malhotra, Anil K.; Chief of Mol. Psychiatry; Long Island Jewish Medical Center 270-05 76Th Ave New Hyde Park, Ny 11040 Timing: Fiscal Year 2001; Project Start 01-SEP-1999; Project End 31-AUG-2004 Summary: This application for a Mentored Patient-oriented Career Development Award (K23) is to support the development of the candidate into a independent investigator capable of conducting large scale clinical trials in psychiatry that address issues of treatment efficacy and effectiveness in addition to serving as the clinical basis for pharmacogenetic studies. The development plan has four major goals: 1) Gain expertise in the design of a clinical trial in schizophrenia, 2) Participate in the execution of a clinical trial, 3) Utilize statistical methodology to analyze clinical trials studies, and 4) Conduct pharmacogenetic analyses of clinical trials data. To accomplish these aims, three major career development activities are proposed: 1) A didactic program to prepare the candidate to independently design, conduct, and analyze clinical trials, 2) Participation in a large clinical trial comparing new antipsychotic medications in patients experiencing their first episode of schizophrenia. This will involve the candidate's participation in the clinical trial as an investigator and will provide the opportunity to develop a pharmacogenetic protocol and, 3) The design, conduct and analysis of a pilot study of the effects of adding the serotonin re-uptake inhibitor, sertraline, to the antipsychotic treatment regimen of schizophrenia patients with
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treatment-refractory hallucinations. The research plan incorporates two studies. The first is a pharmacogenetic assessment of response to the antipsychotic agents olanzapine and risperidone. This study involves determination of genotype at specific candidate loci within the dopamine and Serotonin receptor systems and case-control and family-based association analysis between these loci and clinical phenotypes of treatment response, drug-induced weight gain and drug-induced extra pyramidal symptoms. The second study is a clinical trial examining sertraline augmentation in schizophrenia patients with hallucinations. The basis of this study is evidence from clinical trials research as well as molecular genetics. This represents an initial effort to utilize the two distinct methodologies to enhance the treatment of schizophrenia. The career development activities and completion of the research studies described in this application are expected to provide the candidate with the knowledge and research experience to develop into an independent investigator with the expertise to conduct high quality clinical trials that incorporate pharmacogenetics into psychiatry. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COMPUTER INTERVENTION FOR PREVENTION OF WEIGHT REGAIN Principal Investigator & Institution: Wing, Rena R.; Professor of Psychiatry; Miriam Hospital Providence, Ri 02906 Timing: Fiscal Year 2001; Project Start 01-SEP-2000; Project End 31-AUG-2005 Summary: Over half of US adults are overweight. Treatments are currently available to help these individuals lose wright, but most will regain their loss. Thus, a major problem in the treatment of obesity is prevention of weight regain. An innovative new approach that we believe may be particularly effective in preventing weight regain is the use of an interactive computerized intervention. We propose to use the Internet and e-mail to deliver an intervention that specifically focuses on a weight gain prevention and provides all of the basic components of a cognitive behavioral approach, including goal setting, self-monitoring, feedback, prompting, problem solving motivation enhancement reinforcement and social support. We believe that Internet interventions may be particularly useful for maintenance because frequent contact can be continued long-term with low cost and maximal flexibility; the anonymity may reduce embarrassment about weight gain; educational information can be provided when it is relevant to the participant; all aspects of the intervention can be individualized and tailored to the participant; data can be easily transmitted and analyzed for trends; immediate feedback can be provided to reinforces successful achievement and catch problems early; and participants can provide ongoing social support to each other. We will test this interactive computerized intervention (ICI) by recruiting 160 individuals who lost at least 10 percent of their weight in the past year. Prior studies suggest that individuals who lost weight just 1 year ago are at greatest risk of weight regain. We will purposely recruit individuals who have lost weight using various different approaches. These individuals will be randomly assigned to a no-treatment control condition or to use the ICI program for 18 months. Outcomes will be assessed at 6, 12, and 18 months. The primary outcomes will be weight change from 0 to 18 months and the proportion who regain less than 2.5 kg over 18 months. Adherence to the intervention and acceptability of the various components will be analyzed to determine the feasibility of delivering maintenance interventions via computer. The proposed ICI intervention is innovative because it explicitly focuses on prevention of weight regain; it is developed for individuals who have lost weight in a variety of ways and need help with maintenance of weight loss; it makes use of Internet and e-mail technology that has not
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Weight Gain
previously been applied to the area of the weight control (and certainly not to maintenance); and uses computer technology creatively to maximize the delivery of all of the basic components of a cognitive behavioral intervention for weight loss maintenance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CONSEQUENCES FLUCTUATIONS
AND
CORRELATES
OF
WEIGHT
Principal Investigator & Institution: Field, Alison E.; Assistant Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 01-JAN-1998; Project End 31-DEC-2002 Summary: (Adapted from Investigator's Abstract) In the United States, approximately one third of adult women are trying to lose weight. Most weight losses are not sustained and in fact may be followed by gains of at least as much weight as was intentionally lost. It is unclear whether there are adverse outcomes associated with multiple intentional weight losses. The major aim of this project is to quantify the association between multiple intentional weight losses (i.e., weight fluctuations) and the development of hypertension and diabetes mellitus among 50,790 female nurses participating in the ongoing Nurses' Health Study II. In addition to assessing the consequences of weight fluctuations, their correlates and course will be identified. Among these women, 4.4% report losing 20 or more pounds three or more times or 50 or more pounds at least once. To prospectively assess the risk of developing hypertension the investigators state they will have greater than 90% power using the first 2-year follow-up cycle. Because diabetes mellitus is less common, they state that they will need three follow-up cycles to have sufficient power. A prospective study that assesses the intentionality of weight loss and does not rely on prevalent cases or long-term recall of weight, weight loss intentions, and disease diagnosis is necessary to elucidate the relation of weight fluctuations to chronic disease morbidity. No previous studies have assessed the risk of developing disease associated with multiple weight losses, independent of the effects of important confounders such as smoking, intentionality of the weight loss, physical activity, relative weight, and weight change. The investigators point out that if intentional weight loss, one time or multiple times, is associated with increased morbidity, the public health implications are enormous. Instead of counseling overweight people to lose weight, efforts would need to be placed on preventing weight gain because both excessive weight gain and weight loss would be associated with increased risk. Conversely, if only unintentional weight loss is associated with increased risk, then the current recommendations for overweight people to lose weight or at least not gain weight would be appropriate. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CVD MECHANISMS ASSOCIATED WITH PHYTOESTROGENS USE Principal Investigator & Institution: Kritz-Silverstein, Donna C.; Associate Adjunct Professor; Family and Preventive Medicine; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2002; Project Start 01-APR-1997; Project End 31-DEC-2003 Summary: Estrogen replacement therapy has beneficial effects on heart disease risk factors. However, a large proportion of postmenopausal women are not compliant with therapeutic regimens. Phytoestrogens are naturally occurring compounds found in plants and soy products that have SERM-like effects. Although numerous studies have
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shown a beneficial effect of estrogens on lipids and lipoproteins, few examined other mechanisms by which phytoestrogens might exert a cardioprotective effect. Potential mechanisms include changes in homocysteine metabolism, inhibition in markers of inflammatory activity including interleukin-6 (IL- 6) and C-reactive protein (CRP), decreases in adhesion molecules such as E-selectin and decreases in obesity and body fat. Using new laboratory assays and previously collected data from 210 postmenopausal women in the Soy Health Effects (SHE) Study, this study will examine potential mechanisms other than lipids, by which phytoestrogens may reduce the risk of heart disease. The SHE Study is a randomized, double blind, placebo controlled study designed to determine the acceptability and benefits of a dietary supplement of phytoestrogen, specifically, genistein, on heart disease risk factors, bone density and psychosocial outcomes. Data was collected at screening, baseline, and periodic followups over the course of two years. Funds are requested to assay homocysteine, IL-6, CRP, and E-selectin in frozen sera; and analyze data from SHE Study visits as related to the proposed hypotheses. Cross-sectional and longitudinal comparisons of treatment and placebo groups will be performed before and after adjustment and stratification for covariates. It is expected that women treated with phytoestrogens will have lower homocysteine, IL-6, CRP, E-selectin, and decreased obesity and fat mass over 2 years; that obesity and weight gain will be positively associated with homocysteine, IL-6, CRP, and E- selectin; and that there will be an interactive effect of phytoestrogen use and change in obesity on homocysteine, IL-6, CRP and E-selectin. Given that women can expect to live one-third of their lives after menopause, it is important to know whether and how phytoestrogens may modify cardiovascular disease mechanisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEPO-PROVERA AND BONE DENSITY IN PREMENOPAUSAL WOMEN Principal Investigator & Institution: Clark, M Kathleen.; Associate Professor; None; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2001; Project Start 01-FEB-2000; Project End 31-JAN-2004 Summary: (Adapted from abstract): Registered nurses (RNs) and advanced practice nurses (APNs) play an important role in providing contraceptive services to women of reproductive age. Education and counseling regarding use, risks, and benefits of contraceptive choices are long-standing nursing interventions. With prescriptive authority, APNs are additionally responsible for providing safe, effective pharmacological interventions for preventing pregnancy. DMPA is a progestin only injectable contraception, approved for use in the US in 1992. Of concern is a potential adverse effect of DMPA on bone mineral density. Because DMPA disrupts the hypothalamic-pituitary-ovarian-axis (HPO), it theoretically will suppress estrogen production causing a relative estrogen deficiency, and corresponding loss of bone mineral density. The overall goals of this study are to determine the effect of DMPA on bone mineral density in women aged 18 to 30 years and to determine whether the effect can be modified by calcium intake or predicted by, baseline estradiol levels, irregular vaginal bleeding or weight gain. A two-year prospective longitudinal study of 275 women, 160 who are receiving their first DMPA injection, and 115 control subjects who are not using any hormonal method of contraception, will be completed. All participants will receive a baseline evaluation, and follow-up evaluations every three months for two years. At baseline, participants will have their bone mineral density of the femoral neck, lumbar spine and total body measured using dual energy x-ray densitometry (DEXA). Blood will be drawn for estradiol levels and other physical measurements completed.
24
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Participants will complete nutritional and physical activity assessments, as well as a comprehensive interview detailing demographic, medical reproductive and lifestyle behaviors that may influence bone mineral density. All participants will be given one 90-day menstrual calendar for the daily recording of vaginal bleeding. At each followup evaluation bone mineral density and body composition will be measured, nutrition and physical activity reassessed and components of the interview updated. The menstrual calendar will be collected, reviewed and new calendars provided. Random coefficient regression (RCR) analysis will be the major analytic strategy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DIABETES THERAPY TO IMPROVE BMI AND LUNG FUNCTION IN CF Principal Investigator & Institution: Moran, Antoinette M.; Professor; Pediatrics; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-MAY-2006 Summary: The majority of cystic fibrosis (CF) patients now survive beyond childhood, and CF related diabetes (CFRD), due to insulin deficiency, is common. CFRD without fasting hyperglycemia (FH) is found in 25 percent of CF adults and is associated with increased morbidity and mortality. BMI and pulmonary function deteriorate much more rapidly in these patients than in CF patients with normal glucose tolerance. Insulin deficiency alters protein and fat metabolism resulting in loss of weight and lean body mass and contributing to pulmonary disease and clinical decline. Preliminary isotopic data have shown that insulin and, to a lesser extent, the oral diabetes agent repaglinide acutely improve protein synthesis in patients with CFRD without FH. The objective of this research is to recruit 150 adult patients with CFRD without fasting hyperglycemia for a multi-center, twelve month, placebo- controlled intervention trial testing the ability of insulin or repaglinide to improve BMI and stabilize pulmonary function. It will test the hypotheses that: 1. Participants receiving either insulin or repaglinide will increase their BMI compared to control participants. 2. Insulin will be more effective than repaglinide at increasing BMI. 3. The increase in BMI will be primarily due to increased muscle mass. 4. The increase in BMI will be accomplished without significant changes in dietary macronutrient or calorie composition. 5. Insulin or repaglinide therapy will prevent pulmonary function decline compared to both control subjects and to their own baseline as measured the previous year. This will be associated with improvement in NIH clinical score and will be directly related to weight gain and increase in thigh muscle volume. 6. Participants receiving insulin or repaglinide will improve hand grip strength, and this will be directly related to weight gain and increase in thigh muscle volume. If it can be shown that insulin or repaglinide also improves body mass and pulmonary function, it would have a major impact on the current therapy and prognosis for adult CF patients. The question of whether these patients should receive diabetes therapy was given the highest priority for future research funding at a national consensus conference on CFRD Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DIETARY VARIETY VS DIETARY FAT EFFECTS ON ENERGY INTAKE Principal Investigator & Institution: Mccrory, Megan A.; None; Tufts University Boston Boston, Ma 02111 Timing: Fiscal Year 2003; Project Start 12-SEP-2003; Project End 31-JUL-2006
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Summary: (provided by applicant): The relative importance of dietary patterns vs. macronutrient composition in affecting energy intake and body weight remains uncertain. In this study we propose to investigate the relative effects of dietary variety versus dietary fat on voluntary energy intake in adults. Specifically, we will quantify and compare the effects of typical ranges of variety and fat intakes in the American diet (based on U.S. national survey data) on voluntary energy intake. The primary hypotheses to be tested are (1) an increasing availability of entree/side/snack/dessert variety offered will significantly increase voluntary energy intake in a dose-response fashion when other dietary factors known to influence energy intake are held constant (including macronutrient composition, palatability and variety of other food items); and (2) the separate effects of dietary variety and dietary fat on energy intake will be similar. Healthy, weight stable men and women (n=96, aged 18-45 y, BMI 20-35 kg/m2) will be recruited for a 39-d study in which food is provided. Three levels of entree/side/snack/dessert variety will be offered at each of three levels of dietary fat intake, and the relative effects of these dietary manipulations on voluntary energy intake, independent of potentially confounding dietary factors, will be quantified. Subjects will be assigned to one of three BMI-matched groups that will be offered either 4, 8 or 12 entree/side/snack/dessert items/d at one of three fat intake levels (20, 35, or 50 % of energy) in each of three 13-d phases. All diets will be matched for palatability, fiber, protein content, and the variety of other food items, and also for energy density at each fat intake level. Daily voluntary energy intake will be measured and dietary compliance monitored by using measurements of 24-h urinary PABA and osmolar excretion rates. Other measurements include food and meal palatability, hunger, desire to eat, dietary disinhibition, energy expenditure, and body weight and composition. We anticipate that the results of this investigation will lead to a greater understanding of the relative importance of eating patterns vs macronutrient composition in the etiology of obesity, and more specifically, dietary variety versus dietary fat in determining energy intake. Most importantly, it will help lay a foundation for improved dietary recommendations concerning weight loss and prevention of excess weight gain in adulthood. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EFFECT OF EXERCISE ON PREVENTION OF WEIGHT GAIN Principal Investigator & Institution: Jakicic, John M.; Associate Professor; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2003; Project Start 27-JAN-2003; Project End 31-DEC-2006 Summary: (provided by applicant): It is estimated that in excess of 50 percent of adults in the United States are overweight (body mass index >25 kg/m2). Of particular concern is the significant increase in the prevalence of obesity (body mass index >30 kg/m 2) over the past few decades. Exercise appears to be an important behavior for preventing and treating a number of chronic diseases, and the current public health recommendation for exercise is 30 minutes of moderate intensity activity on most days of the week (150 minutes per week total). However, it is unclear whether this level of exercise is adequate for preventing weight gain and the development of obesity. Therefore, the purpose of this study is to examine the effect of two doses of exercise on prevention of weight gain in moderately overweight adults. Two-hundred ninety four (294) subjects will be recruited to participate in this study. Subjects will be 18-50 years of age, with a body mass index ranging from 25.0 to 29.9 kg/m 2. Subjects will be recruited in three cohorts, with 98 subjects per cohort. Subjects will be randomly assigned to one of the following three treatment groups: 1) control, 2) moderate exercise, or 3) high
26
Weight Gain
exercise. All subjects will be followed for a period of 18 months. The control group will receive basic health information in a newsletter at 3 month intervals. Subjects in the moderate exercise group will progress to 150 minutes of at least moderate intensity exercise. Subjects in the high exercise group will progress to approximately 300 minutes of at least moderate intensity exercise. Subjects in both the moderate and high exercise groups will attend weekly behavioral sessions weekly for 6 months, and biweekly thereafter along with 1 telephone contact per month. The primary outcome of this study will be change in body weight from baseline to 18 months. In addition, subjects will undergo assessment of body composition (using DEXA) and cardiorespiratory fitness at 0 and 18 months. We will also assess changes in physical activity, diet, and potential mediators of change in behaviors at 3-month intervals throughout this study. The results of this study will have a significant impact on exercise recommendations for preventing weight gain in adults. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EXERCISE AND NICOTINE REPLACEMENT FOR FEMALE SMOKERS Principal Investigator & Institution: Kinnunen, Taru; Oral Health Policy & Epidem; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 15-APR-1999; Project End 31-MAR-2002 Summary: Each year nicotine addiction is responsible for more than 125,000 deaths of American women. In 1987, cigarette smoking related lung cancer surpassed breast cancer as the leading cause of death by cancer among women. The prevalence of smoking has declined more slowly for women than for men, suggesting that quitting smoking is more difficult for women. Factors that may contribute to the gender difference in cessation rates include women's greater tendency to smoke as a means of coping with negative affect, and their greater concern about postcessation weight gain. It seems clear that special interventions are needed to address these unique concerns of female smokers. Nicotine replacement therapy has shown some success in improving smoking cessation rates, reducing the severity of negative affect usually experienced during cessation, and, in the case of nicotine gum, minimizing postcessation weight gain. Aerobic exercise has also been found to improve mood and control weight. In combination, nicotine replacement therapy and aerobic exercise should be a powerful smoking cessation treatment for women. The proposed study will investigate the effects of an aerobic exercise intervention as an adjunct to nicotine polacrilex gum therapy. Three hundred female smokers will receive nicotine gum therapy and will be randomly assigned to an exercise intervention, an equal contact control condition, or a gum alone control condition. The exercise intervention will consist of three 45-minute sessions of aerobic exercise per week from 3 weeks precessation through 16 weeks postcessation. All participants will be followed for one year after cessation. In addition to determining the effectiveness of the adjunct exercise intervention on cessation rates, the mechanisms (e.g., relief of negative moods, suppression of cessation-related weight concerns, relief of premenstrual distress) by which exercise affects cessation will be examined. The proposed study will provide the first large-scale test of a very promising intervention to aid women in smoking cessation. The combination of an exercise intervention with nicotine replacement, which has not yet been investigated, should provide a particularly effective treatment program for female smokers. Intensive focus on the mechanisms by which exercise affects cessation will provide information essential both for understanding the nature of the relationship between exercise and smoking cessation, and for later refinement and enhancement of the exercise intervention.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FACILITATED UPTAKE OF LONG CHAIN FATTY ACIDS IN OBESITY Principal Investigator & Institution: Berk, Paul D.; Chief, Division of Liver Diseases; Medicine; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2001; Project Start 01-JAN-1998; Project End 31-DEC-2002 Summary: Obesity is a major public health problem for which current therapies are largely unsuccessful. Work in our laboratory has provided new insights into how fat accumulates in adipose tissue. These insights, in turn, suggest a potential new strategy for management of obesity. Specifically, we have shown that uptake of long chain free fatty acids (FFA) by selected cell types, including adipocytes, is not passive, as previously thought, but is a highly regulated transport process. Studies in adult homozygous (falfa) Zucker fatty rats and in the Zucker Diabetic Fatty (ZDF) strain have shown striking 9- to 13-fold increases in the capacity (Vmax) of adipocytes to take up FFA. By contrast, FFA uptake is unchanged in hepatocytes and only modestly increased in cardiac myocytes from these strains. The effect of these changes is to divert FFA progressively from tissues in which they are oxidized as fuel to adipose tissue where they are stored as fat. Studies in weanling animals reveal that the increase in adipocyte FFA uptake in Zucker pups procedes onset of obesity, increased plasma FFA, or increased adipocyte TNFalpha expression. While these conclusions are independent of the role of any particular FFA transporter, the increase in FFA uptake Vmax in Zucker adipocytes is highly correlated with mRNA levels for one of three cloned, putative FFA transporters, plasma membrane fatty acid binding protein. To determine if similar changes in FFA transport occur in diet-induced obesity, preliminary studies were conducted in three rat strains fed either a control or high fat (35 percent lard, 55 percent of calories) diet. There were no fat-induced changes in the FFA uptake Vmax in adipocytesof S 5B/Pl rats, but Vmax increased significantly in Sprague-Dawley and Osborne Mendel animals. Changes in adipocyte Vmax correlated with weight gain (r=0.91, p less than 0.01). Hepatocyte Vmax did not increase in any strain. The presence of tissue specific physiologic regulation of FFA uptake suggests that tissue-specific pharmacologic manipulatin might be feasible, reducing the propensity of adipocytes to store FFA as fat. To exploit this strategy requires that the physiological regulators of FFA uptake be determined. Preliminary data suggest that leptin may be a critical regulator of this process. We therefore have expressed rat leptin in the baculovirus system for use in future studies. Thus, the goals of this proposal are: to compare FFA uptake kinetics with other variables of interest in progressively younger pre-weaned falfa rats, to elucidate the evolution of the fatty phenotype; to better characterize the FFA transport and leptin responses to high fat intake in the rat models described; to define the effects of exogenous leptin on FFA uptake in different tissues and on specific FFA transporters in the rat; and to study FFA transport in normal and obese human adipocytes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FAMILY-BASED NUTRITION INTERVENTION FOR LATINO CHILDREN Principal Investigator & Institution: Killen, Joel D.; Associate Professor; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-JUL-2007
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Summary: (provided by applicant): We propose to test the efficacy of an intervention designed to prevent obesity in low-income, Mexican American children. MexicanAmerican children are more obese than other minority groups in the U.S. population, and are the fastest growing minority group in the U.S.A. Poor dietary practices, especially food habits that are acquired as families acculturate to the American food supply, are thought to be associated with children's excess weight gain. We propose to conduct a randomized clinical trial in which 250 families receive family-based behavioral counseling (FBC) sessions and 250 families receive an active placebo control intervention. Mothers and their second or third grade children from sixteen low-wealth elementary schools will be randomized into either the treatment or control interventions. The purpose of the FBC sessions is to change children's food environment. Specifically, we intend to increase the amount of fruit and vegetables, and decrease the amount of high fat foods available to children in their homes. In addition, we will encourage parents to model healthy dietary practices for their children. Two intervention strategies, a video, "What's to Eat?" designed specifically for this population, and photographs of each family's food practices, taken by family members, will be used in the counseling sessions. The control intervention will consist of group sessions using a curriculum that adapts the standard nutrition recommendations to traditional Mexican-American foods. Community health advisors will conduct the both the FBC and control sessions. The primary outcome of the trial is children's BMI. The secondary outcome is household food supplies. We hypothesize that within a one year timeframe, children's whose mothers are exposed to the FBC will have lower BMI's compared to children whose mothers receive the active placebo control intervention. The mechanism through which we intend to change weight status is altering the type of foods available to children in their homes. Therefore, two household food inventories, one collected prior to and one after the family's payday will be used as secondary outcomes. In addition, mothers' reports of household food security level, food purchase motives, and family food interaction will be collected as covariates. Measurements will be collected within one month of completing the interventions and at six months and one year follow-ups. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FAT GAIN AND CARDIOVASCULAR DISEASE MECHANISMS Principal Investigator & Institution: Somers, Virend K.; Professor; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): We propose a series of novel studies directed at establishing the effects of increased body fat in healthy individuals. We will determine the distribution patterns of increased body fat and how both increased body fat and fat distribution may affect blood pressure, as well as neural, vascular and inflammatory mechanisms which have been implicated in cardiac and vascular disease. We will study sedentary subjects with and without a family history of hypertension. These subjects will undergo a program of overfeeding with the objective of inducing a 2 kg fat gain. We will study these individuals before and after the 4-week fat gain program and subsequently after an 8-week period of weight loss and restoration of normal weight. Measurements will also be compared to those in a matched control group with and without a family history of hypertension, who continue their normal diet. We will test the following hypotheses: 1) Individuals with a family history of hypertension will gain more visceral and upper body fat and have greater blood pressure increases with overfeeding, compared to those without such a family history. 2) For all overfed
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subjects, increases in blood pressure, sympathetic activity and insulin resistance with fat gain will be most marked in those individuals with a predominantly upper body and visceral fat accumulation. 3) Upper body and visceral fat gain will also be associated with greater impairment in baroreflex sensitivity, endothelial function and chemoreflex function, and an increased likelihood of abnormalities during sleep, including higher nocturnal blood pressures and sleep disordered breathing. 4) Fat gain, particularly upper body and visceral, will be accompanied by enhanced production of inflammatory mediators linked to cardiovascular risk, including adhesion molecules and C-reactive protein. 5) The above changes will resolve with subsequent loss of weight and restoration of normal body fat. These studies build on established programs, one addressing obesity, sleep disordered breathing and cardiovascular disease directed by Dr. Somers, and the other examining mechanisms regulating body fat in humans, directed by Dr. Jensen. This integrated state-of-the-art approach will enable important and novel insights into interactions between fat gain and neural, vascular, and inflammatory cardiovascular disease mechanisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FOOD PREVENTION
SUBSTITUTION
FOR
CHILD
NUTRITION/OBESITY
Principal Investigator & Institution: Faith, Myles S.; Psychiatry; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Childhood obesity is increasing nationwide, is associated with serious health complications, and tracks into adulthood. However, controlled obesity prevention studies remain scarce. Behavioral-economics theory offers a novel framework for conceptualizing and designing such interventions. To this end, we propose a randomized controlled trial that tests the effects of a "Family-Based Food Substitutions" intervention - with and without a Home-Food-Provisions component - on long-term weight change in children at risk for obesity. Based on behavioral-economics theory, we predict that increasing fruit and vegetable intake will substitute for the intake of untargeted energy dense foods and thereby reduce weight gain in children at-risk for obesity. This effect is predicted to be enhanced among families provided home provisions of targeted fruits and vegetables. Participants will be 180 families of diverse ethnic background, with the target child being 4 to 6 years old and "at-risk" for obesity. Families will be randomized to one of the following three treatment groups: (1) Minimal Intervention Control; (2) Family-Based Food Substitutions (FBFS); or (3) FBFS with Home-Food Provisions. There will be 60 families per condition. Families assigned to the control group will receive nutrition education. Those assigned to the FBFS group will be trained in behavioral strategies that target increased child fruit and vegetable intake (e.g., role modeling and contingency management training for parents). Families assigned to the FBFS with Home-Food-Provisions group will receive the aforementioned package plus supplies of targeted fruits and vegetables to enhance their home accessibility. The primary outcome measure will be short-term and 2-year changes in the children's body composition. Secondary outcomes will include measures of dietary intake, parental food preparation skills, and fruit and vegetable accessibility. Mediator analyses will elucidate the mechanisms by which the intervention exerts its effect on changes in body composition. This investigation is designed to provide new insights into environmental manipulations that will induce food substitutions compatible with obesity prevention, while advancing behavioral-economics theory. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FROM PROGRAMMING
EMBRYO
TO
ADULT:
MECHANISMS
OF
FETAL
Principal Investigator & Institution: Fleming, Tom P.; University of Southampton Highfield Southampton, Timing: Fiscal Year 2003; Project Start 11-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): The major objective is to investigate the mechanisms by which mouse eggs and preimplantation embryos become susceptible to maternal low protein diet (LPD), and to determine how this condition may "programme" long-term abnormality in fetal and postnatal growth and development. The concept of egg/embryo sensitivity to environmental conditions has far-reaching healthcare implications (a) in relation to in vitro treatment for human infertility and (b) in the wider context of the established link between poor maternal nutrition and increased risk of adult onset disease, such as coronary heart disease, stroke and hypertension (fetal origin of adult disease hypothesis, FOAD). This hypothesis originated at our institution (University of Southampton), which has a faculty-wide, multidisciplinary, research strategy to identify FOAD mechanisms. Our past studies with rodents have demonstrated that maternal LPD during preimplantation development programmes low birth weight, abnormal growth and hypertension; current work, with our collaborators at the University of York, indicates that the balance of amino acids within the uterine lumen is altered by maternal LPD and may initiate the programming response. We have also developed an in vitro culture and embryo transfer model, which replicates the programming effects of the in vivo LPD diet model, to support investigation of mechanisms. We will use these models to determine the impact of maternal LPD on embryo amino acid content, turnover and selected transporter expression, and address the role of amino acid signaling in fetal programming. The in vitro model will allow for rescue and interventional experimental strategies to be tested. To investigate downstream pathways leading from egg/embryo manipulation and induction of programming using our models to impaired postnatal physiological status, we will conduct (a) fetal gene microarray analysis; (b) fetal/neonatal endocrine analysis using selected components of stress signaling, HPA axis and renin-angiotensin system, shown previously by our FOAD researchers to contribute to programming from sustained maternal LPD throughout gestation; (c) postnatal arterial vasoconstriction and dilation responsiveness for evidence of vascular dysfunction, and (d) behavioural analyses in offspring designed to identify early signs of neurological disease. Our multidisciplinary approach has been designed to provide the first integrative assessment of dietary programming mechanisms, from embryo to adult. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENE THERAPY, OBESITY AND HYPOTHALAMIC SIGNALING Principal Investigator & Institution: Kalra, Satya P.; Professor; Neuroscience; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2001; Project Start 01-JUN-1986; Project End 31-MAY-2006 Summary: (Scanned from the Applicant's Description): With one out of every two adult Americans rated as medically obese, obesity is the number one health problem in the United States. Since it is a major risk factor for heart disease, diabetes, stroke, hypertension, and morbidity, the treatment of obesity and associated diseases entails enormous medical costs. The major objective of this proposal is (1) to examine whether viral vector mediated delivery of weight-reducing signals, such as leptin, is a viable therapy (gene therapy), alternative to the pharmacologic approach, to control body
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weight (BW) gain for extended periods in normal male and female rats and in rodents with obesity due to environmental (diet-induced) and genetic factors. We believe that leptin acts by (1) augmenting energy expenditure (thermogenesis) and/or curbing appetite and (2) that the beneficial effects of leptin gene therapy are manifest at sites that enhance energy expenditure and modify hypothalamic appetite regulating signals such as the orexigenic signals, NPY, AgrP and GABA, and the anorexigenic melanocortin signal alpha-MSH, and intracellular signal transduction sequalae involving STAT3 and SOCS-3. We have successfully generated a recombinant adeno-associated virus (rAAV) vector to efficiently transfer the naturally occurring body weight reducing peptide, leptin (rAAV-lep). Aim 1: Examine the long-term (one-year) efficacy of rAAV-lep to reduce BW gain when delivered intracerebroventricular (icv) or systemically in out-bred Sprague-Dawley (SD) rats and obese rats maintained on a high-energy (HE) diet. Aim 2: Evaluate the efficacy of icv and peripheral rAAV-lep in those genetic models of obesity that (1) lack leptin (ob/ob mice) and (2) display resistance to peripheral and not central leptin (New Zealand obese mice); and (3) lack NPY (-/-) and display obesity when maintained on HE diet. Finally, we will also characterize the underlying mechanism(s) if excessive ectopic leptin itself induces leptin ineffectiveness (resistance) in these experiments. The causal mechanisms responsible for phenotype changes will be identified by evaluation of hypothalamic leptin expression and signaling through analysis of gene expression, and peptide levels, signal transduction sequalae (p-STAT3 and SOCS-3) and metabolic indices (body temperature, 24h urinary NE activity, oxygen consumption, UCP1 mRNA, and blood leptin, insulin glucose, and corticosterone levels). The outcome of these investigations will provide fundamental information on the broader potential of using gene delivery of naturally occurring anorectic molecules for BW control and their mechanism of action. This new knowledge will be applied to the ultimate goal of site-directed gene delivery aimed at the newly identified vulnerable loci in hypothalamic signaling to curb overeating and abnormal weight gain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENE, INTRAUTERINE ENVIRONMENT AND PCOS Principal Investigator & Institution: Dunaif, Andrea F.; Chief, Division of Women's Health; Northwestern University 633 Clark St Evanston, Il 60208 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2007 Summary: Polycystic ovary syndrome (PCOS) is among the most common endocrine disorders in premenopausal women. Women with PCOS have profound insulin resistance as well as pancreatic beta-cell dysfunction, independent of obesity and glucose intolerance. However, skeletal muscle insulin resistance reverse in cultured myotubes suggesting that insulin resistance in this tissue is induced by factors in the in vivo environment. We have recently shown that hyperandrogenemia is the reproductive phenotype in males as well as female relatives of PCOS women. Moreover, Urbanek and colleagues have shown (Project 2) that this phenotype appears to have a genetic basis in PCOS families and shows significant linkage and association with a marker locus on chromosome 19P in the region of the insulin receptor (allele 8 of D19S884). We now have extremely existing evidence that this allele is also associated with a metabolic phenotype in PCOS probands and their brothers: increased post-challenge glucose levels, apparent defects in insulin secretion, especially in response to sulfonylurea, and accelerated weight gain with age. Abbott (Project 3) has shown that in utero testosterone excess can reproduce many features of the PCOS reproductive and metabolic phenotype in female rhesus monkeys, including decreased insulin secretion and increased LH levels. Levine (Project 4) has shown that one mechanism for these changes is androgen-mediated
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sulfonylurea-stimulated insulin secretion by the pancreatic beta cells. Taken together, these observations have led to a new hypothesis for the etiology of PCOS: genetic variation resulting in hyperandrogenemia results in many of the reproductive and metabolic features of PCOS by fetal androgen programming. In this Project, we will test two components of the hypothesis. First, is the metabolic phenotype that is associated with the marker locus decreased insulin secretion, consistent with androgen-mediated suppression of K+/ATP channels? Second, is there in utero androgen excess, decreased fetal insulin secretion and/or intrauterine growth retardation (IUGR) in the female offspring of PCOS women, and does the marker allele identify a subpopulation of offspring with these findings? Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETICS OF ANTIPSYCHOTIC METABOLISM Principal Investigator & Institution: Ellingrod, Vicki L.; Clinical/Hospital Pharmacy; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2001; Project Start 17-AUG-2001; Project End 31-JUL-2006 Summary: (Investigator?s abstract): In this Mentored Clinical Scientist Development Award, Vicki L. Ellingrod seeks to gain expertise in the genetics of psychotropic medication metabolism, therapeutic response, and adverse effects (i.e., psychopharmacogenetics (PPG) expertise). This PPG expertise will allow her to systematically study the contributing factors for atypical antipsychotic induced weight gain (AAP wt gain) and other sequele of long-term AAP use. Her long-term career goal is to identify risk factors for psychotropic morbidity and develop interventions to reduce or prevent it. Dr. Ellingrod seeks to become one of the few pharmacogeneticists in this country focusing on drug metabolism and the occurrence of morbidity. For this proposal, Dr. Ellingrod has developed a program of training and research that utilizes a diverse array of resources at the University of Iowa College of Pharmacy and the College of Medicine?s Departments of Psychiatry and Epidemiology. Specific areas of mentorship and training include molecular genetic methods, pharmacokinetics and dynamics, clinical assessments used in schizophrenia research, the physiology of obesity, biostatistics, and bioethics. As part of this training, the candidate has arranged visits to meet with her mentors/consultants that specialize in these various areas of study. To augment her training, the candidate has developed a research proposal focusing on the genetics of AAP wt gain. More than 50 percent of patients on AAPs gain >10 percent of their initial wt, although some gain >40 percent. This wt gain often results in significant medical morbidity, substantial financial burden, and increased medication non-compliance. Little is known about the underlying mechanism for this wt gain. Identifying risk factors may prevent medical and financial morbidity, disease relapse, and improve overall quality of life (QOL) for patients with schizophrenia. Current research in this area does not take into account genetics, physiology, diet, and physical activity in a controlled manner. Based on pilot data provided by the candidate, she proposes a PG study of AAP wt gain in schizophrenia to examine the role of both genetic and physiologic risk factors in the mechanism behind this phenomenon. Specifically, the goals of this study are: 1) to determine the relationship of cytochrome P450 polymorphisms to wt measures and AAP serum levels. Patients with schizophrenia treated with quetiapine, risperidone, and olanzapine will be recruited and genotyped for CYP 2D6, 1A2, 3A4, 2C9, 2C19, and 2E1; 2) to genotype for polymorphisms of the B3 and 5HT receptors to determine the relationship between these polymorphisms and wt measures; 3) to measure serum levels of leptin, insulin, glucose, and homocystine over a year and examine their relationship to wt changes; 4)
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to serially measure wt, medication compliance, and QOL in patients receiving AAPs and examine the influence of wt on QOL and medication compliance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HEALTHY WEIGHT MANAGEMENT FOR BREAST CANCER SURVIVORS Principal Investigator & Institution: Rock, Cheryl L.; Professor; Cancer Center; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2002; Project Start 26-APR-2002; Project End 31-JAN-2004 Summary: Weight gain commonly occurs in women following the diagnosis of breast cancer. Post-diagnosis weight gain may increase risk for recurrence, and obesity at diagnosis of breast cancer is an established negative prognostic factor. Weight control is of great concern to many breast cancer survivors. Post-diagnosis weight gain is positively associated with energy intake and inversely related to physical activity level, suggest that behavioral strategies to reduce energy intake or increase exercise are likely to influence the long-term pattern of weight gain. Newer behavioral skills training programs to promote the adoption and maintenance of physical activity based on social learning theory have demonstrated success in other groups of inactive adults. Also, we have demonstrated than an intensive, innovative telephone-based counseling intervention can promote major changes in the dietary intakes for women at risk for breast cancer recurrence. The hypothesis to be tested in this exploratory project is that telephone-based counseling can also be useful in facilitating the adoption and maintenance of increased physical activity, and thus, promote weight loss in overweight and obese breast cancer survivors. One approach to healthy weight management emphasizes increased physical activity, improved body image, self- acceptance, and healthy eating attitudes and behaviors. The core content of the curriculum to be used in this project is based on a behavioral skills training program that has been shown to be effective in other target groups of inactive adults, with the incorporation of cognitivebehavioral techniques and emotional processing to promote acceptance and address the unique needs and characteristics of breast cancer survivors. The specific aims of this study are: (1) To examine the effect of a group- based program to increase physical activity and promote healthy eating attitudes and behaviors on measured weight change at the end of an intensive treatment period (16 weeks) and at one year, compared to a wait-list control group; (2) To examine the additional effect of individualized telephone counseling to increase physical activity and promote healthy eating attitudes and behaviors on measured weight change at the end of an intensive treatment period (16 weeks) and at one year, compared to the control group; and (3) To collect preliminary data on the change in level of physical activity that may be expected to occur in breast cancer survivors who participate in a group-based program and individualized telephone counseling to promote healthy weight management. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HYPOTHALAMIC NEUROTRANSMITTER SYSTEMS & EATING BEHAVIOR Principal Investigator & Institution: Leibowitz, Sarah F.; Associate Professor; Lab/Neuroendocrinology; Rockefeller University New York, Ny 100216399 Timing: Fiscal Year 2001; Project Start 01-APR-1988; Project End 31-MAY-2005 Summary: (adapted from applicant's abstract): Obesity is pervasive and growing in industrialized societies. One important factor known to contribute to this increase is the
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availability of high-fat or high-calorie diets. Another factor to consider is individual predisposition to weight gain, due to genetic or early environmental influences. The goal of this research is to use innovative approaches to examine the role of brain peptides in relation to diet and predisposition. These neurochemicals are galanin (GAL) and neuropeptide Y (NPY), which in the hypothalamus are known to stimulate eating behavior and reduce energy expenditure but whose specific roles in obesity still remain to be elucidated. One main objective of this research is to determine whether, in models of dietary obesity that mimic the human condition, these peptides have a causal relationship to disturbances in eating and body weight control. Specifically, it is hypothesized that: a) GAL, in specific neurons of the paraventricular nucleus (PVN) that project to the median eminence (ME), contributes to increased body weight gain and adiposity in response to a high-fat diet; and b) NPY, in neurons of the arcuate nucleus (ARC) that project to the PVN, induces weight gain in response to a high-calorie diet with excess carbohydrate. This research program has been broadened to include new experimental models and techniques; simultaneous analyses of behavioral, endocrine, metabolic and neurochemical parameters; and studies of different animal populations. The proposed experiments will investigate, in: 1) Specific Aim 1, changes in neurobiological and metabolic systems induced by overeating of high-fat or highcarbohydrate diets in rats; 2) Specific Aim 2, the differential traits of obese and lean rats on high-fat or high-carbohydrate diets in rats; 3) Specific Aim 3, conditions in which chronic stimulation with GAL or NPY induces overeating and increases body fat; 4) Specific Aim 4, neuropeptide function in normal-weight rats with differential propensity toward obesity on a high-fat diet; 5) Specific Aim 5, effects of acute peptide injection on endocrine and metabolic systems that affect body fat accrual; 6) Specific Aim 6, the neuroendocrine and metabolic mechanisms underlying changes in peptides in response to fat-rich or carbohydrate-rich meals; 7) Specific Aim 7, neuropeptide traits in obesityprone rats with higher insulin after a high-fat meal; and 8) Specific Aim 8, inbred mouse strains with different patterns of eating and weight gain. The overall objective of this research, in addition to defining the functional role of GAL and NPY, is to establish a program with different animal models, experimental strategies and multidisciplinary techniques that may broaden our perspective of brain function as it relates to energy balance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INHIBITORS OF 5ALPHA-REDUCTASE FOR ACNE THERAPY Principal Investigator & Institution: Li, Lingna; Anticancer, Inc. 7917 Ostrow St San Diego, Ca 92111 Timing: Fiscal Year 2002; Project Start 20-JUN-2002; Project End 31-MAY-2003 Summary: This application addresses the need for selective non-toxic for acne. Excessive 5alpha-reductase activity is found in acne vulgaris as well as androgenic alopecia (male pattern baldness). Numerous side effects occur from current treatments of these diseases both of which originate in the pilosebaceous unit. We have developed a selective, effective, topically applied 5alpha-reductase inhibitor to modify pathological processes in the pilosebaceous unit. For example, toward this goal, we have previously developed a selective topical liposome hair follicle targeting technology fo r genes and other large and small molecules. The present application will focus on our recent observation that the 5-alpha- reductase inhibitor N, N-diethyl-4-methyl-3-oxo-4-aza-5alpha- androstane17beta-carboxamide (4-MA) incorporated into liposomes selectively induces apoptosis and inhibits growth of the dihydrotestosterone (DHT)-dependent hamster flank organ sebaceous gland. With regard to selectivity, when non-liposomal 4-MA was topically
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applied, the selective efficacy was lost resulting in the on- targeted contralateral gland being affected. With regards to safety, liposome 4-MA did not significantly affect prostate weight, T/DHT ratios or body weight gain compared to controls indicating safety as well as efficacy of topical application of liposome 4-MA. We proposed here to develop topical liposomal 4-MAS as an anti-acne agent. The Specific Aims of this application are as follows: 1) Optimize efficacy of topical liposomal 4-MA to selectively induce apoptosis of sebaceous glands of male hamsters; 2) Determine pharmacokinetics of topical liposomal 4- MA to hair follicles of human scalp grafted into SCID mice and in the hamster sebaceous gland; 5) Determine safety of effective doses of liposomal-4-MA by detection of changes in DHT/T blood ratios in treated animals. In Phase II, selective efficacy and safety studies will be conducted on larger animals in order to enable liposomal 4-MA to enter the clinic as an anti-acne therapeutic. PROPOSED COMMERCIAL APPLICATIONS: Liposomal 4-MA will be developed as a topical selectively targeted therapeutic for acne for which they should be a very market. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LONGITUDINAL BREATHING/PREGNANCY
STUDY--SLEEP-DISORDERED
Principal Investigator & Institution: Pien, Grace W.; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 20-JAN-2002; Project End 31-DEC-2006 Summary: (prepared by applicant): Candidate's Plans/Training: The patient-oriented research in sleep medicine and epidemiology. Training will include closely mentored completion of the research protocol, advanced epidemiological course work in patientoriented research advanced training in sleep medicine and respiratory neurobiology. Environment: The University of Pennsylvania is a uniquely suited environment for this training award. The Center for Sleep and Respiratory Neurobiology will provide a mentored experience in patient-oriented research. The Center for Clinical Epidemiology and Biostatistics will provide advanced didactic training. Research: During pregnancy, physiologic changes including gestational weight gain take place that may place women at increased risk for the development of sleep-disordered breathing (SDB). Snoring, which is a common symptom of SDB, is a frequent complaint among pregnant women, experienced on a habitual b y as many as 23 percent of women by the end of the final trimester of pregnancy. The possibility regnant women snorers may manifest sleepdisordered breathing has remained largely unexplored. In general population, baseline obesity and weight gain are both associated with an increased risk for sleep-disordered breathing. It is our central hypothesis that pregnancy is a time of accelerated development of sleep disordered breathing in women, in which the degree of increase is likely to be larger in women with elevated baseline body mass index (BMI) or greater gestational weight gain. This protocol examines whether the number of sleepdisordered breathing events increases in women over the course of pregnancy and how baseline weight status and weight gain during pregnancy impact the degree of SDB. The specific aims of the study proposal are: 1) to test the hypothesis that the respiratory disturbance index (RDI), a measure of the number of abnormal respiratory events hourly during sleep, increases over the course of pregnancy; and to determine whether the degree of increase is greater in obese women; and 2) to identify specific clinical characteristics that influence the risk for clinically significant increases in the severity of SDB. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LUNG HEALTH STUDY--LONG TERM FOLLOW UP Principal Investigator & Institution: Altose, Murray D.; Chief of Staff (W); Medicine; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 01-FEB-1998; Project End 31-JAN-2003 Summary: The Lung Health Study (LHS), conducted from 1986-1994, demonstrated that a smoking intervention program in middle-aged long-term cigarette smokers can result in a highly significant beneficial effect on the rate of FEV1 decline over five years. However, FEV1 is only a surrogate marker for clinical outcomes of respiratory morbidity and mortality. The present study proposes long-term post-trial follow-up of former LHS participants to assess the incidence of morbidity and mortality from respiratory and cardiovascular diseases and other causes, as documented by hospital, clinic, and death records. A pulmonary function test 11 to 12 years after entry into the LHS is also proposed to determine long- term effects of the LHS smoking intervention program on lung function. The main objectives of the study are as follows: 1) to determine, using an intent-to-treat analysis, whether the LHS smoking intervention significantly reduces the incidence of clinically important respiratory and cardiovascular disease over a 12- to 15-year period following study enrollment; 2) to determine whether the beneficial effect of the smoking intervention program on measures of lung function persists through 11 to 12 years of follow-up; 3) to estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality, after controlling for smoking history; 4) to study the role of other factors (gender, airways reactivity, weight gain, and co- morbidities) in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality. All ten of the original LHS clinical centers plan to participate. To minimize bias, all surviving participants of the LHS will be invited to participate, giving a potential sample size of 5600. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LUNG HEALTH STUDY--LONG TERM FOLLOW-UP Principal Investigator & Institution: Bailey, William C.; Professor and Director; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 01-FEB-1998; Project End 31-JAN-2003 Summary: The Lung Health Study (LHS), conducted from 1986-1994, demonstrated that a smoking intervention program in middle-aged long-term cigarette smokers can result in a highly significant beneficial effect on the rate of FEV1 decline over five years. However, FEV1 is only a surrogate marker for clinical outcomes of respiratory morbidity and mortality. The present study proposes long-term post-trial follow-up of former LHS participants to assess the incidence of morbidity and mortality from respiratory and cardiovascular diseases and other causes, as documented by hospital, clinic, and death records. A lung function test 11 to 12 years after entry into the LHS is also proposed to determine long-term effects of smoking cessation on lung function. The main objectives of the study are as follows: 1) to determine, using an intent-to-treat analysis, whether the LHS smoking intervention significantly reduces the incidence of clinically important respiratory cardiovascular disease over a 12- to 15-year period following study enrollment; 2) to determine whether the beneficial effect of the smoking intervention program on measures of lung function persists through 11 to 12 years of follow-up; 3) to estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality, after controlling for smoking history; 4) to study the role of other factors [gender, airways, reactivity, weight gain,
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and co- morbidities] in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality. All ten of the original LHS clinical centers plan to participate. To minimize bias, all surviving participants of the LHS will be invited to participate, giving a potential sample size of 5600. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LUNG HEALTH STUDY--LONG TERM FOLLOW-UP DATA COORD CTR Principal Investigator & Institution: Connett, John E.; Professor; Biostatistics; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 01-FEB-1998; Project End 31-JAN-2003 Summary: The Lung Health Study (LHS), conducted from 1986-1994, demonstrated that a smoking intervention program in middle-aged long-term cigarette smokers can result in a highly significant beneficial effect on the rate of FEV1 decline over five years. However, FEV1 is only a surrogate marker for clinical outcomes of respiratory morbidity and mortality. The present study proposes long-term post-trial follow-up of former LHS participants to assess the incidence of morbidity and mortality from respiratory and cardiovascular diseases and other causes, as documented by hospital, clinic, and death records. A pulmonary function test 11 to 12 years after entry into the LHS is also proposed to determine long- term effects of the LHS smoking intervention program on lung function. The main objectives of the study are as follows: 1) to determine, using an intent-to-treat analysis, whether the LHS smoking intervention significantly reduces the incidence of clinically important respiratory and cardiovascular disease over a 12- to 15-year period following study enrollment; 2) to determine whether the beneficial effect of the smoking intervention program on measures of lung function persists through 11 to 12 years of follow-up; 3) to estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality, after controlling for smoking history; 4) to study the role of other factors [gender, airway reactivity, weight gain, and co- morbidities] in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality. All ten of the original LHS clinical centers plan to participate. To minimize bias, all surviving participants of the Lung Health Study will be invited to participate (potential sample size, approximately 5600). As in the preceding Lung Health Studies, the Data Coordinating Center will be within the Diversion of Biostatistics, School of Public Health, at the University of Minnesota, and will have full access to all records and data from the previous LHS projects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SMOKERS
MAINTAINING
ABSTINENCE
IN
CHRONIC
CIGARETTE
Principal Investigator & Institution: Hall, Sharon M.; Professor & Vice Chair; Langley Porter Psychiatric Institute; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): The overall goals of this line of research are to treat chronic cigarette smokers and to understand the processes related to smoking and relapse in these smokers. Combined treatment with antidepressants, nicotine replacement therapies (NRT), and psychological intervention produces high initial abstinence rates. Our ongoing work suggests that extended treatment can maintain
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these rates, achieving abstinence rates greater than or equal too 60% at one year. A series of hypotheses about the efficacy of extended antidepressant treatment and an empirically based behavioral relapse prevention intervention will be tested. There are five experimental conditions. Chronic smokers (N=400) receive 12 weeks of combined pharmacological treatment (sustained release bupropion + nicotine patch) and psychological intervention, and then are randomly assigned to one of five conditions in a placebo-controlled, double-blind design: (1) 40 weeks active bupropion with medical management (Active/MM); (2) 40 weeks placebo drag with medical management (Placebo/MM); (3) 40 weeks bupropion + behavioral relapse prevention (Active/RP); (4) 40 weeks placebo + behavioral relapse prevention (Placebo/RP); (5) no farther treatment (Brief Treatment). The innovative behavioral relapse prevention intervention will focus on five areas generally agreed to be important post-cessation. These are fluctuating motivation, depression, withdrawal/dependence, weight gain and social support. Participants will be assessed at baseline on smoking behavior, nicotine dependence, psychiatric diagnosis, demographics and measures of anger, anxiety, depression, mood disturbance, social support, stress, health status, motivation for change, and drug and alcohol use. At weeks 12, 24, 36, 52, 64, and 104, participants will be assessed on selfreports of smoking verified by carbon monoxide and anatabine/anabasine assays, as well as on psychometric measures. The proposed research will address significant issues in the treatment of poor prognosis smokers, including the development of strategies to maintain abstinence, determination of the efficacy of extended pharmacological treatment, and determination of the efficacy of a behavioral relapse prevention intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MENTORED CLINICAL SCIENTIST DEVELOPMENT AWARD Principal Investigator & Institution: Fernandez, Isabel D.; Assistant Professor/Epidemiology; Community and Prev Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2001; Project Start 20-SEP-2000; Project End 31-AUG-2005 Summary: The overall goal of this career development plan is to establish an independent research program in the epidemiology of obesity in children at the University of Rochester School of Medicine. Prevalences of overweight and obesity are rising in the United States, especially among females of low socioeconomic status and racial/ethnic minorities. Pregnancy has been described as a life event in which excessive weight can be gained and subsequently retained. Thus, research and training activities will concentrate on the identification of the independent and joint determinants of gestational weight gain and post-partum weight retention in adolescents and young adults of different racial/ethnic groups as major determinants of overweight and obesity in women. The specific aims are: 1) To establish a systematic training program in adolescent nutrition and behavior, special nutritional needs of pregnant adolescents, measurement of nutritional status in pregnant and non-pregnant adolescents, statistical analysis of longitudinal and multi-level data, and measurement and analysis of community-level variables; 2) To analyze cross-sectional and longitudinal data on biological, sociodemographic, behavioral, and community-level determinants of pregnancy weight gain and post-partum weight retention m women from the New York State Regional Perinatal Data System and the Coronary Artery Risk Development in Young Adults study (CARDIA); 3) To design an observational prospective study of adolescents and young adults to identify the biological, behavioral, sociodemographic, psychological, and community-level determinants of pregnancy weight-gain and post-
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partum weight retention among racial/ethnic minorities. The proposed career development activities involve training in the measurement and interpretation of body composition; in reproductive, behavioral/mental health, and nutrition and healthy lifestyle issues in adolescents; in Responsible Conduct of Research; and in longitudinal and qualitative data analysis. At the end of the training program, the candidate will be an independent investigator in the field of pediatric nutrition epidemiology. The clinical and public health significance of this proposal are based on a report from the Institute of Medicine suggesting that African-American women and adolescents gain in the upper end of the recommended weight-gain during pregnancy, a warning in the literature as to the health risks to young adolescents of retaining weight gained during pregnancy, and a national goal of reducing health disparities among Americans. In addition, there is a scarcity of empirical longitudinal data on the differential determinants of pregnancy weight-gain and post-partum weight retention in adolescents of various socioeconomic and racial/ethnic minorities. Examining biological, sociocultural, and community-level factors that may differ among specific population subgroups becomes relevant in order to tailor strategies which prevent post-partum weight retention without threatening either the mother's or the newborn's health. Given the adverse health effect of obesity and the difficulties involved in maintaining weight loss, primary prevention of obesity is of particular public health importance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MENTORED DEVELOPMENT AW
PATIENT-ORIENTED
RESEARCH
CAREER
Principal Investigator & Institution: Burklow, Kathleen PhD.; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2005 Summary: (Adapted from the applicant's abstract): The CAP candidate, Dr. Kathleen A. Burklow, is entering her third year in an assistant professor faculty position. This award is expected to help her develop the skills necessary to develop clinical trials of behaviorally-based feeding interventions using randomized controlled designs that focus on prevention and treatment of feeding problems and the associated physical and psychological morbidity in preterm infants. Specific objectives of the award are to: 1) broaden the understanding of the impact of physiological, developmental, medical, and parent-child interaction factors; and 2) design empirically-based assessment methodologies to quantify clinical data to facilitate the development of behaviorallybased, family-sensitive interventions to treat and/or prevent feeding problems in preterm children. The candidate proposes a five-year training program with mentors from a strong pediatric research department. Her primary mentor is a very experienced pediatric psychology researcher whose work has focused on the implementation of behaviorally-based nutrition interventions designed to improve weight gain in children with cystic fibrosis. Co-mentors represent subspecialty divisions that are directly relevant to the research and career development plan. The career development plan describes activities focused on enhancing scientific knowledge of research-related approaches to the treatment of feeding problems in the preterm population. These activities will include course work, independent studies, and guided clinical observations. Other activities in the plan include training in the responsible conduct of research and mentored experiences with preparation of grant proposals for independent research support. The candidate's proposed research involves two projects. Study 1 is an assessment study comparing child behaviors and care giver-child feeding interactions of preterm infants and healthy controls at two pivotal developmental stages (introduction
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to solid feeding and acquisition of self- feeding). Study 2 is a pilot study designed to evaluate the efficacy of a behaviorally-based feeding intervention intended to teach care givers how to manage feeding problems in toddlers with histories of prematurity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: METABOLIC CONSEQUENCES OF SICKLE CELL ANEMIA Principal Investigator & Institution: Buchowski, Maciej S.; Associate Professor; None; Meharry Medical College 1005-D B Todd Blvd Nashville, Tn 37208 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2006 Summary: (Applicant?s abstract) Homozygous sickle cell disease (HbSS), known also as sickle cell anemia, results from inheritance of the sickle cell Betas-globin gene from both parents and is characterized usually by marked clinical severity. Many children with HbSS have delayed growth and sexual development. The reason for the delayed growth and associated poor weight gain is not well understood but it might be associated with the increased requirement for energy. The underlying physiological mechanism of this increase could be in part explained by the accelerated synthesis of new red blood cells (RBCs) and the altered catabolism of irreversibly sickled RBCs. However, how these metabolic events develop and progress during the accelerated growth occurring in HbSS adolescents is unknown. The central hypothesis of this application is that increased whole-body protein turnover and increased cardiac output, resulting in increased energy expenditure for basal needs and physical activity, divert energy and protein from normal growth pathways in HbSS adolescents. The rationale for the proposed research is that quantifying energy and protein needs ad finding the underlying mechanism(s) for stunting will lead us to establishing nutritional recommendations and designing specific supplementation for HbSS children and adolescents. The specific aims are: 1) to determine how much energy and protein is needed for optimal growth in adolescents with HbSS; 2) to explain how growth rate in HbSS adolescents is altered by increased demands for energy caused by higher whole-body protein turnover, and increased cardiac output; and 3) to quantify how much energy and protein is required for daily physical activity in adolescents with HbSS. In the proposed longitudinal study of HbSS adolescents, energy and protein balance will be measured in a controlled environment and assessed in free living. At regular intervals, all components of energy expenditure and the total 24-h energy balance will be measured continuously inside a whole-room indirect calorimeter while using stable isotopes techniques for assessing protein kinetics. Healthy (HbAA) adolescents matched initially for Tanner stage of sexual development, gender, and race will serve as controls in all experiments. The proposed research is significant, because it is expected to result in new guidelines for nutritional management of adolescents with HbSS that will significantly improve their growth rate and attendant weight gains. In addition, what is learned from this research will contribute to broader understanding of how HbSS affects energy and protein metabolism, how these changes alter growth in HbSS adolescents, and what underlying physiological mechanism(s) are involved. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MINNESOTA OBESITY CENTER Principal Investigator & Institution: Levine, Allen S.; Professor; Psychiatry; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 30-SEP-1995; Project End 31-AUG-2005
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Summary: The mission of the Minnesota Obesity Center is to find ways to prevent weight gain and secondarily the onset of obesity and complications of obesity. Obesity is clearly a major source of illness and death, and is the most common nutritional ailment in the United States. Despite its prevalence, there is little known about effective measures to prevent obesity, and therefore its attendant complications. Further, it is well known that obese individuals can more easily lose weight than maintain the loss. It now seems clear that the emphasis should be prevention of initial weight gain, and failing that, prevention of regain after weight loss. With the mission of prevention defined, our vision establishes three goals: 1) find the underlying problems that lead to obesity, 2) identify behaviors that lead to obesity and find ways to help change those behaviors, and 3) determine public health and public policy measures that will reduce the frequency and severity of obesity. Our Center is primarily a research center, so we plan encouragement and support of studies directed at these aims. With respect to these goals, the role of our center is to: assist principal investigators in conducting relevant research by providing resources through the core system; stimulate new interest in collaborations in research into obesity, eating disorders and energy metabolism; support new research efforts in these areas related to obesity; and support education in obesity and eating disorders in our academic and public communities. The Minnesota Obesity Center has a strong and diverse research base consisting of 46 active investigators with 87 funded projects in obesity, energy metabolism and eating disorders, generating over 18 million dollars per year in grant support for their investigations. We propose the establishment of four core facilities including: 1) Administration will provide vision, leadership, and oversight of other core activities, 2) Basic Mechanisms Core will provide molecular biologic support for studies of nutritional affects on gene expression in a variety of tissues and support the emerging interest in linking epidemiological and behavioral intervention studies available to ONRC participants, 4) Human Metabolic Core Laboratory will provide access to established and state-of-the-art methods for studying energy metabolism and nutrient partitioning all the whole body level in humans. In addition, resources for pilot/feasibility projects and an educational program have been established. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MODERATE EXERCISE TO AID SMOKING CESSATION IN WOMEN Principal Investigator & Institution: Marcus, Bess H.; Professor of Psychiatry & Human Behavior; Miriam Hospital Providence, Ri 02906 Timing: Fiscal Year 2001; Project Start 17-APR-1998; Project End 31-AUG-2004 Summary: (adapted from investigator's abstract): Lung cancer rates now exceed breast cancer rates as the leading cause of death by cancer among women. Furthermore, smoking prevalence rates among women are declining at a slower rate than men and approximately 23% of women still smoke. One important reason why women do not attempt and/or succeed at smoking cessation may be fear of post-cessation weight gain. However, combined smoking cessation and weight control treatments have not been successful at decreasing post-cessation weight gain or enhancing achievement of smoking cessation. Exercise offers a healthful alternative to smoking, which may allay women's fear of weight gain. Exercise facilitates regulation of body weight, moderates mood changes, aids in decreasing responses to stress, and is incompatible with smoking. The proposed study will test the hypothesis that moderate intensity exercise enhances the achievement and maintenance of smoking cessation among healthy adult female smokers. This is a randomized controlled clinical trial comparing two conditions: (a) cognitive-behavioral smoking cessation plus moderate exercise and (b) cognitive-
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behavioral smoking cessation with equal contact time. The treatment is delivered over 12 weeks. A sample of 224 subjects will be recruited, treated for twelve weeks and followed for 12 months. This design permits separation of the effects of physical activity from the effects of frequent contact with staff and other subjects. Smoking cessation outcome (7 day point-prevalence) will be verified by saliva cotinine. Exercise adherence will be validated by attendance at supervised sessions, exercise monitors, and maximal exercise testing. Secondary analyses of hypothesized mediators (weight and/or weight concerns, negative affect, withdrawal symptoms, self-efficacy, motivation) of the effect of moderate exercise on smoking cessation will also be examined. Successful smoking cessation in women could significantly reduce chronic disease mortality in this group. Although intensive, this kind of program could have advantages over pharmacologic treatments and/or could be made more disseminable and cost-effective, but only if the initial results of this rigorous trial are promising. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MODIFYING THE HOME T.V. WATCHING ENVIRONMENT Principal Investigator & Institution: Epstein, Leonard H.; Professor; Pediatrics; State University of New York at Buffalo Suite 211 Ub Commons Amherst, Ny 14228 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Television, computer games and the internet are common components of the home environments of most children. Sedentary behaviors such as watching television and movies and playing video games are associated with the increased prevalence of pediatric obesity. Controlled laboratory and clinical research has shown that reducing these sedentary behaviors is associated with reductions in percent overweight in those who are obese and decrease in rate of BMI increase in nonobese children. There has been no research designed to test the influence of reducing television watching and other sedentary behaviors on prevention of obesity or further weight gain in overweight or obese youth. The aim of this study is to test an innovative environmental intervention designed to modify the home television watching and computer game use environment in contrast to a control condition. Seventy-two overweight or obese 4-7 year-old boys and girls will be randomized to an environmental intervention that focuses on reduction of television and home movie watching and computer games versus a control intervention. The environmental intervention is designed to gradually reduce targeted sedentary behaviors to 50% of baseline levels. We hypothesize that reducing sedentary behaviors will result in a stabilization or smaller increase in BMI in comparison to an untreated control group followed over two years. In addition, we predict lower energy intake for those in the intervention versus control groups, and an increase in physical activity when sedentary behaviors are decreased for the intervention group, and a further decrease in physical activity as the children in the control group become older. We also predict that children who often eat in association with targeted sedentary behaviors will show the largest decreases in energy consumed when sedentary behavior is decreased, and that children with a high baserate of targeted sedentary behaviors and low baserate of physical activity will be more likely to increase physical activity when sedentary behaviors are reduced. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NEURAL SUBSTRATES OF PEPTIDE INDUCED SATIETY Principal Investigator & Institution: Ritter, Robert C.; Professor of Physiology and Neuroscience; Vet & Comp Anat/Pharm/Physiol; Washington State University 423 Neill Hall Pullman, Wa 99164
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Timing: Fiscal Year 2004; Project Start 01-APR-1984; Project End 31-DEC-2007 Summary: (provided by applicant): The overall goals of this work are to define the neural mechanisms through which gastrointestinal peptides, especially cholecystokinin (CCK), reduce food intake and ultimately to appreciate how these substrates are involved in the physiology and pathology of food intake and body weight. CCK is released by intestinal mucosal I cells, in response to nutrients in the intestine. CCK also is synthesized and secreted by discrete populations of neurons in the brain. Recent evidence suggests that in addition to controlling the size of individual meals, CCK may also contribute to the control of long-term food intake and body weight gain. The mechanisms by which CCK contributes to control of long-term food intake and body weight gain have not be investigated. However, recent findings suggest that control of long-term food intake and body weight is facilitated by synergistic interactions between CCK and the fat cell hormone, leptin. In addition, preliminary results from our laboratory indicate that CCK receptors in the hypothalamus play an integral role in the control of long-term food intake and body weight by CCK. The experiments proposed in the attached application will investigate the participation of CCK and CCK receptors in the control of long-term food intake and body weight by testing three hypotheses. First we will use surgical and intestinal infusion methodology to test the hypothesis that exogenous CCK and endogenous CCK both enhance the effect of brain leptin on weight loss and reduction of food intake by actions on capsaicin-sensitive afferent neurons and CCK-A receptors. Second, using intestinal, arterial and intravenous peptide infusions we will test the hypothesis that leptin acts directly on vagal afferent neurons alone and/or in concert with CCK to reduce short-term food intake and enhance leptin effects on long-term food intake. Finally, we will us a novel targeted toxin to selectively destroy specific populations of brain neurons that express CCK receptors, in order to test the hypothesis that discrete populations of CCK receptive hypothalamic neurons participate in control of long-term daily food intake and body weight gain. These experiments are intended to explore an expanded role for control of body weight by both central and peripheral CCK receptors. Such a role could well be of seminal importance to understanding the mechanism by which body weight and food intake are controlled in health and disease Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NICOTINE AND SMOKING CESSATION IN SCHIZOPHRENIA Principal Investigator & Institution: Evins, Anne E.; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2006 Summary: (Applicant's Abstract) This proposal focuses on providing the candidate with the expertise needed to bridge several disciplines in the study of pharmacologic and behavioral interventions in the treatment of nicotine addiction in schizophrenia. Nearly 90 percent of patients with schizophrenia smoke cigarettes compared to less than 25 percent of the general U.S. adult population. Compounded by the problem that patients with schizophrenia are less likely to receive adequate routine and preventative medical care, heavy smoking represents a significant and neglected public health problem for people with schizophrenia. In pilot trials, the candidate found bupropion SR to be safe and effective for smoking reduction and cessation in patients with schizophrenia while improving negative and depressive symptoms and preventing weight gain and exacerbation of psychosis. In the proposed study, 60 subjects with schizophrenia who smoke greater than 10 cigarettes per day and wish to quit smoking will be randomized, in double blind fashion, to receive either bupropion SR or placebo for twelve weeks,
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combined with a nine week cognitive behavioral Quit Smoking Group Therapy Program modified by the candidate for patients with schizophrenia. The primary outcome measure is 7-day point prevalence of greater than or equal to 50 percent smoking reduction at the end of 12 weeks treatment that is biochemically confirmed. Secondary outcome measures are 7-day point prevalence tobacco abstinence at the end of the 3 month treatment and 3 month follow up phases, sustained tobacco abstinence or reduction, change in psychiatric symptoms, cognitive functioning, weight, side effects and health related quality of life. Career Development Plan: The candidate will build upon her experience conducting treatment trials for negative symptoms of schizophrenia. With consultation from individuals with the appropriate expertise, the candidate will design, implement and interpret pharmacologic intervention trials for smoking cessation in schizophrenia, study of cognitive behavioral therapy interventions in patients with the dual diagnoses of addiction and major mental illness, study of harm reduction strategies in patients with schizophrenia unable to attain abstinence, and studies of the effect of nicotinic agents on attention and memory in schizophrenia that will lay the foundation for future independent investigation by the candidate in these areas. The mentored investigative work will take place at the Massachusetts General Hospital and will complement an intensive training program of coursework at the Massachusetts General Hospital and the Harvard School of Public Health on methodology, epidemiology, statistics, and responsible conduct of research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NIDDM SUSCEPTIBILITY GENES IN A BIRACIAL COHORT Principal Investigator & Institution: Brancati, Frederick L.; Associate Professor; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-JUL-2004 Summary: (Adapted from the Investigator's Abstract) Type 2 diabetes mellitus and its atherosclerotic complications impose a substantial burden on health of Americans in general and on African Americans in particular. Recent discoveries in molecular genetics have lead to the identification of functional variations in several candidate genes for susceptibility to obesity, insulin resistance, and/or diabetes. These include genes which code for beta-2and beta-3 adrenergic receptors, insulin receptor substrate 1, fatty acid binding protein 2, frataxin, and leptin receptor. If their role as novel susceptibility factors is confirmed, these variants promise to illuminate the pathophysiologic basis of diabetes and diabetes related cardiovascular diseases, accelerate the development of chemopreventive agents, and facilitate the conduct of prevention trials by marking individuals at high risk. Unfortunately many previous association studies of these mutations in human populations have been limited by small, selected study samples; by limited cross-sectional data on behavioral factors and on cardiovascular risk phenotype; and by paucity of data on African Americans. The investigators, therefore, propose to conduct an epidemiologic study of functional variants in 10 candidate genes for susceptibility to type 2 diabetes, obesity, and insulin resistance. The main objective will be to detect modest effects consistent with polygenic nature of diabetes but with better sensitivity and precision than previous association and linkage studies. The study sample will a community based cohort of 3,250 African Americans and 3,250 Whites aged 45 to 64 who are participants in the ongoing Atherosclerosis Risk in Communities (ARIC) study. Supported by NHLBI the ARIC study has assembled an extensive data base including behavioral assessment (e.g. diet and physical activity), anthropometry, laboratory blood tests (e.g. oral glucose tolerance test and serum lipids), and carotid ultrasonography as well as clinical events and
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mortality. Using race specific case-control, cross-sectional, and longitudinal analyses the investigators will determine if these putative diabetes alleles are associated with incident and prevalent diabetes, with obesity and weight gain, with hyperinsulinemia in non-diabetic individuals with the presence of an adverse cardiovascular risk factor profile, and with atherosclerosis progression and cardiovascular disease incidence over 12 years of follow up. The investigators will assess how behavioral and environmental factors such as obesity, diet, and physical activity, influence the expression of genetically conferred risk. Strength of this proposal include the close collaboration between clinical, epidemiologic, and laboratory researchers, a wealth of prospectively collected data from an NIH sponsored study, and a sample size large enough to detect modest gene effects and to investigate gene-gene and gene-environmental interactions. Most important, this study will provide unique information on the expression of diabetes susceptibility genes in the general population and possibly suggest genetic explanations for the excess prevalence of type 2 diabetes and obesity in African Americans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NONINVASIVE VENTILATION IN CHILDREN WITH CYSTIC FIBROSIS Principal Investigator & Institution: Marcus, Carole L.; Professor of Pediatrics; Children's Hospital of Philadelphia 34Th St and Civic Ctr Blvd Philadelphia, Pa 19104 Timing: Fiscal Year 2003; Project Start 09-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): Cystic fibrosis (CF) is the most common, lifeshortening genetic disease in Caucasians. The vast majority of patients die from cardiorespiratory failure. Although most patients now live into early adulthood, a third will die before their 21st birthday. Noninvasive positive pressure ventilation (NIPPV) has been used effectively to treat respiratory failure in adults with chronic lung disease. However, there have been no controlled, prospective studies of the use of NIPPV in delaying the onset or progression of chronic respiratory failure in children with CF. We hypothesize that early intervention with noninvasive positive pressure ventilation improves daily function and quality of life, and delays the onset of respiratory failure, in patients with cystic fibrosis. Specifically, in children and adolescents with severe CFrelated lung disease treated with NIPPV, compared to matched controls, we predict (1) An improvement in respiratory function, as evidenced by a slower rate of decline of pulmonary function tests, better exercise tolerance, improved ventilatory muscle endurance and improved gas exchange during wakefulness and sleep; (2) An improvement in nutritional and metabolic status, as evidenced by weight gain and a decreased resting energy expenditure; and (3) Improved quality of life, better quality of sleep and a decreased number of pulmonary exacerbations. This study will be the first to use a prospective, randomized, double-blinded design to comprehensively evaluate the effects of NIPPV in pediatric patients with CF. In keeping with the mission of the RFA, this study will use a multidisciplinary approach to improve management and enhance the quality of life in children with chronic respiratory failure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: OBESITY AND NEGATIVE AFFECT-INDUCED EATING Principal Investigator & Institution: Pagoto, Sherry L.; Psychology; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2003; Project Start 05-APR-2003; Project End 31-MAR-2008
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Summary: (provided by applicant): This proposal describes a 5-year training program that will enable Dr. Sherry Pagoto to develop expertise in the research of behavioral mechanisms of positive energy balance in obesity. In the past four years, Dr. Pagoto has completed her training in clinical psychology, with a specialization in cardiovascular risk reduction via behavior change (e.g., weight management, stress reduction, smoking cessation). Dr. Pagoto will work closely with her sponsor Dr. Bonnie Spring, as well as her co-mentors, Drs. Audrey Ruderman and Donald Hedeker at the University of Illinois at Chicago, Dr. Marian Fitzgibbon at Northwestern University in Chicago, and Dr. Karina Davidson at Mt. Sinai School of Medicine in New York. Dr. Pagoto's short term goals are to enhance the theoretical, methodological, and statistical skills needed to study the behavioral mechanisms of unhealthy eating patterns that lead to weight gain and obesity. Her long-term goals are to develop an independent laboratory and a network of collaborators devoted to the understanding of risk factors and treatments for obesity and other outcomes that contribute to cardiovascular risk. Two studies are proposed. Study 1 aims to compare the calorie intake of obese and nonobese males and females during anxious, angry, and neutral mood states. The hypothesis is that both anxiety and anger compared to neutral mood, trigger disproportionately increased eating among both obese males and females compared to normal controls. Anger may be more potent than anxiety in triggering disproportionately increased eating in obese individuals. Study 2 addresses a potential behavioral mechanism of negative affectinduced eating. The aim is to examine the effect of food intake on anxious and angry mood states in obese and nonobese males and females, testing the hypothesis that the negative affect dispelling consequences of eating are greater for obese individuals than for normal weight controls. This is the first study to systematically investigate the effects of eating on different mood states using comparable methodology. Results should increase the understanding of obesity and be used to enhance weight loss interventions. The University of Illinois at Chicago provides an ideal setting for training behavioral scientists and the mentoring team will provide a sound training experience for the PI from which an academic career can be launched. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OBESITY RETIREMENT
IN
EARLY
AND
MIDDLE
ADULTHOOD
AND
Principal Investigator & Institution: Stevens, June; Associate Professor; Epidemiology; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): By the year 2050, the African American elderly population is expected to more than triple while the white elderly population is expected to double. Previous work in Scandinavian countries has indicated that obesity is one lifestyle factor that is associated with disability pensions. There has been a dramatic increase in obesity in the U.S. in recent years, however, very little is known about the associations between obesity and retirement issues in the U.S. Current evidence indicates that African American men and women aged 45 years and older are more likely to report being unable to work because of a physical, mental, or emotional problem than white men and women. It is also known that the prevalence of obesity is almost twice that in African American women compared to white women. The purpose of this research is to determine long-term and short-term associations between obesity, weight gain and retirement among African American and white men and women. Analyses targeting long-term associations will examine the effect of body mass index at
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age 25 on subsequent age of retirement. Short-term associations will be examined as the effect of body mass index in later adulthood on retirement in the subsequent 3 years. We will also examine associations between weight gain from age 25 to later adulthood and retirement. The proposed study will use extant data from the Atherosclerosis Risk in Communities (ARIC) cohort. Information on retirement status is available from 2,314 African American women, 1,620 African American men, 4,517 white women, and 5,409 white men aged 45-64 years at baseline (1987-1989) and examined at 3-year intervals in a maximum of 4 visits. Retirement will be assessed using information on employment status at each visit. Information on measured weight and height, self-reported weight at age 25 and several other pertinent variables will also be used in these analyses. This proposal is directly responsive to PA-01-082 to ". support researchers interested in undertaking secondary data analyses of data related to. behavioral research on aging" and ". determinants of retirement. " Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OBESITY PREV AMONG PREPUBERTAL AFRICAN AMERICAN GIRLS Principal Investigator & Institution: Baranowski, Thomas; Professor; Pediatrics; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-MAY-2002 Summary: Obesity is a risk factor for several adult chronic diseases. Obesity is more prevalent among African-Americans (AA) than other ethnic groups, especially AA females. Obesity tracks from childhood into the adult years. Children above the 50th percentile (50 percent tile) and/or who have one or two obese parents are more likely to become obese than others. Thus, intervening just before and early in puberty among those at high risk may prevent obesity among those not already obese, and prevent or minimize further weight gain among those already overweight and lower chronic disease burden. We hypothesize that participation in 60 min or more per day of moderate to vigorous physical activity, eating 5 or more servings of fruit, juice and vegetables (FJ and V) per day, and decreasing dietary fat intake will minimize weight gain over a two year period among prepubertal 8-year-old (yo) AA girls in the upper 50 percent tile of BMI or who have one or more obese parents. Behavioral objectives will be achieved through a 2-year intervention consisting of a four-week summer day camp and a 23 month child-parent weekly interactive Fun, Food and Fitness web site to learn about healthy eating and physical activity. This study will employ a randomized two group (treatment-control) design with four annual repeated measures at baseline, mid program (+12 mo), post program (+24 mo), and a year after the program(+36 mo) starting with 336 girls. The primary intervention outcomes will be body weight and fat gain as measured by DEXA; secondary outcomes include cardiovascular disease risk factors, energy expenditure measured by doubly labeled water, dietary practices and psychosocial variables. Candidate gene polymorphisms and resting metabolic rate will be examined for association with obesity related phenotypes and response to intervention. Prior to the Intervention (Phase I) we will initiate three studies: 1) test of the validity of two alternative approaches to self-report of physical activity (24-hour physical activity recall vs. week activity recall); 2) assessment of family and personal factors that influence physical activity among these girls; and 3) development and pilot testing of a culturally sensitive month-long summer camp and two month world wide web program to help 8yo AA girls change their dietary and physical activity practices. This will be the first obesity prevention project to employ a month-long summer camp,
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web technology, and sophisticated biological measures to assess factors predictive of body composition change. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OBESITY--NEURAL CONTROL OF METABOLISM AND WEIGHT GAIN Principal Investigator & Institution: Levin, Barry E.; Professor and Acting Chair; Neurology and Neurosciences; Univ of Med/Dent Nj Newark Newark, Nj 07103 Timing: Fiscal Year 2001; Project Start 01-APR-1982; Project End 31-MAR-2004 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ONCOTIC PRESSURE AND EXTRAVASCULAR LUNG WATER IN ARDS Principal Investigator & Institution: Martin, Gregory S.; Medicine; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2001; Project Start 30-SEP-2000; Project End 31-JUL-2005 Summary: Applicant's Abstract This proposal is part of a career development plan integrating didactics in the form of a Master's Degree in Clinical Investigation with direct, mentored experience in the design and conduct of randomized clinical trials. Expertise in these areas will provide the necessary components for a successful career in patient-oriented critical care research. The Center for Lung Research at Vanderbilt University has focused substantial efforts toward the understanding of fluid and solute exchange in the injured lung, both in the pre-clinical arena and in prospective, randomized clinical trials. The mentors and consulting faculty in this environment are well recognized, established senior investigators in critical care research with vast preclinical and clinical experience. ARDS is defined by acute impairment of oxygenation and radiographic infiltrates compatible with pulmonary edema without increased hydrostatic pressures. It affects approximately 15,0000 people per year in the United States, with mortality approaching 50% and a financial burden estimated to exceed $5 billion. Fluid overload, weight gain, and hyperproteinemia are associated with increased mortality in patients with ARDS. Reduced oncotic pressure gradients related to hypoproteinemia may contribute to generation and maintenance of pulmonary edema in this condition. Previous trials have demonstrated clinical benefits associated with albumin and diuretic therapy in patients with ARDS, through the mechanisms by which these improvements occur is unclear. It is hypothesized that these benefits occur through increases in the oncotic pressure gradient and reductions in extravascular lung water, through the exact mechanism is unknown. The purpose of this project is to elucidate the pulmonary and hemodynamic effects of colloid and diuretic therapy in patients with ARDS using recently developed technology, which permits simple and accurate measurement of systemic hemodynamics and extravascular lung water in critically ill patients. This investigational proposes a critical trial randomizing hypoproteinemic ARDS patients to albumin and furosemide or dual placebo with targeted goals of diuresis and weight loss. Therapeutic effects on respiratory function, extravascular lung water, oncotic pressure, alveolar fluid clearance, and systemic hemodynamics will be characterized. This trial could advance our understanding of factors affecting fluid balance in patients with ARDS and has the potential to change clinical practice standards. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: OUTCOMES ADOLESCENTS
OF
SLEEP
DISORDERED
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BREATHING
IN
Principal Investigator & Institution: Redline, Susan S.; Professor of Pediatrics, Medicine & Epid; Medicine; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): In children, unrecognized Sleep Disordered Breathing (SDB) may significantly contribute to learning and behavioral problems, and predispose to the development of cardiovascular problems. Adolescents may be predisposed to SDB because of weight gain or sleep restriction. However, the prevalence and impact of SDB in teenagers have not been systematically studied. Over the last 3 years, we have studied a unique cohort of 907 children (41% minority), ages 811, many who have been under observation since age 3 years. Our physiological and neuropsychological measurements provide fundamental data regarding the prevalence of SDB and risk factors for SDB in pre-pubertal children. Preliminary analyses indicate that children with snoring or SDB perform more poorly on a number of tests of cognitive function, and have more behavioral morbidity than do other children. We propose extending this study to assess the morbidity of SDB in adolescents (ages 13-16 years), addressing the extent to which SDB in childhood impacts behavior, cognitive functions, and neuro-endocrine responses important in the pathogenesis of cardiovascular disease or diabetes. We hypothesize that the effects of sleep fragmentation, reduced slow wave sleep and sleep-associated intermittent hypoxemia may lead to deficits in executive functions, insulin sensitivity, and abnormalities in the somatotropic axis. We also will quantify the impact of putative risk factors on adolescent SDB, including race/ethnicity, overweight, small pharyngeal size, prematurity, familial SDB, and SDB at ages 8-11 years. For efficiency, we will perform stratified sampling of 250 children from this cohort (125 with habitual snoring or sleep apnea at ages 8-11 yrs., and 125 children randomly selected from the remaining cohort, frequency matched by gender, term, and race). Children will undergo overnight stateof-the-art-sleep monitoring, a glucose tolerance test, acoustic rhino-pharnygometry, anthropometry, spirometry, blood pressure, and a focused battery of neuropsychological and behavioral assessments. Specimens for biomarkers and potential confounders (e.g, measures of puberty and thyroid status) will be collected, some both before and after sleep. First-degree relatives also will undergo sleep studies and relatives and children will have DNA collected for future studies. This proposal provides the opportunity to characterize the prevalence and morbidity of SDB in a wellcharacterized population-based sample, including a large proportion of minority and preterm adolescents who appeared to be at high risk for SDB at younger ages, and may be at increased risk for SDB-associated chronic morbidities, and poorer cognitive development. Comprehensive data collection and statistical analyses will permit identification of potential pathophysiological mechanisms for, and effects of, SDB. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PEDIATRIC BIPOLAR COLLABORATIVE MOOD STABILIZER TRIAL Principal Investigator & Institution: Scheffer, Russell E.; Psychiatry; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2001; Project Start 01-SEP-2000; Project End 31-AUG-2004
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Summary: (Adapted from Applicant's Abstract): Bipolar disorder (BPD) in children and adolescents is increasingly recognized as a common and virulent disorder, but evidencebased treatment approaches are lacking. This revised, proposed study develops evidence to address this significant knowledge gap, and helps to develop more empirically based treatments of child and adolescent BPD. This three-site, collaborative treatment study proposes to evaluate the acute phase, comparative efficacy of two mood stabilizers, lithium (LI) and divalproex sodium (DVP) versus placebo (PBO) in outpatient children and adolescents with symptomatic, nonpsychotic BPD I in the mixed or manic phase. Investigators at 3 sites (UTSW, Case Western Reserve & Univ. of Cinn.) will randomize 150 patients over 3 years. To our knowledge, this represents the first randomized, controlled the comparing the efficacy of each mood stabilizer versus placebo in this population. This will be accomplished by randomly assigning subjects in a double-blinded fashion to 8 weeks of treatment with either LI, DVP, or PBO. The primary aim of this project is to compare the efficacy of LI, DVP, and PBO in the acute phase treatment of symptomatic bipolar I disorder, in children and adolescents ages 8-17 yr. Our hypothesis is that differential efficacy will be observed with the following predicted order of response: DVP equals LI > PBO. The secondary aims are: 1)To provide descriptive data and effect size estimates of combined treatment with LI and DVP in patients who do not respond acutely to either one alone; 2) To collect systematic safety data on the incidence of weight gain, polycystic ovaries, and hyperandrogenism, in bipolar adolescent females treated with LI, DVP, or LI + DVP; 3) To collect data on possible predictors of acute treatment response to the two active treatments; 4) To provide descriptive information on the stability of acute phase response to monotherapy with either LI or DVP over 16 weeks of continuation phase treatment. We will systematically collect data concerning the short- and long-term safety and tolerability of mood stabilizers in children and adolescents. No studies have looked at the question of weight gain, polycystic ovaries, and endocrine abnormalities in female bipolar adolescents treated with mood stabilizers. Because of the frequent use of mood stabilizers in bipolar adolescents, this is an important area to systematically collect prospective data on. We will also be able to provide descriptive data and effect size estimates of combined treatment with LI and DVP in patients who do not respond acutely to either one and collect data on possible predictors of acute treatment response to the two active treatments. Lastly, this trial will provide descriptive information on the stability of acute phase response to monotherapy over a 16 week continuation phase. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PEDIATRIC BIPOLAR COLLABORATIVE MOOD STABILIZER TRIALS Principal Investigator & Institution: Kowatch, Robert A.; Professor; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2001; Project Start 07-SEP-2000; Project End 31-AUG-2004 Summary: (Adapted from Applicant's Abstract): Bipolar disorder (BPD) in children and adolescents is increasingly recognized as a common and virulent disorder, but evidencebased treatment approaches are lacking. This revised, proposed study develops evidence to address this significant knowledge gap, and helps to develop more empirically based treatments of child and adolescent BPD. This three-site, collaborative treatment study proposes to evaluate the acute phase, comparative efficacy of two mood stabilizers, lithium (LI) and divalproex sodium (DVP) versus placebo (PBO) in outpatient children and adolescents with symptomatic, nonpsychotic BPD I in the mixed or manic phase. Investigators at 3 sites (UTSW, Case Western Reserve & Univ. of Cinn.)
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will randomize 150 patients over 3 years. To our knowledge, this represents the first randomized, controlled the comparing the efficacy of each mood stabilizer versus placebo in this population. This will be accomplished by randomly assigning subjects in a double-blinded fashion to 8 weeks of treatment with either LI, DVP, or PBO. The primary aim of this project is to compare the efficacy of LI, DVP, and PBO in the acute phase treatment of symptomatic bipolar I disorder, in children and adolescents ages 8-17 yr. Our hypothesis is that differential efficacy will be observed with the following predicted order of response: DVP equals LI > PBO. The secondary aims are: 1)To provide descriptive data and effect size estimates of combined treatment with LI and DVP in patients who do not respond acutely to either one alone; 2) To collect systematic safety data on the incidence of weight gain, polycystic ovaries, and hyperandrogenism, in bipolar adolescent females treated with LI, DVP, or LI + DVP; 3) To collect data on possible predictors of acute treatment response to the two active treatments; 4) To provide descriptive information on the stability of acute phase response to monotherapy with either LI or DVP over 16 weeks of continuation phase treatment. We will systematically collect data concerning the short- and long-term safety and tolerability of mood stabilizers in children and adolescents. No studies have looked at the question of weight gain, polycystic ovaries, and endocrine abnormalities in female bipolar adolescents treated with mood stabilizers. Because of the frequent use of mood stabilizers in bipolar adolescents, this is an important area to systematically collect prospective data on. We will also be able to provide descriptive data and effect size estimates of combined treatment with LI and DVP in patients who do not respond acutely to either one and collect data on possible predictors of acute treatment response to the two active treatments. Lastly, this trial will provide descriptive information on the stability of acute phase response to monotherapy over a 16 week continuation phase. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PREDICTORS OF ADVERSE METABOLIC EFFECTS OF SLEEP LOSS Principal Investigator & Institution: Spiegel, Karine; Free University of Brussels 50 Ave Franklin Roosevelt Brussels, Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Chronic sleep loss, obesity and sleep-disordered breathing (SDB) are increasingly common in industrialized countries. Sleep curtailment in healthy young lean adults results in the development of components of the metabolic syndrome, including reduced glucose tolerance and/or insulin resistance, elevated evening cortisol levels, increased cardiac sympatho-vagal balance, and a risk of weight gain resulting from reduced leptin levels and increased hunger and appetite. The studies proposed in the present application build on novel findings from our group that indicate that obese individuals may be more at risk for further weight gain than lean individuals in conditions of sleep loss, and that individuals levels of slow wave activity (SWA), a stable trait-dependent marker of deep sleep, may predict subjective vulnerability to sleep loss, and are also likely to predict the severity of adverse metabolic and cardiovascular consequences of sleep loss. We therefore propose to characterize sleep architecture, autonomic nervous system (ANS) activity, and biomarkers of the metabolic syndrome in three groups of middle aged (35-50 years old) subjects studied while they follow their usual sleep habits as well as during 4 days of sleep restriction and sleep extension, presented in randomized order in a cross-over design. The three groups of subjects will be healthy lean men and women, gender-matched individuals who are obese, and gender-matched individuals who are obese and also suffer from SDB. The specific aims are: 1. To test the hypothesis that baseline levels of SWA are
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lower in obese adults than in lean controls, and are even lower in obese subjects with SDB, and examine correlations between levels of SWA and sleep duration, ANS activity and biomarkers of the metabolic syndrome. 2. To test the hypothesis that sleep restriction, as compared to sleep extension, has adverse effects on biomarkers of the metabolic syndrome in lean adults, obese adults, and obese adults with SDB. 3. To test the hypothesis that the adverse impact of partial sleep loss on components of the metabolic syndrome is more important for obese adults than in lean adults, and more severe in obese adults with SDB than in those without SDB. This project capitalizes on our experience with human studies of "sleep debt" and on our extensive expertise in assessment of ANS activity to evaluate the role of the ANS as a mediator of the adverse health effects of chronic sleep loss. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PREDICTORS OF MENARCHE Principal Investigator & Institution: Frazier, Lindsay; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 26-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): Younger age at menarche is a strong risk factor for breast cancer. For each year of decline in age at menarche, risk of breast cancer has been estimated to increase 4%. In most developed countries, age at menarche has declined, on average, 3 months per decade over the last century, whereas in developing countries, the decline has been more rapid. Postulated reasons for the younger age at menarche include improved nutrition, lower levels of physical activity and the concomitant rise in obesity. Understanding the impact of physical activity has been hampered by crude measurement, however, and studies to date have not examined rigorously the relative impact of physical activity versus weight. To examine the impact of physical activity on onset of menarche, we will use data from the Growing Up Today Study (GUTS) a longitudinal study of 16,882 children who have completed annual surveys since inception of the study in 1996 when they were 9-14 years of age. Using age at onset of menses as our outcome, we will examine the impact of physical activity, independent of the effect of body weight. We will also examine the effects of overweight and inactivity, and their effect modification, on timing of menses. Understanding the predictors of menarche will help to develop a public health approach to the issue of early pubertal development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PREGNANCY ESTROGENS, DIET, AND BREAST CANCER RISK Principal Investigator & Institution: Hilakivi-Clarke, Leena A.; Professor; V T Lombardi Cancer Res Center; Georgetown University Washington, Dc 20057 Timing: Fiscal Year 2001; Project Start 15-AUG-2001; Project End 31-JUL-2006 Summary: Estrogen levels are elevated by 50-100 -fold during pregnancy, and interindividual variability in pregnancy estrogen levels is 4-6 -fold. Women exhibiting highest pregnancy estrogen levels are suggested to be at a significantly increased risk to develop breast cancer, perhaps due to an estrogen-induced promotion of existing transformed cells. Diet, particularly dietary fats, may affect pregnancy estrogen levels and later breast cancer risk. In our animal study, a high fat intake significantly increased pregnancy estrogen levels and increased pregnancy-promoted mammary tumor incidence. Polymorphism in genes that metabolize estrogens and have been linked to increased breast cancer risk, may also affect pregnancy estrogen levels. Our proposed
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study has two general aims: (1) to study whether dietary fat intake affects pregnancy estrogen levels in women, perhaps by interacting with polymorphism in CYP17 and COMT, and (2) to study whether highest pregnancy estrogen levels might increase breast cancer risk by increasing growth factor levels. These growth factors could originate from mutated or already transformed mammary cells, which during pregnancy are stimulated by high estrogen levels. Growth factor levels will be measured in nipple aspirate fluid (NAF) that can be obtained using a breast pump from nonlactating breast. Consequently, the following hypotheses will be tested: Hypothesis-1. We hypothesize that high dietary fat intake and weight gain increase pregnancy estrogen levels. We further hypothesize that polymorphism in CYP17 or COMT influences these interactions. Hypothesis-2. We hypothesize that higher circulating estradiol levels during pregnancy are associated with increased growth factor levels in nipple aspirate fluid, including EGF, TGFalpha and IGF-1/IGF binding protein 3. These aims will be studied in 200 pregnant women attending the Maternity Clinic at Solna in NAF will be obtained 12 months after giving birth. Our results may lead to modifications of pregnancy diet to reduce the risk to develop breast cancer. In particular, women who already are at high risk, for example, due to family history of breast cancer, age at first pregnancy (greater than 30 years), or other reproductive risk factors, may significantly benefit from pregnancy dietary modifications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PREGNANCY RELATED WEIGHT GAIN: A LINK TO OBESITY Principal Investigator & Institution: Siega-Riz, Anna M.; Maternal and Child Health; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 26-AUG-2002; Project End 31-JUL-2007 Summary: (provided by applicant): Past research on maternal weight gain during pregnancy has focused on determinants and consequences of inadequate weight gain with concerns for the health of the infant. However, with the rising prevalence of obesity among women of childbearing ages and the high proportion of women who are gaining in excess of recommendations, a shift in research focus must occur to include consideration of the mother's long-term health status. This study's long-term goal is to identify modifiable behaviors for pregnant women that are associated with gaining weight above the recommended ranges and that result in high postpartum weight retention. This project will build upon and extend the on-going Pregnancy, Infection, and Nutrition study being conducted at the University of North Carolina. Presently, women are being recruited before 20 weeks gestation. Data collected includes biological specimens (urine, blood, vaginal cultures, and placenta) and information on sociodemographic characteristics, psychosocial indicators, health habits, all moderate and vigorous physical activity, dietary intake, previous and current medical history, and birth outcome. The proposed study will add three new components during the prenatal period (preconceptional body image assessment, dietary restraint, and pregnancy related weight gain attitudes) for approximately 1230 women and extend the data collection period into the postpartum months. A home visit at 3 and 12 months postpartum will include the collection of maternal weight and percent body fat, information on breastfeeding status, dietary intake and physical activity behaviors, measurement of psychosocial status, body image, and restrained eating. Multivariate techniques, specifically log-linear modeling, ordinary least squares regression, and general linear mixed modeling will be employed in the analysis. Focus groups during pregnancy and in-depth interviews during the postpartum period will be conducted to
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collect qualitative information on barriers and enhancements to physical activity, healthy eating, and weight loss during the postpartum period. These data, both the quantitative and qualitative, will be used to identify modifiable behaviors for pregnant women that are associated with gaining weight above the recommended ranges and postpartum weight retention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PRETERM INFANTS' WEIGHT GAIN FOLLOWING MASSAGE THERAPY Principal Investigator & Institution: Hernandez-Reif, Maria; Senior Research Associate; Pediatrics; University of Miami-Medical Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2003 Summary: (adapted from investigator's abstract): This is the second submission of a proposed study designed to investigate possible mechanisms leading to enhanced weight gain in premature infants who receive massage. Multiple investigations demonstrated that preterm neonates who received massage therapy for five to ten days exhibited 28 to 47 percent greater daily weight gain. Findings were consistent in showing that preterms receiving massage do not consume more formula or calories than control infants. The proposed research will examine possible underlying mechanisms for this enhanced weight gain following massage therapy. The model that will be tested is that moderate pressure massage therapy enhances vagal activity, which in turn promotes gastric motility and the release of hormones that enhance the metabolism of digestion. Medically-stable preterm neonates (N=120) residing in the progressive or intermediate care nurseries will be matched on gestational age, birthweight, NICU days, mother's SES, and entry weight and then assigned to one of three groups: Massage Therapy (n=40), Sham Massage (n=40), or Control (n=40). Massage therapy and Sham Massage will be provided for 15 minutes, three times per day, for five days. Massage Therapy will use moderate pressure and Sham Massage will use light pressure. Group comparisons will focus on physiologic (vagal tone and gastric motility), biochemical (serum insulin, IGF-I, oxytocin, and cortisol) and behavioral (performance on the Brazelton Neonatal Behavior Assessment Scale) variables. At the end of the 5-day period, the massaged infants are expected to show: 1) higher vagal tone during massage and higher vagal tone across the study; 2) higher concentrations of serum insulin, IGF-I, and oxytocin, and lower cortisol; 3) greater gastric motility values, and 4) superior performance on the Brazelton. Regression analyses will be conducted to determine the percentage of variance in weight gain and Brazelton performance that is accounted for by the physiologic and biochemical variables. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PRETERM INFANTS: LIGHT EFFECTS ON HEALTH AND DEVELOPMENT Principal Investigator & Institution: Brandon, Debra H.; None; Duke University Durham, Nc 27706 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2008 Summary: (provided by applicant): Health and developmental outcomes vary even among the healthiest preterm infants. These variations in outcome have led to speculation that the neonatal intensive care unit environment, and light in particular, may impact outcomes. Recently, cycled light has shown short-term benefits over near darkness, but it is unclear at what gestational age cycled light should be initiated and
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whether these benefits continue long term. Some evidence suggests that at 28-weeks gestational age the visual sensory system is capable of handling light stimulation since the brain has a full complement of neurons, migration and differentiation is beginning, and the suprachiasmatic nuclei is innervated by the retina and responsive to light. The proposed study evaluates the timing and effects of early versus late cycled light throughout hospitalization on short-and long-term health and developmental outcomes in infants born at < 28 weeks gestation. Utilizing a longitudinal randomized experimental design, 140 infants will be assigned to either: (1) early cycled light (28 weeks post-conceptional age [PCA]) or (2) late cycled light (36 weeks PCA). Infants will be followed throughout hospitalization to evaluate the short-term outcomes of weight gain, number hospital days, sleep-wake state development, retinopathy of prematurity, and auditory acuity. Infants will be followed after discharge until 24 months corrected age to evaluate weight gain, sleep patterns, visual acuity, development (cognitive, motor, language) and neurological outcomes. Data, a mixture of continuous and categorical variables, will be analyzed using mixed general linear models, generalized estimating equations, multiple analysis of variance, and chi-square. Preterm infants receiving early cycled-light are expected to have better outcomes because they will receive cycled light when it can be utilized. While most NICUs across the country modify the light environment in some fashion, a national standard of care for environmental light does not exist, therefore it is important to determine when cycled light or near darkness is most appropriate. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PREVENTION OF OBESITY BY ALTERATION OF DIETARY FAT Principal Investigator & Institution: Donnelly, Joseph E.; Professor and Director; Educ Psychology and Research; University of Kansas Lawrence Lawrence, Ks 66045 Timing: Fiscal Year 2003; Project Start 15-FEB-2001; Project End 31-JAN-2006 Summary: Treatment for obesity has proven difficult as most reduced obese individuals regain the weight which had been lost. The lack of success in treating obesity argues for strategies to prevent obesity or weight re-gain. The PIs propose to use 3 clinically appropriate levels of fat intake in a population at-risk for weight gain in a long-term study where energy intake and macronutrient composition is verified by multi-method techniques. Primary Aim-Prevention of weight gain. The PI will determine the effects of 3 levels of verified dietary fat intake on body weight and body composition in college students at-risk for weight gain. We hypothesize that ad libitum diets which contain greater than 35 percent fat will promote weight gain compared to subjects who ingest ad libitum diets which contain 28 to 32 percent fat or 25 percent fat or less. Specifically, the PI expects a dose response for the level of fat in the diet for body weight and fat mass. Secondary aims will may contribute to our understanding of how various levels of fat intake may prevent or promote obesity and may provide explanation for the anticipated differences in individual responses with the groups. Association of fat intake to total energy intake. The PI expects that subjects consuming diets with higher amounts of fat to have greater total energy intakes and will therefore show weight gain in a dose response fashion. Specifically, the PI will hypothesize that subjects consuming ad libitum diets with 35 percent fat or greater will show an increase in total energy intake compared to subjects consuming a 28 to 32 percent fat diet or subjects consuming a diet of 25 percent fat or less. Individual response - the PI expects subjects with greater body fat to gain more weight and fat mass compared to leaner subjects and expect subjects who are restrained eaters to gain less weight than those who exhibit disinhibited eating. Although the PI expects increase energy intake for the groups that receive high fat
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intakes, they do not expect all subjects within each group to respond in similar fashion. The long-term results expect to show those subjects who gained the least amount of weight during the intervention will have the lowest weights 1,2 and 3 years post intervention. The results of this study should advance our understanding of the role of dietary fat in the prevention of obesity and weight re-gain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PRIMARY CARE OFFICE MANAGEMENT OF OBESITY Principal Investigator & Institution: Martin, Pamela D.; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, La 70808 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2004 Summary: Approximately 55% of the American Population is either overweight or obese. African American women in particular are at significant risk for becoming obese with as many as 49% currently qualifying for obesity (BMI greater than or equal to 30). Low-income, African American women appear less likely to engage in dietary and activity habits associated with weight maintenance and cultural factors may influence their acceptance of excessive body weight. Furthermore, traditional weight loss approaches have been minimally effective with low-income, African American women. Focus group research suggest that African-American women may be responsive to prevention programs which focus on the health b3enefits of weight management and which employ culturally sensitive educational materials. Preliminary research also suggests that a patient centered motivational intervention which uses messages targeted at patient's motivational level, knowledge and perceived barriers may enhance preention efforts. Primary care physicians who provide routine medical care to lowincome, African American women are in a unique position to offer preventive services to deter weight gain and promote maintenance of weight loss. This randomized, two arm treatment study will use culturally sensitive educational materials by trained primary care physicians. It will compare physicians directed education (standard care group) to another group who receive customized education plus patient centered messages by primary care physicians. It will attempt to determine a physician delivered patient centered intervention is more effective than standard cre in regard to prevention of weight gain and achievement of weight loss at 6 months. It will also examine whether the groups differ in regard to weight maintenance at 12 and 18 months follow up. It is hypothesized that patients in the patient centered group will demonstrate less weight gain, more weight loss at 6 months, greater maintenance of weight loss at 12 and 18 months as well as dietary and physical activity improvement throughout the observation period than patients receiving standard care. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PRIMARY PREVENTION OF WEIGHT GAIN FOR WOMEN AGED 2545 Principal Investigator & Institution: Willett, Walter C.; Professor and Chairman; Nutrition; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 14-JAN-2002; Project End 31-DEC-2004 Summary: (provided by applicant) This research will be conducted primarily in Brazil as an extension of NIH grants # R0l CA 50385 and R0l HL60712-0l. Overweight (BMI (Body Mass Index) 25.0-29.9) and obesity (BMI greater than or equal to 30 kg/m2) now affect more than 40 percent of adult Brazilians. Women at reproductive age are particularly at
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risk of obesity and a 70 percent increase in the prevalence was observed in the last two decades in Brazil. Increasing fat intake does not appear to explain this trend, whereas a steady decline in the consumption of beans has been shown for the whole country. Many studies have demonstrated changes in blood glucose levels due to the intake of specific carbohydrate foods, as measured by glycemic index (GI). An exceptionally low blood glucose response was associated with beans and it has been suggested that the consumption of low-GI diets may: 1) decrease hunger/ increase satiation; 2) reduce lipogenesis. In a nonrandomized follow-up of children attending a program of obesity treatment, children assigned to a low GI diet had a decrease in BMI greater than the high GI group. There are no long term clinical trials of weight loss or prevention of weight gain comparing low with high GI diets. However, a dietary pattern identified through factor analysis in a survey in the city of Rio de Janeiro, Brazil, that represents mainly rice and bean intake was associated with lower risk of obesity. The purpose of this study is to compare in Brazilian women the effectiveness of encouraging them to eat two different dietary patterns (low vs. high GI), with equal macronutrient composition, on weight control over the course of 18 months. The low GI dietary pattern will be heavily based on the traditional rice and beans combination. The comparison group will be encouraged to eat a diet with the same amount of macronutrients, but closer to a Western diet. Both diets are realistic prescriptions of foods consumed by Brazilians.Specifically, this study will compare changes in weight (main outcome), food intake, blood chemistries and hunger/satiation in 206 adult women at reproductive age, with BMI of 23-27 kg/m2, randomized to either one of the diets after 4-week run-in period eating a high GI diet. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROSPECTIVE STUDY OF DIET AND COLORECTAL NEOPLASIA Principal Investigator & Institution: Fuchs, Charles; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 23-AUG-1991; Project End 31-MAR-2006 Summary: (provided by Applicant) We propose to address a series of dietary and hormonal hypothesis related to colorectal neoplasia in the Health Professionals FollowUp Study (HPFS) and Nurses? Health Study (NHS) Cohorts. Participants for the analysis of cancers will be drawn from the HPFS whereas participants for the analysis of adenomas will be drawn from both cohorts. We expect 1126 incident cases of colorectal cancer among the HPFS with prospectively collected dietary data, whereas we expect 4,548 total adenomas and 1,494 adenomas less than 1 cm from both cohorts. The repeated measures of diet and other exposures will allow an assessment of long-term patterns as well as the impact of changes in diet and other exposures. We propose to build upon, extend, and refine observations we have already made on the dietary and hormonal influences of colorectal neoplasia. We propose to focus on 5 areas: (1) nutritional influences on DNA synthesis, methylation, and repair; (2) external (including dietary) carcinogen; (3) physical activity, body mass index, weight gain; and tumor promoting growth factor; (4) non-steroidal ani-inflammatory drugs (NSAIDs) that inhibit cyclo-oxygenase-2 (COX-2); and (5) calcium and vitamin D receptor polymorphisms. We propose to develop each of these areas through questionnaires over a 18-year period to better assess the impact of long-term exposures, to account for various induction periods, and to examine for the impact of change. We will also examine how hormones may underlie the basis of action for physical activity, body mass in index, and weight change, and we will extra DNA from blood and buccal samples to examine hypothesized gene-environment interactions. In addition, we
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propose to acquire and use paraffin-embedded tissue specimens to examine how etiologic factors correlate with specific well-established molecular alterations (including the prevalence and spectrum K-ras mutations, level of microsatellite instability, prevalence of hMLH1 hypermethylation, and the levels of p53, p27, and COX-2 expression) in colorectal neoplasia. These studies are aimed to enhance our understanding of colorectal carcinogenesis and to provide a firm scientific foundation for future preventive efforts. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REDUCTION OF TRIGLYCERIDES IN WOMEN ON HRT Principal Investigator & Institution: Kuller, Lewis H.; Professor and Chair; Epidemiology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): The risk and benefits of hormone replacement therapy (HRT) have come under increased concern in recent years because of the results of the HERS and WHI trials, the increased risk of breast cancer, new therapies, i.e., SERMs and lipid lowering drugs, bisphosphorates, and better understanding of hormone metabolism and disease. We have shown in several studies that the potential benefits of HRT are limited by lifestyle, cofactors, specifically weight gain, obesity and increased visceral abdominal fat associated metabolic changes in lipoproteins, inflammatory markers and estrogen metabolites. We are proposing a randomized trial of 500 women, on HRT for at least two years, aged 52-60 years, and three or more years postmenopausal to test whether reduction in waist circumference, triglycerides, dense LDLc, number of LDL particles, CPR, PAI-I by aggressive diet exercise, versus a health education control will decrease progression or result in regression of measures of subclinical vascular disease. The intervention is designed to reduce total fat intake to 17 percent of calories, 1300 kilo calories, and increase moderate activity to 150-240 minutes per week to obtain a 10 percent reduction in weight. The primary endpoint will be a 20 percent or at least a 20 mg decrease in triglyceride levels, a 5 cm decrease in waist circumference, and a 10 percent decrease in LDLc. This will result in changes in subclinical measurements including carotid ultrasound, electron beam computer tomography of the coronary and aorta, pulse wave velocity, endothelial function, and tonometry of the radial artery. NMR spectroscopy of lipoproteins, inflammatory markers, and estrogen metabolites will also be evaluated. Therefore, the primary goal of this trial is the modification of measures of subclinical disease among HRT users. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: REGULATION OF ENERGY PARTITIONING DURING WEIGHT CHANGE Principal Investigator & Institution: Nagy, Timothy R.; Associate Professor; Nutrition Sciences; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 01-JUN-1998; Project End 31-MAY-2003 Summary: Collared lemmings are able to double their body weight and body fat content in response to a change in photoperiod. This occurs without a change in food intake. Photo-induced changes in body weight will be used to examine the temporal relationships among changes in energy expenditure (resting and activity) and fuel partitioning. In this revised application, it is proposed that both leptin and corticosterone may play important roles in the seasonal changes in body weight and
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body composition. It is hypothesized that during weight gain: 1) A decrease in resting energy expenditure will be associated with the early phase of weight gain, and a decrease in energy expenditure associated with physical activity will be associated with weight maintenance after weight gain; 2) increased metabolic efficiency (decreased expression of uncoupling protein mRNA) will cause the decrease in resting energy expenditure during the early phase of weight gain; 3) the photoperiod-induced decrease in corticosterone concentration will decrease ob mRNA expression, which in turn will decrease uncoupling protein mRNA expression. The converse will also be studied during weight loss in this model system. The results will shed light on the role of energy expenditure and energy partitioning on the regulation of body weight and body composition. The basic scientific information gained from this model should be useful for understanding the role of metabolic perturbations in the etiology of human obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF HYPERABSORTION OF NA IN AIRWAY DISEASE IN VIVO Principal Investigator & Institution: Grubb, Barbara R.; Research Professor; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 16-SEP-2003; Project End 31-AUG-2008 Summary: The airway surfaces are covered by a thin layer of liquid (ASL) consisting of a mucus layer residing on top of the periciliary liquid layer (PCL). The mucus layer traps debris and pathogens deposited on the airway surfaces, while the PCL layer provides a low viscosity liquid for efficient ciliary beating and functions as a lubricant layer. CF airway epithelia exhibit dysregulated epithelial Na+ channel (ENaC) function and absent CFTR CI- channel function, which results in hyperabsorption of Na+ and osmotically induced water absorption. We hypothesize that the net effect of Na+ hyperabsorption is to (1) deplete the PCL volume, (2) collapse the mucus layer onto the cilia, (3) slow both cilial and cough-dependent mucus clearance, (4) leading to accumulation of mucus plaques and plugs that are a nidus for bacterial colonization. While this hypothesis has been supported by data from in vitro experiments, the lack of an animal model has limited experiments to test this hypothesis in vivo. To test the hypothesis in vivo, we have generated transgenic (TG) mice that use the CCSP promoter to over-express the individual ENaC subunits (a,b,g). Preliminary data indicate that over-expression of the b subunit leads to an elevated rate of airway Na+ absorption, a decrease in PCL volume, marked mucus accumulation and plugging of the airways, and approximately 50% pup mortality by day 28. We propose four Specific Aims to study mice over-expressing b ENac as well as other ENaC subunit combinations.: Aim 1. Mice will be characterized with respect to survival, weight gain, pulmonary function tests, and histological/bioelectrical study of airways. Aim 2. The volume of the PCL/ASL, rate of volume flow, PCL ionic composition, mucus % solids and mucociliary clearance will be measured. Aim 3. We propose bacterial infection studies (P. aeruginosa) on the b TG mice, to generate insights into the initiation of inflammation and infection as well as information on the genetic and morphological changes in the bacteria in response to the host. Aim 4. We will test therapeutic agents aimed at blocking ENaC and dissolving mucus in airways of neonatal and adult b TG mice. Thus, our mouse model will be key in fostering translation of basic science to clinical application in a disease for which we now, for the first time, have an animal airway model. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF WNT IN WHITE AND BROWN ADIPOSE DEVELOPMENT Principal Investigator & Institution: Macdougald, Ormond A.; Associate Professor; Physiology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2008 Summary: (provided by applicant): The long-term goal of my research program is to determine the molecular mechanisms by which extracellular signals regulate adipocyte differentiation and metabolism. We have pioneered investigations into the role of Wnt signaling as a potent, endogenously produced inhibitor of adipogenesis. Wnt10b acts as an adipogenic switch, which must be shut off for cultured preadipocyte models to differentiate in vitro. Based on the role of Wnt10b in white adipogenesis in cell culture, we hypothesize that Wntl0b also regulates development of white adipose tissue (WAT) and brown adipose tissue (BAT) in the integrative setting of the organism. To test this hypothesis, we have created transgenic mice in which Wnt10b is expressed under control of the adipocyte-specific promoter, 422/aP2. Our preliminary data indicate that Wnt10b transgenic mice are almost devoid of WAT. In addition to its effects on development of WAT, our data suggest that Wnt10b also inhibits development of brown adipocytes within mice and within cultured cell models. Because little is known about the regulation of BAT development, our studies will be seminal to our understanding of this important metabolic and thermogenic tissue. The role of Wnt10b in development of adipose tissues will also be explored in Wnt10b -/- mice. Thus, the Specific Aims of this proposal are to:1) Investigate the role of Wnt10b in development of WAT. Experiments include molecular and mechanistic analyses of how Wnt10b regulates adipocyte differentiation and metabolism,1) Investigate the role of Wnt10b in development of BAT. Experiments include molecular and mechanistic analyses of how Wnt 10b regulates BAT development in vivo and brown adipogenesis in cultured cells.1) Determine effects of Wnt10b on energy balance. Variables measured will include food intake, weight gain, body composition, metabolic rate, respiratory quotient, locomotor activity, and body temperature. Effects on energy balance will be determined as control and Wnt transgenic or null mice adapt to fasting, cold stress, genetic or diet-induced obesity.Understanding the role of Wnt signaling in the development of WAT and BAT will provide important insight into the medical problems of obesity and type II diabetes, two major health risks in the United States. The identification of Wnt10b as a susceptibility gene for dysregulated development of WAT in mice will provide proof of principle that Wnt10b is important for normal and pathological development of adipose tissue in the human population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SKELETAL MUSCLE NUTRIENT SENSING Principal Investigator & Institution: Obici, Silvana; Medicine; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2007 Summary: (provided by applicant): Obesity occurs when caloric intake exceeds expenditure. The increasing prevalence of obesity in industrialized societies has generated new interest in the mechanisms underlying the control of energy balance. In humans, reduced rate of energy expenditure, which is largely accounted for by oxidative phosphorylation in skeletal muscle, is a risk factor for future weight gain. Nutrients, via the activation of nutrient-sensing pathways, activate adipostatic responses (e.g. leptin) that attempt to limit lipid storage by enhancing energy
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expenditure and inhibiting food intake. A major nutrient-sensing pathway, the hexosamine biosynthetic pathway (HBP) has been recently shown to increase local leptin expression in skeletal muscle. Yet, acute pharmacological activation of HBP induces a dramatic drop in skeletal muscle energy production, by downregulating the expression of genes for oxidative phosphorylation. Based on these observations, we wish to develop animal models designed to define how the physiological regulation of HBP modulates energy homeostasis. In particular, we will use transgenic animal models to discern the metabolic consequences of activation of HBP in muscle from those derived from the associated local induction of leptin. We will generate transgenic mice lines carrying constitutive and moderate elevations of the enzyme glutamine:fructose 6P amidotransferase (GFAT, which catalyzes the first committed step of HBP and regulates the flux through this pathway), or of leptin in skeletal muscle. The careful phenotyping of these animal models should allow one to define the direct and respective roles of muscle HBP and leptin in the regulation of energy expenditure and substrate oxidation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SOCIAL DETERMINANTS OF OBESITY AND RISK OF STROKE Principal Investigator & Institution: Dubowitz, Tamara; Maternal and Child Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2006 Summary: (provided by applicant): Stroke is the third leading cause of death in the United States, and a leading cause of long-term disability. The risk for stroke varies by race/ethnicity; stroke incidence is greater among African Americans at younger ages, contributing to a mortality rate 80 percent greater than that of Caucasians (Keppel et al 2002; DHHS 2000; Stroke Progress Review Group, NINDS 2002). Limited understanding exists concerning the etiology and variations of subtypes of stroke incidence in different populations and geographic locations over time (Stroke Progress Review Group, NINDS 2002). Obesity, which results in part from a complex pathway of numerous lifestyle precursors, is a strong predictor of cerebrovascular disease such as stroke and other cardiovascular disease (WHO, 2000). Moreover, dietary intake and physical activity contribute to energy imbalances that result in obesity and independently predict stroke (AICR 1997; USDA/USDHHS 2000; USDHHS 1996; 2000; Krebs-Smith SM. 2001). Few studies consider both biological and social determinants of intermediate outcomes of cerebrovascular disease from a multileveled perspective. This application considers longitudinal measures of social and biological variables to investigate the independent effect of social disparities to the development of obesity among low-income multi-ethnic postpartum women at increased risk of stroke and other comorbidities. As women face particular biological and social transition during the postpartum period, the proposed research seeks to measure social determinants of pregnancy-related weight gain over time, adjusting for diet, physical and biological predictors of obesity and stroke. Research findings from the proposed work can inform the design of future interventions to reduce risk of stroke in women of reproductive age in low income, racial/ethnic subpopulations at highest risk of obesity and its sequelae. Specific aims include examination of: (1) individual and household social determinants pregnancy-related weight change and obesity; (2) social disparity in dietary intake and nutritional status and its relation to pregnancy-related weight change and obesity; and (3) neighborhood characteristics that influence the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STRATEGIES TO IMPROVE COPD MANAGEMENT Principal Investigator & Institution: Casaburi, Richard; Harbor-Ucla Research & Educ Inst 1124 W Carson St Torrance, Ca 90502 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The Harbor-UCLA Research and Education Institute is highly qualified to be a vigorous and committed site in the COPD Clinical Research Network. The Principal Investigator leads 10 investigators and 3 consultants with broad experience in COPD clinical research. The research facilities are arrayed around a 4000 ft 2 Clinical Trials Center dedicated to COPD research, and include this institution's NIHsupported GCRC. This Center has extensive experience in recruiting COPD patients for both single and multi-center research protocols. Referral resources are solidly in place and have led to success in recruiting a gender-balanced and multi-ethnic population for COPD trials. A total of 20 clinical trials in COPD have been completed in the past two years or are underway. This site is able to perform a wide range of procedures that might be utilized in the network's trials, with special expertise in physiologic testing. We target two especially poor-prognosis COPD groups: chronically hypoxemic patients and patients with weight loss. Both trials focus on determining whether treatments we propose alter survival, though a range of other outcomes will be explored. Protocol 1 is based on the observation that expert opinion holds that lightweight ambulatory oxygen supply is of benefit to hypoxemic COPD patients even though most patients, in practice, are supplied with much heavier E-cylinders. A randomized 18-month trial involving 252 patients will determine whether, compared to patients receiving E-cylinders, patients assigned to lightweight oxygen supply will have increased activities of daily living, use more hours of oxygen per day, have better retention of muscle mass and exercise tolerance, have fewer exacerbations and lower medical resource utilization and, ultimately, have superior survival. Protocol 2 recognizes recent work suggesting that prognosis of underweight COPD patients is improved by weight gain and that muscle dysfunction is a reversible cause of exercise intolerance. We build on our recent demonstrations that testosterone increases muscle mass and strength in COPD men and that megestrol acetate stimulates appetite and increases body weight in COPD. A double-blind, placebo-controlled study involving 225 underweight COPD men is proposed in which 3 groups receive 6 months of 1) placebo, 2) testosterone enanthate 150mg/wk, or 3) testosterone plus megestrol acetate 800mg/day, each for 6 months followed by 12 months of observation. We will determine whether these interventions increase lean and total body mass, decrease systemic inflammation, increase activities of daily living, muscle strength, exercise endurance and quality of life, and thereby improve survival. These studies should have immediate impact on treatment strategies for large poor-prognosis subgroups of COPD patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SUGAR-SWEETENED BEVERAGES AND WEIGHT GAIN IN CHILDREN Principal Investigator & Institution: Ludwig, David S.; Assistant Professor of Pediatrics; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2004 Summary: (provided by applicant): The prevalence of obesity has risen dramatically among children in the U.S. since the 1960s. Effective treatment of childhood obesity is widely recognized as instrumental to public health efforts to combat type 2 diabetes and heart disease. Many factors are thought to have contributed to the epidemic of pediatric
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obesity. One factor that has received increasing attention is consumption of sugarsweetened beverages. Feeding studies suggest physiological mechanisms by which sugar in liquid form may be less satiating than other foods. One observational study found total energy consumption to be greater among children who consume sugarsweetened beverages compared to non-consumes. Short-term interventional studies report increasing energy intake and body weight in subjects given sugar-sweetened beverages compared to non-caloric beverages. Our preliminary data found that the risk for becoming obese increased by about 60% in middle school children for every additional serving per day of sugar-sweetened beverage consumed. However, there are presently no longer-term intervention studies examining the effects of beverage consumption on body weight in children. The purpose of this project is to examine, in a pilot study; the effect of a home-based environmental intervention designed to decrease consumption of sugar-sweetened beverages among adolescents. Specifically, we plan to recruit subjects from a high school in Cambridge, Massachusetts who will be randomly assigned to experimental or control groups. The experimental group will receive weekly deliveries to their homes of a variety of non-caloric beverages for a period of 6 months. We anticipate that children in the experimental group will 1) decrease consumption of sugar-sweetened beverages; 2) decrease total energy consumption; 3) show improvements in various measure of diet quality; and 4) gain less weight than controls (change in BMI is the primary study endpoint). Because soft drinks are heavily advertised to children and widely available, this study and subsequent multi-center trials are necessary to determine whether public health efforts aimed at reducing consumption of sugar-sweetened beverages among children may be warranted. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE EPIDEMIOLOGY OF BODY MASS INDEX REBOUND Principal Investigator & Institution: Daniels, Stephen R.; Professor of Pediatrics and Environment; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, Oh 45229 Timing: Fiscal Year 2001; Project Start 17-AUG-2000; Project End 31-JUL-2005 Summary: (Adapted from the Investigator's Abstract) Obesity is the most obesity which are present prior to the onset of excess weight gain has been problematic. Recently, it has been shown that the timing of body mass index (BMI) rebound may be a predictor of future obesity. BMI increases during the first year of life. It then declines until it reaches a minimum value during childhood and subsequently increases into adolescence and adulthood. The nadir of BMI is called BMI rebound. Studies have shown that BMI rebound at a younger age is associated with increased risk of obesity later in life. Currently, very little is known about the epidemiology of BMI rebound. The purpose of the proposed investigation is to precisely determine the age of BMI rebound and evaluate the body composition changes which occur during this time to determine if BMI rebound corresponds to a rebound in adiposity. In addition, determinants of the changes in body composition, such as diet and physical activity, will be investigated. Finally, the relationship of the timing of BMI rebound to body composition and cardiovascular risk factor status will be studied. The proposed investigation is a cohort study designed to follow 320 children from age three age seven years. Subjects will be evaluated every four months during the period of the study. Data will be collected on height, weight, body composition, diet and physical activity. At age seven years, the level of adiposity, the distribution of body fat, and cardiovascular risk factors will be studied. The investigators note that better understanding of the epidemiology of BMI rebound could lead to improved identification of children at high risk of future obesity
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prior to excess weight gain. They further note that elucidation of the determinants of the timing of BMI rebound could lead to the development of clinical and public health strategies to prevent the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ROLE OF PLACENTAL LACTOGEN IN FETAL DEVELOPMENT Principal Investigator & Institution: Freemark, Michael S.; Pediatrics; Duke University Durham, Nc 27706 Timing: Fiscal Year 2003; Project Start 01-MAY-1988; Project End 31-MAY-2008 Summary: (provided by applicant): Prolactin (PRL) and placental lactogen (PL) stimulate fat deposition, weight gain, and leptin production in rodents and humans, suggesting that lactogens play roles in maternofetal lipid metabolism and obesity. The mechanisms by which lactogens promote fat storage and weight gain are unknown. We hypothesize: (a) that lactogens promote fat deposition through induction of adipogenesis, the process of differentiation of adipocytes from stromal precursors; (b) that adipogenic effects of lactogens are mediated through induction of transcription factors including PPARkhi-2; (c) that PPARkhi-2 induction is mediated through activation of Stat5; and (d) that adipogenic effects of lactogens are modulated by insulin, IGF-1, glucocorticoids, and sex steroids. To test these hypotheses we will examine effects of exogenous PRL and PL on adipogenesis in 3T3-L1 preadipocytes, primary mouse preadipocytes and embryonic fibroblasts and the effects of constitutive expression of PL in a novel 3T3-L1 cell line. To determine if lactogenic signaling is required for preadipocyte differentiation, we will compare rates of adipogenesis in preadipocytes of PRL receptor (PRLR)-deficient mice with rates of adipogenesis in cells of wild-type littermates. To characterize effects of lactogens on PPARkhi expression we will examine effects of PRL and PL on PPARkhi1 and 2 mRNA and protein levels in 3T3-L1 cells, primary preadipoyctes, mouse embryonic fibroblasts and will compare PPARkhi expression in tissues of PRLR deficient mice with that in wild-type littermates, We will examine effects of lactogens on transcriptional activation of the human and mouse PPARkhi-2 promoters expressed in 3T3-L1 cells and will compare the time course of expression of PPARkhi1I and 2 mRNAs in PRL-treated cells with that of ADD1 and c/EBPs beta, delta, and alpha. To test the hypothesis that induction of PPARkhi-2 is mediated through activation of Stat5, we will determine if lactogens induce binding of STAT 5 to consensus binding sites in the human and mPPAR c-2 promoters. We will examine the effect of mutating PPARkhi-2 Stat5 consensus sequences on lactogendependent activation of PPAR gamma2 transcription, and the effect of a dominantnegative STAT5 construct on the induction of PPARkhi mRNA and protein levels in 3T3-L1 cells. Finally, to test the hypothesis that the adipogenic effects of the lactogens are modulated by sex steroids, we will examine the effects of progesterone and estradiol on the adipogenic effects of PRL in 3T3-L 1 cells and the effects of progesterone supplementation on fat deposition and leptin production in PRLR-deficient mice. The results of our studies should provide new insist into the roles of pituitary and placental hormones in adipose development and function. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE USE OF SIBUTRAMINE IN SMOKING CESSATION Principal Investigator & Institution: Johnson, Karen C.; Associate Professor of Medicine; Preventive Medicine; University of Tennessee Health Sci Ctr Memphis, Tn 38163 Timing: Fiscal Year 2002; Project Start 01-SEP-2001; Project End 31-AUG-2006
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Summary: Cigarette smoking poses a serious but preventable health risk. Behavioral smoking cessation interventions have been show to help persons quit smoking. However, concerns about post-cessation weight gain have been reported as a significant barrier to quitting for many smokers. Recently, a new serotonin and norepinephrine reuptake inhibitor, sibutramine has received FDA approval to help persons lose weight. Given sibutramine effects neurotransmitters that are important in regulation of body weight, it is reasonable to hypothesize that this drug will decrease post-cessation weight gain in overweight and obese smokers who quit smoking. To date, there has been no clinical trial comparing use of sibutramine to a placebo, as pharmacologic therapy for reduction of post-cessation weight gain among overweight and obese smokers who take part in a behavioral smoking cessation program. Therefore, whether sibutramine is efficacious in reducing post-cessation weight gain in these smokers in unknown. Further, given the neuropharmacologic effects of sibutramine, it is reasonable to speculate that this medication could also be effective in helping smokers quit smoking both initially and long term. We hypothesize that use of sibutramine as compared to use of a placebo will result in a decrease in post-cessation weight gain in overweight and obese persons who quit smoking and result in an increase in smoking cessation rates. We plan to test these hypotheses in this double blind clinical trial by randomizing overweight and obese persons who smoke to one of two groups: Group 1) Sibutramine plus a behavioral smoking cessation program or Group 2) Placebo Sibutramine plus a behavioral smoking cessation program. We will determine post-cessation weight change and smoking cessation initially (during treatment) and long term (12 months after randomization, which is 9 months off study medication). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TOBACCO CESSATION IN POSTMENOPAUSAL WOMEN Principal Investigator & Institution: Allen, Sharon S.; Associate Professor; Family Practice & Cmty Health; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 01-MAR-1993; Project End 31-JUL-2002 Summary: (Applicant's Abstract) In spite of the negative health effects of cigarette smoking, if current trends continue, smoking rates for women will surpass men by the year 2000. Studies show that women have a greater fear of weight gain after quitting, as well as, they tend to gain more weight to suggest gender specific cessation strategies are needed. Animal and clinical studies suggest that estrogen could decrease appetite behavior and minimize weight gain, as well as, affect mood and therefore could attenuate withdrawal symptoms. However, no study has systematically and comprehensively investigated the different effects of estrogen replacement therapy (ERT) in smoking cessation in postmenopause where the estrogen level is low. This renewal application will address this area in a randomized double blind nontreatment study conducted in 2 parts over 4 years. Part I investigates if there is a differential effect of ERT on appetitive behavior and withdrawal symptoms in postmenopausal women during short term smoking cessation, i.e., to decrease appetite behavior and minimize weight gain, and affect mood and attenuate withdrawal symptoms. Eligible subjects are randomized to smoking and non-smoking status, and enter a 3-week period of scheduled measurements. Week 1 is baseline with smoking ad lib, and in weeks 2 and 3 some subjects stop smoking while others continue smoking. During these 3 weeks weight, caloric intake, RMR and tobacco withdrawal symptom measurements will be done. Part II is also a short term nontreatment study investigating the additive effects of ERT on the same parameters in postmenopausal women on nicotine replacement.
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Subjects are randomized to ERT and placebo and monitored for 1 month, then randomized to placebo or active patch. The study design and measurements are identical to Part I. The results of this research will increase our understanding of the functional relationships between ERT and appetitive behavior and withdrawal symptoms in smoking cessation in postmenopausal women. This research will provide new information which will be important and useful in assessing direction for specific and more effective treatment strategies for smoking cessation in women during the postmenopausal years. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TREATMENT OF EARLY ONSET SCHIZOPHRENIA SPECTRUM (TEOSS) Principal Investigator & Institution: Findling, Robert L.; Director; Psychiatry; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 19-SEP-2001; Project End 31-AUG-2006 Summary: (Adapted from the Applicant?s Abstract): Objectives: This is one of four identical revised applications of a collaborative R01 proposal being conducted at the University of Washington, Seattle, WA, University of North Carolina (UNC), Chapel Hill, NC, Harvard Medical School, Boston, MA and Case Western University, Cleveland, Ohio. The study will examine the long-term effectiveness of three different antipsychotic medications in the treatment of early onset schizophrenia and schizoaffective disorder: risperidone (RIS), olanzapine (OLA), the molindone (MOL) over a one year period. Specific Aims: 1) To determine the efficacy of MOL, RIS, and OLA in reducing psychotic symptoms in youth with schizophrenia and related disorders; 2) To determine the ability to sustain treatment over one year with each of these agents; 3) To examine the effects of treatment on adaptive and neurocognitive functioning; and 4) To examine the safety and tolerability of these agents in the pediatric population, particularly potential effects on neuropyramidal symptoms and weight gain. Research Design: 168 youths (ages 8-19 years) with schizophrenia, schizophreniform disorder or schizoaffective disorder and active psychotic symptoms will be recruited across four sites. Subjects will be randomly assigned to double-blind treatment with one of the three study medications. Standard dosage schedules will be followed, with modifications allowed dependent on the clinical status of subjects. Antipsychotic agents will be cross-tapered over the first week of the study to prevent exacerbation of psychotic symptoms. Symptom ratings and neurocognitive testing will be performed at baseline and repeated at specific intervals. The acute phase of treatment will last 8 weeks. Subjects with clinically significant improvement and without intolerable side effects, will continue maintenance therapy for an additional 44 weeks. Tolerance of the study medications will be systematically monitored with assessments for extrapyramidal side effects and weight gain. Revision of treatment algorithms, reliability testing and data analysis will be coordinated between the four sites. Randomization, preparation of study medications, and overall management of the database will be centralized at UNC. Revisions: To address reviewers concerns, the revised proposal has added a fourth site (Harvard), revised the data management and analysis plan, and adjusted some of the primary outcome measures. Significance: There are very few controlled studies to inform clinical practice for the treatment of youth with psychotic disorders. This study will provide information about the comparative effectiveness of the most commonly used and representative antipsychotic drugs in youth with schizophrenia spectrum disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: WED BASED OUTREACH FOR PREGNANT AFRICAN AMERICAN WOMEN Principal Investigator & Institution: Herman, Joanne; Associate Professor; None; University of South Carolina at Columbia Byrnes Bldg., Room 501 Columbia, Sc 29208 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2004 Summary: Low birth weight and preterm birth are the primary factors responsible for neonatal deaths, perinatal deaths, and infants with permanent neurological damage. African American (AA) women are twice as likely as Caucasian women to deliver low birth weight or preterm infants. Low-income women are at an even higher risk for poor pregnancy outcomes. Perceived stress and poor social support are import factors that impact the higher incidence of low birth weight and preterm birth. Social support buffers the effect of stressors and improves pregnancy outcomes. The purpose of the study is to test the effect of an innovative World Wide Web (web) based social support intervention on stressors during pregnancy; pregnancy related health behaviors; and pregnancy outcomes of gestational, intrapartal, and neonatal complications in lowincome pregnant AA women. The study is a pretest-posttest control group design with random assignment to Web page group and standard care group. The sample will consist of 40 pregnant AA women between the ages of 18-39 in the first trimester of pregnancy. To be included, women must be classified as low obstetrical risk, pregnant for the first time, carrying a singleton pregnancy, have electricity, functioning television set, functioning phone line, and agree to have a WebTV installed in their home. The population of interest will be accessed from a prenatal clinic of a regional hospital in the southeastern United States. The variables of social support; stressors during pregnancy (global stress, pregnancy related stress, life events, mood states); pregnancy related health behavior (weight gain, nutrient intake, physical activity); and pregnancy outcomes (gestational, intrapartal, neonatal complications) will be measured using instruments designed for use with culturally diverse low income pregnant women. All subjects will complete pretest instruments between 10 and 20 weeks gestation. Subjects in the web page group will receive standard of care, have WebTV installed in their homes, be taught how to use the system, be taught how to access the Health Pregnancy web page. Subjects in the standard care group will receive stand care and be given a written copy of the information contained on the Health Pregnancy web page. Posttest data will be collected after 28 weeks gestation. Pretest and posttest measurement must be at least 10 weeks apart. The hypotheses will be tested using ANCOVA, ANOVA, ChiSquare, and test of proportion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: WEIGHT CONNECTION: WEIGHT LOSS MAINTANANCE USING THE WEB Principal Investigator & Institution: Kaplan, Lee M.; Associate Professor; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2004 Summary: Despite widespread recognition of the increasing prevalence and medical sequelae of obesity, efforts to reverse these trends have met with limited success. Although 75 percent of obese individuals who enter a weight loss program are initially successful, more than 90 percent of these individuals regain the lost weight within 5 years, leading to renewal or even exacerbation of cardiopulmonary and vascular disease risks. The focus of this proposal is the prevention of weight regain in obese individuals after successful weight loss. The best predictor of weight loss maintenance is the
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duration and intensity of patient-provider contact, irrespective of practitioner specialty or the nature of the intervention. However, the high costs of intensive interventions over an extended period limit optimal management to a small number of patients. The hypothesis underlying the proposed study is that some of the benefits of intensive patient-provider interaction can be achieved in a cost-efficient manner through creative use of electronic communication. We propose to develop a three-part, web-based program ("WeightConnection") that includes mechanisms for (1) ongoing, patient selfmonitoring and graphical feedback about weight, eating and exercise behavior, (2) individual, electronic consultative advice from a weight counselor and (3) on-line group-based therapy and peer-to-peer communication. Our goals for this intervention are to achieve several benefits of intensive patient-provider interaction that appear to underlie successful weight loss maintenance, including sustained patient motivation, diminished attrition rates, and timely relapse management. Each component of the proposed program is designed to promote these goals by providing personal guidance, educational opportunities and psychological support. We will initially test and refine the WeightConnection program with a small group of patient volunteers recruited from MGH Weight Center patients. Thereafter, we will examine whether this intervention improves the success of a standard group-based program in maintaining weight loss. We will conduct a randomized, controlled study in 30-40 patients, comparing the combination of the WeightConnection program and standard therapy vs. standard therapy alone. The results of this pilot study, including effects on weight maintenance and patient retention, preliminary subgroup analysis and careful assessment of patient usage and feedback, will be used to design a more definitive study of the efficacy and cost-effectiveness of electronic communication for prevention of recurrent weight gain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: WEIGHT GAIN IN AFRICAN-AMERICAN GIRLS Principal Investigator & Institution: Rochon, James; Research Professor; Statistics; George Washington University 2121 I St Nw Washington, Dc 20052 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-MAY-2002 Summary: According to NHANES data, the prevalence of obesity in the U.S. population has increased from 25 percent to 33 percent over the past 10 years. Obesity is well accepted as a risk factor for coronary heart disease and type 2 diabetes, and it exacerbates many chronic conditions such as hypertension and dyslipidemia. Not surprisingly, the economic costs of obesity are staggering and amount to approximately 100 billion dollars annually. The prevalence of obesity appears to be proportionately greater in certain minority populations. Almost twice as many African-American women are overweight compared to Caucasians. Moreover, the disproportionate levels of obesity in African-American women may have their origins in childhood and adolescence. Approximately 30 percent of African-American girls between the ages of 6 and 17 years are overweight, compared to only 22 percent for all other youth as a whole. Large prevention trials, most notably, the Child and Adolescent Trial for Cardiovascular Health (CATCH) and the Dietary Intervention Study in Children (DISC), have been largely unsuccessful in producing reductions in dietary fat, body weight or BMI. Thus, the NHLBI has proposed a research program to develop and test interventions to prevent weight gain in preadolescent African-American girls. The Biostatistics Center of the George Washington University proposes to serve as the Coordinating Center for this project. In this role, we will attend to the following functions. (1) Study Coordination and Planning: We will help establish an efficient organizational structure to ensure that all activities advance in a coordinated fashion. (2) Data Management Activities: We will
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apply our Distributed Data Entry system for on-going data collection and generate periodic reports summarizing the execution of the trial. (3) Statistical Analysis: We will provide statistical leadership in the design of the study, and perform interim and final analyses in an expeditious and timely manner. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: WISE MIND: ENVIRONMENTAL APPROACH FOR OBESITY PREVENTION Principal Investigator & Institution: Williamson, Donald A.; Professor; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, La 70808 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005 Summary: (provided by applicant): In this pilot study, we propose a two-arm primary prevention trial to test the efficacy of an environmental approach for the prevention of obesity in children who are in the second through sixth grades. An attention-placebo control group will receive an environmental approach for the prevention of alcohol drug tobacco use and abuse. This test of an environmental approach targets a school system for change. Four schools with a total of approximately 1,040 students will be the participants in the study. The four schools will be randomly assigned to one of the two treatment arms. The prevention study will be conducted across two consecutive academic years. The primary endpoint will be body mass index. The primary aim of the study is to test the efficacy of the obesity program for the prevention of weight gain in children. Changes in dietary intake and physical activity will be tested as mediators of changes in body mass index. Also, age of the child, initial body mass index, and gender will be tested as factors that are associated with differential outcomes related to the prevention of weight gain. Secondary endpoints include: body composition, waist circumference, physical activity, dietary intake, body image, mood, and self-esteem. The environmental program for the prevention of obesity will have multiple components that are designed to alter automatic/habitual decision making by students. The results of this pilot study will guide the development of full-scale investigations in a larger set of schools. The findings of the study will have significant impact upon public health policy regarding prevention of obesity. Several innovations are utilized in the study, including novel applications of the internet to provide environmental prompts to parents and families, and the use of a new method, called digital photography of foods, for measurement of the food selections and food intake of individual students, in school cafeterias. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and
3 4
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age.
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unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “weight gain” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for weight gain in the PubMed Central database: •
Altered anxiety and weight gain in corticotropin-releasing hormone-binding proteindeficient mice. by Karolyi IJ, Burrows HL, Ramesh TM, Nakajima M, Lesh JS, Seong E, Camper SA, Seasholtz AF.; 1999 Sep 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18079
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Antisense-mediated depletion of a potato lipoxygenase reduces wound induction of proteinase inhibitors and increases weight gain of insect pests. by Royo J, Leon J, Vancanneyt G, Albar JP, Rosahl S, Ortego F, Castanera P, Sanchez-Serrano JJ.; 1999 Feb 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15365
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Are atypical antipsychotics associated with an increased risk of diabetes, and is this associated with weight gain? by Chue PS.; 2001 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=167193
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Ciliary neurotrophic factor activates leptin-like pathways and reduces body fat, without cachexia or rebound weight gain, even in leptin-resistant obesity. by Lambert PD, Anderson KD, Sleeman MW, Wong V, Tan J, Hijarunguru A, Corcoran TL, Murray JD, Thabet KE, Yancopoulos GD, Wiegand SJ.; 2001 Apr 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=31889
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Corticotropin-releasing factor-binding protein ligand inhibitor blunts excessive weight gain in genetically obese Zucker rats and rats during nicotine withdrawal. by Heinrichs SC, Lapsansky J, Behan DP, Chan RK, Sawchenko PE, Lorang M, Ling N, Vale WW, De Souza EB.; 1996 Dec 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26429
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Galanin-Containing Neurons in the Paraventricular Nucleus: A Neurochemical Marker for Fat Ingestion and Body Weight Gain. by Akabayashi A, Koenig JI, Watanabe Y, Alexander JT, Leibowitz SF.; 1994 Oct 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45022
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Intervening to reduce weight gain in pregnancy and gestational diabetes mellitus in Cree communities: an evaluation. by Gray-Donald K, Robinson E, Collier A, David K, Renaud L, Rodrigues S.; 2000 Nov 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=80308
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Subtherapeutic levels of antibiotics in poultry feeds and their effects on weight gain, feed efficiency, and bacterial cholyltaurine hydrolase activity. by Feighner SD, Dashkevicz MP.; 1987 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203661
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The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with weight gain, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “weight gain” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for weight gain (hyperlinks lead to article summaries): •
A college nutrition science course as an intervention to prevent weight gain in female college freshmen. Author(s): Matvienko O, Lewis DS, Schafer E. Source: Journal of Nutrition Education. 2001 March-April; 33(2): 95-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12031189&dopt=Abstract
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A history of depression and smoking cessation outcomes among women concerned about post-cessation weight gain. Author(s): Levine MD, Marcus MD, Perkins KA. Source: Nicotine & Tobacco Research : Official Journal of the Society for Research on Nicotine and Tobacco. 2003 February; 5(1): 69-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745508&dopt=Abstract
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A longitudinal study of the effects of a gluten-free diet on glycemic control and weight gain in subjects with type 1 diabetes and celiac disease. Author(s): Amin R, Murphy N, Edge J, Ahmed ML, Acerini CL, Dunger DB. Source: Diabetes Care. 2002 July; 25(7): 1117-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12087007&dopt=Abstract
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A preliminary study of the relationship between clozapine-induced weight gain and menstrual irregularities in schizophrenic, schizoaffective, and bipolar women. Author(s): Feldman D, Goldberg JF. Source: Annals of Clinical Psychiatry : Official Journal of the American Academy of Clinical Psychiatrists. 2002 March; 14(1): 17-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12046636&dopt=Abstract
6
PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A program for managing weight gain associated with atypical antipsychotics. Author(s): Vreeland B, Minsky S, Menza M, Rigassio Radler D, Roemheld-Hamm B, Stern R. Source: Psychiatric Services (Washington, D.C.). 2003 August; 54(8): 1155-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12883145&dopt=Abstract
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A prospective study of holiday weight gain. Author(s): Yanovski JA, Yanovski SZ, Sovik KN, Nguyen TT, O'Neil PM, Sebring NG. Source: The New England Journal of Medicine. 2000 March 23; 342(12): 861-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10727591&dopt=Abstract
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Abnormal weight gain and weight management: are carbohydrates the enemy? Author(s): Daniels SR. Source: The Journal of Pediatrics. 2003 March; 142(3): 225-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640363&dopt=Abstract
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Abuse history and nonoptimal prenatal weight gain. Author(s): Johnson PJ, Hellerstedt WL, Pirie PL. Source: Public Health Reports (Washington, D.C. : 1974). 2002 March-April; 117(2): 14856. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12356999&dopt=Abstract
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Additive effect of A-->G (-3826) variant of the uncoupling protein gene and the Trp64Arg mutation of the beta 3-adrenergic receptor gene on weight gain in morbid obesity. Author(s): Clement K, Ruiz J, Cassard-Doulcier AM, Bouillaud F, Ricquier D, Basdevant A, Guy-Grand B, Froguel P. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1996 December; 20(12): 1062-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8968850&dopt=Abstract
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Alcohol, body weight, and weight gain in middle-aged men. Author(s): Wannamethee SG, Shaper AG. Source: The American Journal of Clinical Nutrition. 2003 May; 77(5): 1312-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716687&dopt=Abstract
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Amantadine treatment of psychotropic-induced weight gain in children and adolescents: case series. Author(s): Gracious BL, Krysiak TE, Youngstrom EA. Source: Journal of Child and Adolescent Psychopharmacology. 2002 Fall; 12(3): 249-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12427299&dopt=Abstract
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Analysing the relationship between maternal weight gain and birthweight: exploration of four statistical issues. Author(s): Selvin S, Abrams B. Source: Paediatric and Perinatal Epidemiology. 1996 April; 10(2): 220-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8778694&dopt=Abstract
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Android obesity at diagnosis and breast carcinoma survival: Evaluation of the effects of anthropometric variables at diagnosis, including body composition and body fat distribution and weight gain during life span,and survival from breast carcinoma. Author(s): Kumar NB, Cantor A, Allen K, Cox CE. Source: Cancer. 2000 June 15; 88(12): 2751-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10870057&dopt=Abstract
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Antipsychotic-induced weight gain and therapeutic response: a differential association. Author(s): Czobor P, Volavka J, Sheitman B, Lindenmayer JP, Citrome L, McEvoy J, Cooper TB, Chakos M, Lieberman JA. Source: Journal of Clinical Psychopharmacology. 2002 June; 22(3): 244-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006893&dopt=Abstract
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Antipsychotic-induced weight gain: bipolar disorder and leptin. Author(s): McIntyre RS, Mancini DA, Basile VS, Srinivasan J, Kennedy SH. Source: Journal of Clinical Psychopharmacology. 2003 August; 23(4): 323-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12920406&dopt=Abstract
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Are leptin and cytokines involved in body weight gain during treatment with antipsychotic drugs? Author(s): Baptista T, Beaulieu S. Source: Canadian Journal of Psychiatry. Revue Canadienne De Psychiatrie. 2002 October; 47(8): 742-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12420652&dopt=Abstract
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Association of antipsychotic drug-induced weight gain with a 5-HT2C receptor gene polymorphism. Author(s): Reynolds GP, Zhang ZJ, Zhang XB. Source: Lancet. 2002 June 15; 359(9323): 2086-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12086765&dopt=Abstract
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Association of body mass index, body fat, and weight gain with inflammation markers among rural residents in Japan. Author(s): Saito I, Yonemasu K, Inami F. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2003 April; 67(4): 323-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655163&dopt=Abstract
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Attenuation of olanzapine-induced weight gain with reboxetine in patients with schizophrenia: a double-blind, placebo-controlled study. Author(s): Poyurovsky M, Isaacs I, Fuchs C, Schneidman M, Faragian S, Weizman R, Weizman A. Source: The American Journal of Psychiatry. 2003 February; 160(2): 297-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562576&dopt=Abstract
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Atypical antipsychotics and weight gain--a systematic review. Author(s): Taylor DM, McAskill R. Source: Acta Psychiatrica Scandinavica. 2000 June; 101(6): 416-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10868465&dopt=Abstract
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Beliefs about weight gain and attitudes toward relapse in a sample of women and men with obesity. Author(s): Cachelin FM, Striegel-Moore RH, Brownell KD. Source: Obesity Research. 1998 May; 6(3): 231-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9618128&dopt=Abstract
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Beyond sloth--physical activity and weight gain. Author(s): Ravussin E, Danforth E Jr. Source: Science. 1999 January 8; 283(5399): 184-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9925477&dopt=Abstract
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Biobehavioral influences on energy intake and adult weight gain. Author(s): McCrory MA, Suen VM, Roberts SB. Source: The Journal of Nutrition. 2002 December; 132(12): 3830S-3834S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468634&dopt=Abstract
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Bionursing: how drugs can cause weight gain. Author(s): Jordan S, Torrance C. Source: Nurs Stand. 1996 February 21; 10(22): 47-50. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8695453&dopt=Abstract
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Birth weight, adulthood BMI, and subsequent weight gain in relation to leptin levels in Swedish women. Author(s): Lissner L, Karlsson C, Lindroos AK, Sjostrom L, Carlsson B, Carlsson L, Bengtsson C. Source: Obesity Research. 1999 March; 7(2): 150-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10102251&dopt=Abstract
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Blood pressure changes in relation to interdialytic weight gain. Author(s): Luik AJ, Gladziwa U, Kooman JP, van Hooff JP, de Leeuw PW, van Bortel LM, Leunissen KM. Source: Contrib Nephrol. 1994; 106: 90-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8174384&dopt=Abstract
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Blood transfusion in late anemia of prematurity: effect on oxygen consumption, heart rate, and weight gain in otherwise healthy infants. Author(s): Bohler T, Janecke A, Linderkamp O. Source: Infusionstherapie Und Transfusionsmedizin. 1994 December; 21(6): 376-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7873916&dopt=Abstract
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Body composition of anorexia nervosa patients assessed by underwater weighing and skinfold-thickness measurements before and after weight gain. Author(s): Probst M, Goris M, Vandereycken W, Van Coppenolle H. Source: The American Journal of Clinical Nutrition. 2001 February; 73(2): 190-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11157313&dopt=Abstract
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Body fat and water changes during pregnancy in women with different body weight and weight gain. Author(s): Lederman SA, Paxton A, Heymsfield SB, Wang J, Thornton J, Pierson RN Jr. Source: Obstetrics and Gynecology. 1997 October; 90(4 Pt 1): 483-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9380301&dopt=Abstract
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Body fat distribution before and after weight gain in anorexia nervosa. Author(s): Zamboni M, Armellini F, Turcato E, Todisco P, Gallagher D, Dalle Grave R, Heymsfield S, Bosello O. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1997 January; 21(1): 33-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9023598&dopt=Abstract
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Body mass index, weight gain, and risk of endometrial cancer. Author(s): Olson SH, Trevisan M, Marshall JR, Graham S, Zielezny M, Vena JE, Hellmann R, Freudenheim JL. Source: Nutrition and Cancer. 1995; 23(2): 141-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7644383&dopt=Abstract
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Body weight and weight gain during adult life in men in relation to coronary heart disease and mortality. A prospective population study. Author(s): Rosengren A, Wedel H, Wilhelmsen L. Source: European Heart Journal. 1999 February; 20(4): 269-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10099921&dopt=Abstract
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Body weight and weight gain related to pulmonary function decline in adults: a six year follow up study. Author(s): Chen Y, Horne SL, Dosman JA. Source: Thorax. 1993 April; 48(4): 375-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8511735&dopt=Abstract
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Body weight gain after administration of antipsychotic drugs. Author(s): Baptista T, Lacruz A, De Mendoza D, Mendoza JM, Silvera R, Angeles F, Mendoza MT, Hernandez L. Source: Pharmacopsychiatry. 2002 January; 35(1): 36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11819161&dopt=Abstract
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Body weight gain after administration of antipsychotic drugs: correlation with leptin, insulin and reproductive hormones. Author(s): Baptista T, Lacruz A, de Mendoza S, Mendoza Guillen JM, Silvera R, Angeles F, Mendoza MT, Hernandez L. Source: Pharmacopsychiatry. 2000 May; 33(3): 81-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10855458&dopt=Abstract
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Body weight gain induced by antipsychotic drugs: mechanisms and management. Author(s): Baptista T. Source: Acta Psychiatrica Scandinavica. 1999 July; 100(1): 3-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10442434&dopt=Abstract
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Body weight gain, insulin, and leptin in olanzapine-treated patients. Author(s): Baptista T, Beaulieu S. Source: The Journal of Clinical Psychiatry. 2001 November; 62(11): 902-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11775052&dopt=Abstract
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Brain hypometabolism of glucose in anorexia nervosa: normalization after weight gain. Author(s): Delvenne V, Goldman S, De Maertelaer V, Simon Y, Luxen A, Lotstra F. Source: Biological Psychiatry. 1996 October 15; 40(8): 761-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8894069&dopt=Abstract
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Breast cancer incidence in ex-smokers in relation to body mass index, weight gain and blood lipid levels. Author(s): Manjer J, Malina J, Berglund G, Bondeson L, Garne JP, Janzon L. Source: European Journal of Cancer Prevention : the Official Journal of the European Cancer Prevention Organisation (Ecp). 2001 June; 10(3): 281-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11432717&dopt=Abstract
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Breastmilk feeding status and weight gain of low birth weight infants in a Neonatal Intensive Care Unit. Author(s): Lim NL, Cheah IG, Soosai AP. Source: Med J Malaysia. 2001 March; 56(1): 65-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11503299&dopt=Abstract
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Can physical activity minimize weight gain in women after smoking cessation? Author(s): Kawachi I, Troisi RJ, Rotnitzky AG, Coakley EH, Colditz GA. Source: American Journal of Public Health. 1996 July; 86(7): 999-1004. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8669525&dopt=Abstract
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Carbamazepine and weight gain. Author(s): Ranganath HN. Source: Neurology India. 2000 September; 48(3): 299. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11184456&dopt=Abstract
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Causes of adult weight gain. Author(s): Roberts SB, Williamson DF. Source: The Journal of Nutrition. 2002 December; 132(12): 3824S-3825S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468632&dopt=Abstract
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Changes in body composition and resting energy expenditure in anorectic patients after a weight gain of fifteen percent. Author(s): Pagliato E, Corradi E, Gentile MG, Testolin G. Source: Annals of the New York Academy of Sciences. 2000 May; 904: 617-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10865815&dopt=Abstract
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Changes in weight gain and anaemia attributable to malaria in Tanzanian children living under holoendemic conditions. Author(s): Shiff C, Checkley W, Winch P, Premji Z, Minjas J, Lubega P. Source: Trans R Soc Trop Med Hyg. 1996 May-June; 90(3): 262-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8758071&dopt=Abstract
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Characterization of tobacco withdrawal symptoms: transdermal nicotine reduces hunger and weight gain. Author(s): Jorenby DE, Hatsukami DK, Smith SS, Fiore MC, Allen S, Jensen J, Baker TB. Source: Psychopharmacology. 1996 November; 128(2): 130-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8956374&dopt=Abstract
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Characterizing concerns about post-cessation weight gain: results from a national survey of women smokers. Author(s): Pomerleau CS, Zucker AN, Stewart AJ. Source: Nicotine & Tobacco Research : Official Journal of the Society for Research on Nicotine and Tobacco. 2001 February; 3(1): 51-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11260811&dopt=Abstract
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Clinical determinants of interdialytic weight gain. Author(s): Testa A, Plou A. Source: Journal of Renal Nutrition : the Official Journal of the Council on Renal Nutrition of the National Kidney Foundation. 2001 July; 11(3): 155-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11466666&dopt=Abstract
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Clozapine and weight gain. Author(s): Theisen FM, Cichon S, Linden A, Martin M, Remschmidt H, Hebebrand J. Source: The American Journal of Psychiatry. 2001 May; 158(5): 816. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11329412&dopt=Abstract
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Clozapine weight gain, plus topiramate weight loss. Author(s): Dursun SM, Devarajan S. Source: Canadian Journal of Psychiatry. Revue Canadienne De Psychiatrie. 2000 March; 45(2): 198. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10742883&dopt=Abstract
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Clozapine, diabetes mellitus, weight gain, and lipid abnormalities: A five-year naturalistic study. Author(s): Henderson DC, Cagliero E, Gray C, Nasrallah RA, Hayden DL, Schoenfeld DA, Goff DC. Source: The American Journal of Psychiatry. 2000 June; 157(6): 975-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10831479&dopt=Abstract
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Clozapine: diabetes mellitus, weight gain, and lipid abnormalities. Author(s): Henderson DC. Source: The Journal of Clinical Psychiatry. 2001; 62 Suppl 23: 39-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11603884&dopt=Abstract
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Clozapine-induced weight gain predicts improvement in psychopathology. Author(s): Meltzer HY, Perry E, Jayathilake K. Source: Schizophrenia Research. 2003 January 1; 59(1): 19-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413638&dopt=Abstract
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Combination-therapy with bedtime nph insulin and sulphonylureas gives similar glycaemic control but lower weight gain than insulin twice daily in patients with type 2 diabetes. Author(s): Olsson PO, Lindstrom T. Source: Diabetes & Metabolism. 2002 September; 28(4 Pt 1): 272-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12442064&dopt=Abstract
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Comorbidity of schizophrenia and galactosemia: effective clozapine treatment with weight gain. Author(s): Haasen C, Lambert M, Yagdiran O, Karow A, Krausz M, Naber D. Source: International Clinical Psychopharmacology. 2003 March; 18(2): 113-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12598824&dopt=Abstract
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Conjugated linoleic acid may be useful in treating diabetes by controlling body fat and weight gain. Author(s): Pariza MW. Source: Diabetes Technology & Therapeutics. 2002; 4(3): 335-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12165172&dopt=Abstract
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Contribution of excess weight gain during pregnancy and macrosomia to the cesarean delivery rate, 1990-2000. Author(s): Rhodes JC, Schoendorf KC, Parker JD. Source: Pediatrics. 2003 May; 111(5 Part 2): 1181-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728135&dopt=Abstract
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Corticotropin-releasing factor-binding protein ligand inhibitor blunts excessive weight gain in genetically obese Zucker rats and rats during nicotine withdrawal. Author(s): Heinrichs SC, Lapsansky J, Behan DP, Chan RK, Sawchenko PE, Lorang M, Ling N, Vale WW, De Souza EB. Source: Proceedings of the National Academy of Sciences of the United States of America. 1996 December 24; 93(26): 15475-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8986836&dopt=Abstract
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Cup or bottle for preterm infants: effects on oxygen saturation, weight gain, and breastfeeding. Author(s): Rocha NM, Martinez FE, Jorge SM. Source: Journal of Human Lactation : Official Journal of International Lactation Consultant Association. 2002 May; 18(2): 132-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12033074&dopt=Abstract
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CYP2D6 polymorphisms and atypical antipsychotic weight gain. Author(s): Ellingrod VL, Miller D, Schultz SK, Wehring H, Arndt S. Source: Psychiatric Genetics. 2002 March; 12(1): 55-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11901361&dopt=Abstract
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Daily weight gain and protein catabolic rate are lower over the long interdialytic interval. Author(s): Stragier A, Jadoul M. Source: Clinical Nephrology. 2003 July; 60(1): 22-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12872854&dopt=Abstract
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Dance and reducing television viewing to prevent weight gain in African-American girls: the Stanford GEMS pilot study. Author(s): Robinson TN, Killen JD, Kraemer HC, Wilson DM, Matheson DM, Haskell WL, Pruitt LA, Powell TM, Owens AS, Thompson NS, Flint-Moore NM, Davis GJ, Emig KA, Brown RT, Rochon J, Green S, Varady A. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S65-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713212&dopt=Abstract
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Deficits in haptic perception and right parietal theta power changes in patients with anorexia nervosa before and after weight gain. Author(s): Grunwald M, Ettrich C, Assmann B, Dahne A, Krause W, Busse F, Gertz HJ. Source: The International Journal of Eating Disorders. 2001 May; 29(4): 417-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11285579&dopt=Abstract
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Depomedroxyprogesterone acetate use and weight gain among adolescents. Author(s): Templeman C, Boyd H, Hertweck SP. Source: Journal of Pediatric and Adolescent Gynecology. 2000 February; 13(1): 45-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10841626&dopt=Abstract
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Depo-provera associated with weight gain in Navajo women. Author(s): Espey E, Steinhart J, Ogburn T, Qualls C. Source: Contraception. 2000 August; 62(2): 55-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11102587&dopt=Abstract
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Desogestrel plus testosterone effectively suppresses spermatogenesis but also causes modest weight gain and high-density lipoprotein suppression. Author(s): Anawalt BD, Herbst KL, Matsumoto AM, Mulders TM, Coelingh-Bennink HJ, Bremner WJ. Source: Fertility and Sterility. 2000 October; 74(4): 707-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11020511&dopt=Abstract
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Determinants of gestational weight gain outside the recommended ranges among black and white women. Author(s): Caulfield LE, Witter FR, Stoltzfus RJ. Source: Obstetrics and Gynecology. 1996 May; 87(5 Pt 1): 760-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8677082&dopt=Abstract
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Dietary and genetic influences on susceptibility or resistance to weight gain on a high fat diet. Author(s): Mercer JG. Source: Nutr Metab Cardiovasc Dis. 2001 August; 11(4 Suppl): 114-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11894743&dopt=Abstract
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Dietary fiber and weight gain. Author(s): Waugh RJ. Source: Jama : the Journal of the American Medical Association. 2000 April 12; 283(14): 1821; Author Reply 1821-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10770137&dopt=Abstract
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Dietary fiber and weight gain. Author(s): McCarty MF. Source: Jama : the Journal of the American Medical Association. 2000 April 12; 283(14): 1821; Author Reply 1821-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10770136&dopt=Abstract
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Dietary fiber, weight gain, and cardiovascular disease risk factors in young adults. Author(s): Ludwig DS, Pereira MA, Kroenke CH, Hilner JE, Van Horn L, Slattery ML, Jacobs DR Jr. Source: Jama : the Journal of the American Medical Association. 1999 October 27; 282(16): 1539-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10546693&dopt=Abstract
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Dietary habits, pregnancy weight gain and birthweights in a highland population of Kenya. Author(s): Perry H, Muita JW, Omwega AM. Source: East Afr Med J. 1996 July; 73(7): 424-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8918001&dopt=Abstract
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Dietary intervention in the first four years prevents abnormal weight gain but negatively affects height development in Prader-Willi syndrome. Author(s): Schmidt H, Schwarz HP, Enders A. Source: Acta Paediatrica (Oslo, Norway : 1992). 2001 April; 90(4): 468-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11332946&dopt=Abstract
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Dietary restraint and weight gain during pregnancy. Author(s): Conway R, Reddy S, Davies J. Source: European Journal of Clinical Nutrition. 1999 November; 53(11): 849-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10556996&dopt=Abstract
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Discrepancy between objective weight gain and recognition as a side effect of antipsychotic treatment. Author(s): Haberfellner EM, Rittmannsberger H. Source: European Psychiatry : the Journal of the Association of European Psychiatrists. 1999 September; 14(5): 298. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10572361&dopt=Abstract
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Do epileptic children treated with valproate have a risk of excessive weight gain? Author(s): Bosnak M, Dikici B, Haspolat K, Dagli A, Dikici S. Source: Journal of Child Neurology. 2003 April; 18(4): 306; Author Reply 306. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760438&dopt=Abstract
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Does long-term use of valproate cause weight gain in prepubertal epileptic children? Author(s): Caksen H, Deda G, Berberoglu M. Source: The International Journal of Neuroscience. 2002 October; 112(10): 1183-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12587521&dopt=Abstract
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Does physical activity prevent weight gain--a systematic review. Author(s): Fogelholm M, Kukkonen-Harjula K. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 October; 1(2): 95-111. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119991&dopt=Abstract
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Does physical exercise in addition to a multicomponent smoking cessation program increase abstinence rate and suppress weight gain? An intervention study. Author(s): Jonsdottir D, Jonsdottir H. Source: Scandinavian Journal of Caring Sciences. 2001; 15(4): 275-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12453168&dopt=Abstract
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Does relative leptinemia predict weight gain in humans? Author(s): Jenkins AB, Campbell LV. Source: Obesity Research. 2003 March; 11(3): 373-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634432&dopt=Abstract
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Early excess weight gain of children in the Pima Indian population. Author(s): Lindsay RS, Cook V, Hanson RL, Salbe AD, Tataranni A, Knowler WC. Source: Pediatrics. 2002 February; 109(2): E33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11826243&dopt=Abstract
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Early weight gain patterns may affect adult blood pressure. Author(s): Bradbury J. Source: Lancet. 2002 February 9; 359(9305): 501. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11853806&dopt=Abstract
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Eating behavior correlates of adult weight gain and obesity in healthy women aged 55-65 y. Author(s): Hays NP, Bathalon GP, McCrory MA, Roubenoff R, Lipman R, Roberts SB. Source: The American Journal of Clinical Nutrition. 2002 March; 75(3): 476-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11864852&dopt=Abstract
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Effect of multivitamin and vitamin A supplements on weight gain during pregnancy among HIV-1-infected women. Author(s): Villamor E, Msamanga G, Spiegelman D, Antelman G, Peterson KE, Hunter DJ, Fawzi WW. Source: The American Journal of Clinical Nutrition. 2002 November; 76(5): 1082-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399282&dopt=Abstract
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Effect of traditional food supplementation during pregnancy on maternal weight gain and birthweight. Author(s): Kaseb F, Kimiagar M, Ghafarpoor M, Valaii N. Source: Int J Vitam Nutr Res. 2002 December; 72(6): 389-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12596505&dopt=Abstract
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Effects of insulin-like growth factor on weight gain in chronic hypoxic rats. Author(s): Iioka Y, Tatsumi K, Sugito K, Moriya T, Kuriyama T. Source: Journal of Cardiovascular Pharmacology. 2002 May; 39(5): 636-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11973406&dopt=Abstract
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Effects of megestrol acetate on weight gain, body composition, and pulmonary function in patients with cystic fibrosis. Author(s): Eubanks V, Koppersmith N, Wooldridge N, Clancy JP, Lyrene R, Arani RB, Lee J, Moldawer L, Atchison J, Sorscher EJ, Makris CM. Source: The Journal of Pediatrics. 2002 April; 140(4): 439-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006958&dopt=Abstract
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Effects of neurobehavioral assessment on feeding and weight gain in preterm neonates. Author(s): Senn TE, Espy KA. Source: Journal of Developmental and Behavioral Pediatrics : Jdbp. 2003 April; 24(2): 858. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692452&dopt=Abstract
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Effects of testosterone replacement and/or resistance exercise on the composition of megestrol acetate stimulated weight gain in elderly men: a randomized controlled trial. Author(s): Lambert CP, Sullivan DH, Freeling SA, Lindquist DM, Evans WJ. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 May; 87(5): 2100-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11994348&dopt=Abstract
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Efficacy of Rigiflex balloon dilatation in 12 children with achalasia: a 6-month prospective study showing weight gain and symptomatic improvement. Author(s): Khan AA, Shah SW, Alam A, Butt AK, Shafqat F. Source: Diseases of the Esophagus : Official Journal of the International Society for Diseases of the Esophagus / I.S.D.E. 2002; 15(2): 167-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12220427&dopt=Abstract
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Energy/protein restriction for high weight-for-height or weight gain during pregnancy. Author(s): Kramer MS. Source: Cochrane Database Syst Rev. 2000; (2): Cd000080. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10796119&dopt=Abstract
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Enhanced weight gain in preterm infants receiving lactase-treated feeds: a randomized, double-blind, controlled trial. Author(s): Erasmus HD, Ludwig-Auser HM, Paterson PG, Sun D, Sankaran K. Source: The Journal of Pediatrics. 2002 October; 141(4): 532-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12378193&dopt=Abstract
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Epidemiologic data on the relationships of caloric intake, energy balance, and weight gain over the life span with longevity and morbidity. Author(s): Lee IM, Blair SN, Allison DB, Folsom AR, Harris TB, Manson JE, Wing RR. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2001 March; 56 Spec No 1: 7-19. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12088215&dopt=Abstract
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Epidemiology, implications and mechanisms underlying drug-induced weight gain in psychiatric patients. Author(s): Zimmermann U, Kraus T, Himmerich H, Schuld A, Pollmacher T. Source: Journal of Psychiatric Research. 2003 May-June; 37(3): 193-220. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12650740&dopt=Abstract
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Ethnicity modifies seasonal variations in birth weight and weight gain of infants. Author(s): van Hanswijck de Jonge L, Waller G, Stettler N. Source: The Journal of Nutrition. 2003 May; 133(5): 1415-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730431&dopt=Abstract
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European best practice guidelines for renal transplantation. Section IV: Long-term management of the transplant recipient. IV.5.7. Cardiovascular risks. Obesity and weight gain. Author(s): EBPG Expert Group on Renal Transplantation. Source: Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 2002; 17 Suppl 4: 2930. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12091635&dopt=Abstract
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Excess pregnancy weight gain and long-term obesity: one decade later. Author(s): Rooney BL, Schauberger CW. Source: Obstetrics and Gynecology. 2002 August; 100(2): 245-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12151145&dopt=Abstract
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Excessive weight gain following therapy for hyperthyroidism--a major problem. Author(s): Ross IL, Levitt NS. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 2003 July; 93(7): 515-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939923&dopt=Abstract
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Exercise and weight gain in breast cancer patients receiving chemotherapy. Author(s): Schwartz AL. Source: Cancer Practice. 2000 September-October; 8(5): 231-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11898235&dopt=Abstract
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Extreme weight gain in a youth with schizophrenia: risk/benefit considerations. Author(s): Webster D, Devarajan S, Gallant J, Harris A, Kopala LC. Source: Schizophrenia Research. 2002 July 1; 56(1-2): 187-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12084432&dopt=Abstract
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Factors associated with the pattern of maternal weight gain during pregnancy. Author(s): Abrams B, Carmichael S, Selvin S. Source: Obstetrics and Gynecology. 1995 August; 86(2): 170-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7617345&dopt=Abstract
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Factors associated with weight gain in women after diagnosis of breast cancer. Women's Healthy Eating and Living Study Group. Author(s): Rock CL, Flatt SW, Newman V, Caan BJ, Haan MN, Stefanick ML, Faerber S, Pierce JP. Source: Journal of the American Dietetic Association. 1999 October; 99(10): 1212-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10524383&dopt=Abstract
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Factors influencing weight gain after renal transplantation. Author(s): Johnson CP, Gallagher-Lepak S, Zhu YR, Porth C, Kelber S, Roza AM, Adams MB. Source: Transplantation. 1993 October; 56(4): 822-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8212200&dopt=Abstract
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Factors that are associated with cesarean delivery in a large private practice: the importance of prepregnancy body mass index and weight gain. Author(s): Young TK, Woodmansee B. Source: American Journal of Obstetrics and Gynecology. 2002 August; 187(2): 312-8; Discussion 318-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12193918&dopt=Abstract
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Failure of antipsychotic drug dose to explain abnormal diurnal weight gain among 129 chronically psychotic inpatients. Author(s): Victor W, Vieweg R, Godleski LS, Hundley PL, Yank GR. Source: Progress in Neuro-Psychopharmacology & Biological Psychiatry. 1989; 13(5): 709-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2571178&dopt=Abstract
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Famine, third-trimester pregnancy weight gain, and intrauterine growth: the Dutch Famine Birth Cohort Study. Author(s): Stein AD, Ravelli AC, Lumey LH. Source: Human Biology; an International Record of Research. 1995 February; 67(1): 13550. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7721275&dopt=Abstract
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Fasting and post-glucose ghrelin levels in SGA infants: relationships with size and weight gain at one year of age. Author(s): Iniguez G, Ong K, Pena V, Avila A, Dunger D, Mericq V. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 December; 87(12): 5830-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12466394&dopt=Abstract
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Fasting hyperinsulinemia is a predictor of increased body weight gain and obesity in Pima Indian children. Author(s): Odeleye OE, de Courten M, Pettitt DJ, Ravussin E. Source: Diabetes. 1997 August; 46(8): 1341-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9231660&dopt=Abstract
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Fasting respiratory exchange ratio and resting metabolic rate as predictors of weight gain: the Baltimore Longitudinal Study on Aging. Author(s): Seidell JC, Muller DC, Sorkin JD, Andres R. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1992 September; 16(9): 667-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1328091&dopt=Abstract
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Fear of weight gain: its correlates among school-aged adolescents. Author(s): Moore SM, Gullone E. Source: Psychological Reports. 1995 June; 76(3 Pt 2): 1305-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7480500&dopt=Abstract
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Fetal macrosomia and maternal weight gain during pregnancy. Author(s): Lepercq J, Hauguel-De Mouzon S, Timsit J, Catalano PM. Source: Diabetes & Metabolism. 2002 September; 28(4 Pt 1): 323-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12442070&dopt=Abstract
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Fetal weight gain at term: linear with minimal dependence on maternal obesity. Author(s): Nahum GG, Stanislaw H, Huffaker BJ. Source: American Journal of Obstetrics and Gynecology. 1995 May; 172(5): 1387-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7755043&dopt=Abstract
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Fetal weight gain in a serially scanned high-risk population. Author(s): de Jong CL, Gardosi J, Baldwin C, Francis A, Dekker GA, van Geijn HP. Source: Ultrasound in Obstetrics & Gynecology : the Official Journal of the International Society of Ultrasound in Obstetrics and Gynecology. 1998 January; 11(1): 39-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9511194&dopt=Abstract
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Fibrinogen, other putative markers of inflammation, and weight gain in middle-aged adults--the ARIC study. Atherosclerosis Risk in Communities. Author(s): Duncan BB, Schmidt MI, Chambless LE, Folsom AR, Carpenter M, Heiss G. Source: Obesity Research. 2000 July; 8(4): 279-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10933303&dopt=Abstract
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Fluoxetine in panic disorder patients with imipramine-associated weight gain. Author(s): Brady K, Zarzar M, Lydiard RB. Source: Journal of Clinical Psychopharmacology. 1989 February; 9(1): 66-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2785123&dopt=Abstract
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Food intake and weight gain in pregnant women. Author(s): Caan B, Petitti DB. Source: The American Journal of Clinical Nutrition. 1983 November; 38(5): 815-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6637873&dopt=Abstract
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Food supplementation with encouragement to feed it to infants from 4 to 12 months of age has a small impact on weight gain. Author(s): Bhandari N, Bahl R, Nayyar B, Khokhar P, Rohde JE, Bhan MK. Source: The Journal of Nutrition. 2001 July; 131(7): 1946-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11435512&dopt=Abstract
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From beltline to steering wheel: the vanishing space. An informal study of persistent weight gain of truck drivers. Author(s): Rather RJ, Warriner S, Johnson D. Source: S D J Med. 1981 March; 24(3): 21-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6944792&dopt=Abstract
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From physiology to neuroendocrinology: a reappraisal of risk factors of body weight gain in humans. Author(s): Tataranni PA. Source: Diabetes & Metabolism. 1998 April; 24(2): 108-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9592634&dopt=Abstract
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Fructose, weight gain, and the insulin resistance syndrome. Author(s): Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ. Source: The American Journal of Clinical Nutrition. 2002 November; 76(5): 911-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12399260&dopt=Abstract
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Gender differences in neonatal subcutaneous fat store in late gestation in relation to maternal weight gain. Author(s): Guihard-Costa AM, Papiernik E, Grange G, Richard A. Source: Annals of Human Biology. 2002 January-February; 29(1): 26-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11822483&dopt=Abstract
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Gender effect of the Trp64Arg mutation in the beta 3 adrenergic receptor gene on weight gain in morbid obesity. Author(s): Clement K, Manning BS, Basdevant A, Strosberg AD, Guy-Grand B, Froguel P. Source: Diabetes & Metabolism. 1997 November; 23(5): 424-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9416435&dopt=Abstract
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Genetic dissection of atypical antipsychotic-induced weight gain: novel preliminary data on the pharmacogenetic puzzle. Author(s): Basile VS, Masellis M, McIntyre RS, Meltzer HY, Lieberman JA, Kennedy JL. Source: The Journal of Clinical Psychiatry. 2001; 62 Suppl 23: 45-66. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11603885&dopt=Abstract
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Genetic factors as predictors of weight gain in young adult Dutch men and women. Author(s): van Rossum CT, Hoebee B, Seidell JC, Bouchard C, van Baak MA, de Groot CP, Chagnon M, de Graaf C, Saris WH. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 April; 26(4): 517-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12075579&dopt=Abstract
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Genetic influences on adult weight gain and maximum body mass index in male twins. Author(s): Fabsitz RR, Sholinsky P, Carmelli D. Source: American Journal of Epidemiology. 1994 October 15; 140(8): 711-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7942773&dopt=Abstract
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Genetic variation in the leptin receptor gene, leptin, and weight gain in young Dutch adults. Author(s): van Rossum CT, Hoebee B, van Baak MA, Mars M, Saris WH, Seidell JC. Source: Obesity Research. 2003 March; 11(3): 377-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634434&dopt=Abstract
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Gestational weight gain among average-weight and overweight women--what is excessive? Author(s): Cogswell ME, Serdula MK, Hungerford DW, Yip R. Source: American Journal of Obstetrics and Gynecology. 1995 February; 172(2 Pt 1): 70512. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7856711&dopt=Abstract
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Gestational weight gain and postpartum behaviors associated with weight change from early pregnancy to 1 y postpartum. Author(s): Olson CM, Strawderman MS, Hinton PS, Pearson TA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 January; 27(1): 117-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532163&dopt=Abstract
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Gestational weight gain as a predictor of birth and placenta weight according to prepregnancy body mass index. Author(s): Zhou W, Olsen J. Source: Acta Obstetricia Et Gynecologica Scandinavica. 1997 April; 76(4): 300-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9174421&dopt=Abstract
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Gestational weight gain, pregnancy outcome, and postpartum weight retention. Author(s): Scholl TO, Hediger ML, Schall JI, Ances IG, Smith WK. Source: Obstetrics and Gynecology. 1995 September; 86(3): 423-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7651655&dopt=Abstract
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Glucose dysregulation and mirtazapine-induced weight gain. Author(s): Fisfalen ME, Hsiung RC. Source: The American Journal of Psychiatry. 2003 April; 160(4): 797. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668379&dopt=Abstract
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Gluteal region morphology: the effect of the weight gain and aging. Author(s): Babuccu O, Gozil R, Ozmen S, Bahcelioglu M, Latifoglu O, Celebi MC. Source: Aesthetic Plastic Surgery. 2002 March-April; 26(2): 130-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12016499&dopt=Abstract
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Growth and weight gain in children with vesicoureteral reflux receiving medical versus surgical treatment: 10-year results of a prospective, randomized study. International Reflux Study in Children (European Branch). Author(s): Wingen AM, Koskimies O, Olbing H, Seppanen J, Tamminen-Mobius T. Source: Acta Paediatrica (Oslo, Norway : 1992). 1999 January; 88(1): 56-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10090549&dopt=Abstract
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Growth hormone secretion and effects of growth hormone therapy on growth velocity and weight gain in children with Prader-Willi syndrome. Author(s): Angulo M, Castro-Magana M, Mazur B, Canas JA, Vitollo PM, Sarrantonio M. Source: J Pediatr Endocrinol Metab. 1996 May-June; 9(3): 393-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8887149&dopt=Abstract
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H(2) antagonist nizatidine may control olanzapine-associated weight gain in schizophrenic patients. Author(s): Sacchetti E, Guarneri L, Bravi D. Source: Biological Psychiatry. 2000 July 15; 48(2): 167-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10903413&dopt=Abstract
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H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs. Author(s): Kroeze WK, Hufeisen SJ, Popadak BA, Renock SM, Steinberg S, Ernsberger P, Jayathilake K, Meltzer HY, Roth BL. Source: Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology. 2003 March; 28(3): 519-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629531&dopt=Abstract
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Haptic perception in anorexia nervosa before and after weight gain. Author(s): Grunwald M, Ettrich C, Krause W, Assmann B, Dahne A, Weiss T, Gertz HJ. Source: J Clin Exp Neuropsychol. 2001 August; 23(4): 520-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11780950&dopt=Abstract
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HbA1, height velocity and weight gain as indicators of metabolic control in type I diabetic children. A 5 year survey. Author(s): Arreola F, Junco E, Partida-Hernandez G, Almengor A, Mondragon L. Source: Arch Invest Med (Mex). 1991 July-December; 22(3-4): 303-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1844116&dopt=Abstract
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Hedonic response to sucrose solutions and the fear of weight gain in patients with eating disorders. Author(s): Eiber R, Berlin I, de Brettes B, Foulon C, Guelfi JD. Source: Psychiatry Research. 2002 December 15; 113(1-2): 173-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12467956&dopt=Abstract
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Hemodialysis and the elderly patient: potential advantages as to quality of life, urea generation, serum creatinine, and less interdialytic weight gain. Author(s): Avram MR, Pena C, Burrell D, Antignani A, Avram MM. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 1990 October; 16(4): 342-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2220783&dopt=Abstract
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High fasting insulin levels associated with lower rates of weight gain in persons with normal glucose tolerance: the San Luis Valley Diabetes Study. Author(s): Hoag S, Marshall JA, Jones RH, Hamman RF. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1995 March; 19(3): 175-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7780493&dopt=Abstract
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Higher androgens and weight gain with valproate compared with lamotrigine for epilepsy. Author(s): Morrell MJ, Isojarvi J, Taylor AE, Dam M, Ayala R, Gomez G, O'Neill F, Tennis P, Messenheimer J. Source: Epilepsy Research. 2003 May; 54(2-3): 189-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837570&dopt=Abstract
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Hindmilk improves weight gain in low-birth-weight infants fed human milk. Author(s): Valentine CJ, Hurst NM, Schanler RJ. Source: Journal of Pediatric Gastroenterology and Nutrition. 1994 May; 18(4): 474-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8071785&dopt=Abstract
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Holiday weight gain: fact or fiction? Author(s): Roberts SB, Mayer J. Source: Nutrition Reviews. 2000 December; 58(12): 378-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11206847&dopt=Abstract
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Hormone replacement therapy dissociates fat mass and bone mass, and tends to reduce weight gain in early postmenopausal women: a randomized controlled 5-year clinical trial of the Danish Osteoporosis Prevention Study. Author(s): Jensen LB, Vestergaard P, Hermann AP, Gram J, Eiken P, Abrahamsen B, Brot C, Kolthoff N, Sorensen OH, Beck-Nielsen H, Nielsen SP, Charles P, Mosekilde L. Source: Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research. 2003 February; 18(2): 333-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12568411&dopt=Abstract
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How can obese weight controllers minimize weight gain during the high risk holiday season? By self-monitoring very consistently. Author(s): Boutelle KN, Kirschenbaum DS, Baker RC, Mitchell ME. Source: Health Psychology : Official Journal of the Division of Health Psychology, American Psychological Association. 1999 July; 18(4): 364-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10431937&dopt=Abstract
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How much physical activity is enough to prevent unhealthy weight gain? Outcome of the IASO 1st Stock Conference and consensus statement. Author(s): Saris WH, Blair SN, van Baak MA, Eaton SB, Davies PS, Di Pietro L, Fogelholm M, Rissanen A, Schoeller D, Swinburn B, Tremblay A, Westerterp KR, Wyatt H. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 101-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760445&dopt=Abstract
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How much weight gain occurs following smoking cessation? A comparison of weight gain using both continuous and point prevalence abstinence. Author(s): Klesges RC, Winders SE, Meyers AW, Eck LH, Ward KD, Hultquist CM, Ray JW, Shadish WR. Source: Journal of Consulting and Clinical Psychology. 1997 April; 65(2): 286-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9086692&dopt=Abstract
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Human adenovirus Ad-36 promotes weight gain in male rhesus and marmoset monkeys. Author(s): Dhurandhar NV, Whigham LD, Abbott DH, Schultz-Darken NJ, Israel BA, Bradley SM, Kemnitz JW, Allison DB, Atkinson RL. Source: The Journal of Nutrition. 2002 October; 132(10): 3155-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368411&dopt=Abstract
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Hyperphagia, weight gain and neonatal drug withdrawal. Author(s): Shephard R, Greenough A, Johnson K, Gerada C. Source: Acta Paediatrica (Oslo, Norway : 1992). 2002; 91(9): 951-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12412871&dopt=Abstract
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Hyperprolactinaemia as a reversible cause of weight gain in male patients? Author(s): Delgrange E, Donckier J, Maiter D. Source: Clinical Endocrinology. 1999 February; 50(2): 271. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10396373&dopt=Abstract
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Hypertonic saline (7.5%) decreases perioperative weight gain following cardiac surgery. Author(s): Jarvela K, Kaukinen S. Source: Journal of Cardiothoracic and Vascular Anesthesia. 2002 February; 16(1): 43-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11854877&dopt=Abstract
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Hypoproteinemia predicts acute respiratory distress syndrome development, weight gain, and death in patients with sepsis. Ibuprofen in Sepsis Study Group. Author(s): Mangialardi RJ, Martin GS, Bernard GR, Wheeler AP, Christman BW, Dupont WD, Higgins SB, Swindell BB. Source: Critical Care Medicine. 2000 September; 28(9): 3137-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11008971&dopt=Abstract
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Hypothesis: Beta-adrenergic receptor blockers and weight gain: A systematic analysis. Author(s): Sharma AM, Pischon T, Hardt S, Kunz I, Luft FC. Source: Hypertension. 2001 February; 37(2): 250-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11230280&dopt=Abstract
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Impact of breastfeeding on weight gain and incidence of diarrhea among low birth weight infants of an urban slum of Calcutta. Author(s): Sur D, Mondal SK, Gupta DN, Ghosh S, Manna B, Sengupta PG. Source: Indian Pediatrics. 2001 April; 38(4): 381-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11313509&dopt=Abstract
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Importance of plasma leptin in predicting future weight gain in obese children: a two-and-a-half-year longitudinal study. Author(s): Savoye M, Dziura J, Castle J, DiPietro L, Tamborlane WV, Caprio S. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 July; 26(7): 942-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12080447&dopt=Abstract
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Importance of preventing weight gain in adulthood. Author(s): Gill T. Source: Asia Pacific Journal of Clinical Nutrition. 2002; 11 Suppl 3: S632-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492656&dopt=Abstract
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Improvement in quality-of-life measures and stimulation of weight gain after treatment with megestrol acetate oral suspension in geriatric cachexia: results of a double-blind, placebo-controlled study. Author(s): Yeh SS, Wu SY, Lee TP, Olson JS, Stevens MR, Dixon T, Porcelli RJ, Schuster MW. Source: Journal of the American Geriatrics Society. 2000 May; 48(5): 485-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10811540&dopt=Abstract
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Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea. Author(s): Phillips BG, Kato M, Narkiewicz K, Choe I, Somers VK. Source: American Journal of Physiology. Heart and Circulatory Physiology. 2000 July; 279(1): H234-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10899061&dopt=Abstract
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Infant weight gain and childhood overweight status in a multicenter, cohort study. Author(s): Stettler N, Zemel BS, Kumanyika S, Stallings VA. Source: Pediatrics. 2002 February; 109(2): 194-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11826195&dopt=Abstract
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Infant weight gain and later blood pressure. Author(s): Harder T, Plagemann A. Source: Circulation. 2002 September 24; 106(13): E58; Author Reply E58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12270877&dopt=Abstract
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Infant with inadequate feeding and weight gain, progressive respiratory difficulty, hypotonia, and weakness, with onset at birth. Author(s): Pomerance HH, Gilbert-Barness E, Gieron-Korthals M, Lacson AG, Barnes J, Fernandez R. Source: American Journal of Medical Genetics. 2000 September 4; 94(1): 68-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10982486&dopt=Abstract
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Inflammation-sensitive plasma proteins are associated with future weight gain. Author(s): Engstrom G, Hedblad B, Stavenow L, Lind P, Janzon L, Lindgarde F. Source: Diabetes. 2003 August; 52(8): 2097-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882928&dopt=Abstract
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Influences of gender and weight gain on short-term relapse to smoking in a cessation trial. Author(s): Borrelli B, Spring B, Niaura R, Hitsman B, Papandonatos G. Source: Journal of Consulting and Clinical Psychology. 2001 June; 69(3): 511-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11495180&dopt=Abstract
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Insulin and the “thrifty” woman: the influence of insulin during pregnancy on gestational weight gain and postpartum weight retention. Author(s): Scholl TO, Chen X. Source: Maternal and Child Health Journal. 2002 December; 6(4): 255-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12512767&dopt=Abstract
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Insulin therapy does not itself induce weight gain in patients with type 2 diabetes. Author(s): Larger E, Rufat P, Dubois-Laforgue D, Ledoux S. Source: Diabetes Care. 2001 October; 24(10): 1849-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11574460&dopt=Abstract
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Interdialytic weight gain and dry weight. Author(s): Levin NW, Zhu F, Keen M. Source: Blood Purification. 2001; 19(2): 217-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11150813&dopt=Abstract
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Intervening to reduce weight gain in pregnancy and gestational diabetes mellitus in Cree communities: an evaluation. Author(s): Gray-Donald K, Robinson E, Collier A, David K, Renaud L, Rodrigues S. Source: Cmaj : Canadian Medical Association Journal = Journal De L'association Medicale Canadienne. 2000 November 14; 163(10): 1247-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11107459&dopt=Abstract
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Interventions for weight loss and weight gain prevention among youth: current issues. Author(s): Fulton JE, McGuire MT, Caspersen CJ, Dietz WH. Source: Sports Medicine (Auckland, N.Z.). 2001; 31(3): 153-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11286354&dopt=Abstract
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Introduction. Weight gain with psychotropics: size does matter. Author(s): Masand PS. Source: The Journal of Clinical Psychiatry. 1999; 60 Suppl 21: 3-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10548134&dopt=Abstract
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Is antipsychotic drug--induced weight gain associated with a favorable clinical response? Author(s): Lamberti JS. Source: The Journal of Clinical Psychiatry. 2000 September; 61(9): 678. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11030490&dopt=Abstract
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Is foetal growth reduction induced by smoking modified by body mass or gestational weight gain? Author(s): Weijin Z, Olsen J. Source: Scand J Soc Med. 1996 September; 24(3): 155-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8878367&dopt=Abstract
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Is prevalence of diarrhea a better predictor of subsequent mortality and weight gain than diarrhea incidence? Author(s): Morris SS, Cousens SN, Kirkwood BR, Arthur P, Ross DA. Source: American Journal of Epidemiology. 1996 September 15; 144(6): 582-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8797518&dopt=Abstract
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Is the energy homeostasis system inherently biased toward weight gain? Author(s): Schwartz MW, Woods SC, Seeley RJ, Barsh GS, Baskin DG, Leibel RL. Source: Diabetes. 2003 February; 52(2): 232-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540591&dopt=Abstract
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Jejunoileal bypass. Late metabolic sequelae and weight gain. Author(s): Halverson JD, Scheff RJ, Gentry K, Alpers DH. Source: American Journal of Surgery. 1980 September; 140(3): 347-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7425210&dopt=Abstract
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Lack of effect of long-term use of angiotensin-converting enzyme inhibitors by hemodialysis patients on thirst and fluid weight gain. Author(s): Hamad A, Khosrovaneh A, Gupta S, Fazal S, Manis T, Feinfeld DA. Source: Renal Failure. 2002 July; 24(4): 461-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12212825&dopt=Abstract
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Leisure-time physical activity and regular walking or cycling to work are associated with adiposity and 5 y weight gain in middle-aged men: the PRIME Study. Author(s): Wagner A, Simon C, Ducimetiere P, Montaye M, Bongard V, Yarnell J, Bingham A, Hedelin G, Amouyel P, Ferrieres J, Evans A, Arveiler D. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2001 July; 25(7): 940-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11443490&dopt=Abstract
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Leptin and gestational weight gain: relation of maternal and cord blood leptin to birth weight. Author(s): Shaarawy M, el-Mallah SY. Source: Journal of the Society for Gynecologic Investigation. 1999 March-April; 6(2): 703. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10205776&dopt=Abstract
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Leptin and total cholesterol are predictors of weight gain in pre-pubertal children. Author(s): Byrnes SE, Baur LA, Bermingham M, Brock K, Steinbeck K. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1999 February; 23(2): 146-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10078848&dopt=Abstract
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Leptin concentrations do not predict weight gain: the Mexico City Diabetes Study. Author(s): Haffner SM, Mykkanen LA, Gonzalez CC, Stern MP. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1998 July; 22(7): 695-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9705032&dopt=Abstract
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Leptin levels and IgF-binding proteins in malnourished children: effect of weight gain. Author(s): Palacio AC, Perez-Bravo F, Santos JL, Schlesinger L, Monckeberg F. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2002 January; 18(1): 17-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11827758&dopt=Abstract
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Lifestyle factors related to postpartum weight gain and body image in bottle- and breastfeeding women. Author(s): Walker LO, Freeland-Graves J. Source: Journal of Obstetric, Gynecologic, and Neonatal Nursing : Jognn / Naacog. 1998 March-April; 27(2): 151-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9549700&dopt=Abstract
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Lifestyle-related weight gain in obese men with newly diagnosed obstructive sleep apnea. Author(s): Traviss KA, Barr SI, Fleming JA, Ryan CF. Source: Journal of the American Dietetic Association. 2002 May; 102(5): 703-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12008998&dopt=Abstract
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Linear growth and weight gain in diabetic children--a cross-sectional and longitudinal evaluation. Author(s): Choudhury S, Stutchfield P. Source: J Pediatr Endocrinol Metab. 2000 May; 13(5): 537-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10803872&dopt=Abstract
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Lithium and weight gain. Author(s): Armond AD. Source: The British Journal of Psychiatry; the Journal of Mental Science. 1996 August; 169(2): 251-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8871808&dopt=Abstract
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Longitudinal lipid profiles on CAPD: their relationship to weight gain, comorbidity, and dialysis factors. Author(s): Little J, Phillips L, Russell L, Griffiths A, Russell GI, Davies SJ. Source: Journal of the American Society of Nephrology : Jasn. 1998 October; 9(10): 19319. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9773795&dopt=Abstract
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Longitudinal study of human milk creamatocrit and weight gain in exclusively breastfed infants. Author(s): Chatterjee R, Chatterjee S, Datta T, Roy B, Marimuthu P. Source: Indian Pediatrics. 1997 October; 34(10): 901-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9567552&dopt=Abstract
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Long-term effects of nicotine gum on weight gain after smoking cessation. Author(s): Nordstrom BL, Kinnunen T, Utman CH, Garvey AJ. Source: Nicotine & Tobacco Research : Official Journal of the Society for Research on Nicotine and Tobacco. 1999 September; 1(3): 259-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11072423&dopt=Abstract
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Low circulating IGF-II concentrations predict weight gain and obesity in humans. Author(s): Sandhu MS, Gibson JM, Heald AH, Dunger DB, Wareham NJ. Source: Diabetes. 2003 June; 52(6): 1403-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765950&dopt=Abstract
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Low maternal weight gain in the second or third trimester increases the risk for intrauterine growth retardation. Author(s): Strauss RS, Dietz WH. Source: The Journal of Nutrition. 1999 May; 129(5): 988-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10222390&dopt=Abstract
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Low plasma adiponectin concentrations do not predict weight gain in humans. Author(s): Vozarova B, Stefan N, Lindsay RS, Krakoff J, Knowler WC, Funahashi T, Matsuzawa Y, Stumvoll M, Weyer C, Tataranni PA. Source: Diabetes. 2002 October; 51(10): 2964-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12351434&dopt=Abstract
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Low prenatal weight gain among adult WIC participants delivering term singleton infants: variation by maternal and program participation characteristics. Author(s): Hickey CA, Kreauter M, Bronstein J, Johnson V, McNeal SF, Harshbarger DS, Woolbright LA. Source: Maternal and Child Health Journal. 1999 September; 3(3): 129-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10746752&dopt=Abstract
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Low weight gain in infancy and suicide in adult life. The evidence doesn't support the theory. Author(s): Hollis C. Source: Bmj (Clinical Research Ed.). 1996 February 24; 312(7029): 510. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8597704&dopt=Abstract
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Lowered weight gain during pregnancy and risk of neural tube defects among offspring. Author(s): Shaw GM, Todoroff K, Carmichael SL, Schaffer DM, Selvin S. Source: International Journal of Epidemiology. 2001 February; 30(1): 60-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11171858&dopt=Abstract
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Low-fat diets may prevent weight gain in sedentary women: prospective observations from the population study of women in Gothenburg, Sweden. Author(s): Lissner L, Heitmann BL, Bengtsson C. Source: Obesity Research. 1997 January; 5(1): 43-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9061715&dopt=Abstract
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Male adolescents identify their weight gain practices, reasons for desired weight gain, and sources of weight gain information. Author(s): O'Dea JA, Rawstorne PR. Source: Journal of the American Dietetic Association. 2001 January; 101(1): 105-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11209574&dopt=Abstract
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Management of weight gain associated with antipsychotics. Author(s): Birt J. Source: Annals of Clinical Psychiatry : Official Journal of the American Academy of Clinical Psychiatrists. 2003 March; 15(1): 49-58. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839432&dopt=Abstract
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Management of weight gain in patients with schizophrenia. Author(s): Aquila R. Source: The Journal of Clinical Psychiatry. 2002; 63 Suppl 4: 33-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11913674&dopt=Abstract
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Managing weight gain as a side effect of antidepressant therapy. Author(s): Deshmukh R, Franco K. Source: Cleve Clin J Med. 2003 July; 70(7): 614, 616, 618, Passim. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882383&dopt=Abstract
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Marijuana safety study completed: weight gain, no safety problems. Author(s): James JS. Source: Aids Treat News. 2000 August 4; (348): 3-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12170987&dopt=Abstract
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Massage therapy by mothers and trained professionals enhances weight gain in preterm infants. Author(s): Ferber SG, Kuint J, Weller A, Feldman R, Dollberg S, Arbel E, Kohelet D. Source: Early Human Development. 2002 April; 67(1-2): 37-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11893434&dopt=Abstract
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Massive weight gain and hostility force mirtazapine stoppage. Author(s): Abraham G. Source: Canadian Journal of Psychiatry. Revue Canadienne De Psychiatrie. 2002 August; 47(6): 582. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12211888&dopt=Abstract
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Maternal and neonatal outcomes in pregestational and gestational diabetes mellitus, and the influence of maternal obesity and weight gain: the DEPOSIT study. Diabetes Endocrine Pregnancy Outcome Study in Toronto. Author(s): Ray JG, Vermeulen MJ, Shapiro JL, Kenshole AB. Source: Qjm : Monthly Journal of the Association of Physicians. 2001 July; 94(7): 347-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11435630&dopt=Abstract
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Maternal body mass, proportional weight gain, and fetal growth in parous women. Author(s): Shepard MJ, Bakketeig LS, Jacobsen G, O'Connor T, Bracken MB. Source: Paediatric and Perinatal Epidemiology. 1996 April; 10(2): 207-19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8778693&dopt=Abstract
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Maternal weight, pregnancy weight gain, and the risk of antepartum stillbirth. Author(s): Stephansson O, Dickman PW, Johansson A, Cnattingius S. Source: American Journal of Obstetrics and Gynecology. 2001 February; 184(3): 463-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11228504&dopt=Abstract
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Mechanisms of antipsychotic-induced weight gain. Author(s): McIntyre RS, Mancini DA, Basile VS. Source: The Journal of Clinical Psychiatry. 2001; 62 Suppl 23: 23-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11603882&dopt=Abstract
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Mechanisms of weight gain induced by antipsychotic drugs. Author(s): Baptista T. Source: The Journal of Clinical Psychiatry. 2002 March; 63(3): 245-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11926725&dopt=Abstract
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Medically advised, mother's personal target, and actual weight gain during pregnancy. Author(s): Cogswell ME, Scanlon KS, Fein SB, Schieve LA. Source: Obstetrics and Gynecology. 1999 October; 94(4): 616-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10511369&dopt=Abstract
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Megestrol acetate stimulates weight gain and ventilation in underweight COPD patients. Author(s): Weisberg J, Wanger J, Olson J, Streit B, Fogarty C, Martin T, Casaburi R. Source: Chest. 2002 April; 121(4): 1070-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11948034&dopt=Abstract
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Megestrol acetate-induced weight gain does not negatively affect blood lipids in elderly men: effects of resistance training and testosterone replacement. Author(s): Lambert CP, Sullivan DH, Evans WJ. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2003 July; 58(7): 644-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865481&dopt=Abstract
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Metabolic predictors of weight gain. Author(s): Ravussin E, Gautier JF. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 1999 February; 23 Suppl 1: 37-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10193860&dopt=Abstract
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Metformin and carbohydrate-modified diet: a novel obesity treatment protocol: preliminary findings from a case series of nondiabetic women with midlife weight gain and hyperinsulinemia. Author(s): Mogul HR, Peterson SJ, Weinstein BI, Zhang S, Southren AL. Source: Heart Disease. 2001 September-October; 3(5): 285-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11975807&dopt=Abstract
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Metformin prevents weight gain by reducing dietary intake during insulin therapy in patients with type 2 diabetes mellitus. Author(s): Yki-Jarvinen H, Nikkila K, Makimattila S. Source: Drugs. 1999; 58 Suppl 1: 53-4; Discussion 75-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10576526&dopt=Abstract
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Modifiable behavioral factors in a biopsychosocial model predict inadequate and excessive gestational weight gain. Author(s): Olson CM, Strawderman MS. Source: Journal of the American Dietetic Association. 2003 January; 103(1): 48-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525793&dopt=Abstract
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Muscle metabolic function, exercise performance, and weight gain. Author(s): Larew K, Hunter GR, Larson-Meyer DE, Newcomer BR, McCarthy JP, Weinsier RL. Source: Medicine and Science in Sports and Exercise. 2003 February; 35(2): 230-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569210&dopt=Abstract
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Neuropharmacology of paradoxic weight gain with selective serotonin reuptake inhibitors. Author(s): Harvey BH, Bouwer CD. Source: Clinical Neuropharmacology. 2000 March-April; 23(2): 90-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10803799&dopt=Abstract
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Neuropsychological and behavioral changes and weight gain after medial pallidotomy. Author(s): Lang AE, Lozano A, Tasker R, Duff J, Saint-Cyr J, Trepanier L. Source: Annals of Neurology. 1997 June; 41(6): 834-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9189048&dopt=Abstract
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Nicotine gum dose and weight gain after smoking cessation. Author(s): Doherty K, Militello FS, Kinnunen T, Garvey AJ. Source: Journal of Consulting and Clinical Psychology. 1996 August; 64(4): 799-807. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8803371&dopt=Abstract
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Nicotine replacement effects on post-cessation withdrawal symptoms and weight gain. Author(s): Stitzer M, Gross J. Source: Nida Res Monogr. 1988; 81: 53-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3136387&dopt=Abstract
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Nicotine replacement: effects of postcessation weight gain. Author(s): Gross J, Stitzer ML, Maldonado J. Source: Journal of Consulting and Clinical Psychology. 1989 February; 57(1): 87-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2925978&dopt=Abstract
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Nizatidine for prevention of weight gain with olanzapine: a double-blind placebocontrolled trial. Author(s): Cavazzoni P, Tanaka Y, Roychowdhury SM, Breier A, Allison DB. Source: European Neuropsychopharmacology : the Journal of the European College of Neuropsychopharmacology. 2003 March; 13(2): 81-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12650950&dopt=Abstract
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No relation between maternal weight gain and stillbirth. Author(s): Rydhstrom H, Tyden T, Herbst A, Ljungblad U, Walles B. Source: Acta Obstetricia Et Gynecologica Scandinavica. 1994 November; 73(10): 779-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7817728&dopt=Abstract
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No relationship between subjective assessment of urinary incontinence and pad test weight gain in a random population sample of menopausal women. Author(s): Ryhammer AM, Laurberg S, Djurhuus JC, Hermann AP. Source: The Journal of Urology. 1998 March; 159(3): 800-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9474152&dopt=Abstract
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No weight gain among elderly schizophrenia patients after 1 year of risperidone treatment. Author(s): Barak Y. Source: The Journal of Clinical Psychiatry. 2002 February; 63(2): 117-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11874211&dopt=Abstract
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Nonpharmacologic and pharmacologic management of weight gain. Author(s): Greenberg I, Chan S, Blackburn GL. Source: The Journal of Clinical Psychiatry. 1999; 60 Suppl 21: 31-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10548140&dopt=Abstract
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Normalization of abnormal diurnal weight gain among chronically psychotic geriatric patients. Is abnormal diurnal weight gain a risk factor in chronic psychosis? Author(s): Vieweg WV, Godleski LS, Shannon C, Hundley PL, Yank GR. Source: The Journal of Nervous and Mental Disease. 1989 September; 177(9): 542-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2570123&dopt=Abstract
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Novel antipsychotics: comparison of weight gain liabilities. Author(s): Wirshing DA, Wirshing WC, Kysar L, Berisford MA, Goldstein D, Pashdag J, Mintz J, Marder SR. Source: The Journal of Clinical Psychiatry. 1999 June; 60(6): 358-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10401912&dopt=Abstract
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Novel assays based on human growth hormone receptor as alternatives to the rat weight gain bioassay for recombinant human growth hormone. Author(s): Roswall EC, Mukku VR, Chen AB, Hoff EH, Chu H, McKay PA, Olson KC, Battersby JE, Gehant RL, Meunier A, Garnick RL. Source: Biologicals : Journal of the International Association of Biological Standardization. 1996 March; 24(1): 25-39. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8733599&dopt=Abstract
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Nutrient absorption and weight gain in persistent diarrhea: comparison of a traditional rice-lentil/yogurt/milk diet with soy formula. Author(s): Bhutta ZA, Molla AM, Issani Z, Badruddin S, Hendricks K, Snyder JD. Source: Journal of Pediatric Gastroenterology and Nutrition. 1994 January; 18(1): 45-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8126617&dopt=Abstract
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Nutrition counseling increases weight gain among Brazilian children. Author(s): Santos I, Victora CG, Martines J, Goncalves H, Gigante DP, Valle NJ, Pelto G. Source: The Journal of Nutrition. 2001 November; 131(11): 2866-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11694610&dopt=Abstract
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Nutrition intervention for weight gain in cystic fibrosis: a meta analysis. Author(s): Jelalian E, Stark LJ, Reynolds L, Seifer R. Source: The Journal of Pediatrics. 1998 March; 132(3 Pt 1): 486-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9544906&dopt=Abstract
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Nutritional status and weight gain in patients with pulmonary tuberculosis in Tanzania. Author(s): Kennedy N, Ramsay A, Uiso L, Gutmann J, Ngowi FI, Gillespie SH. Source: Trans R Soc Trop Med Hyg. 1996 March-April; 90(2): 162-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8761578&dopt=Abstract
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Obesity and weight gain are associated with increased incidence of hyperinsulinemia in non-diabetic men. Author(s): Lakka HM, Salonen JT, Tuomilehto J, Kaplan GA, Lakka TA. Source: Hormone and Metabolic Research. Hormon- Und Stoffwechselforschung. Hormones Et Metabolisme. 2002 September; 34(9): 492-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12384825&dopt=Abstract
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Obesity, weight gain, and ovarian cancer. Author(s): Fairfield KM, Willett WC, Rosner BA, Manson JE, Speizer FE, Hankinson SE. Source: Obstetrics and Gynecology. 2002 August; 100(2): 288-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12151152&dopt=Abstract
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Olanzapine and weight gain. Author(s): Karagianis J. Source: Canadian Journal of Psychiatry. Revue Canadienne De Psychiatrie. 2000 June; 45(5): 493. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10900535&dopt=Abstract
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Olanzapine associated weight gain, hyperglycemia and neuroleptic malignant syndrome: case report. Author(s): Malyuk R, Gibson B, Procyshyn RM, Kang N. Source: International Journal of Geriatric Psychiatry. 2002 April; 17(4): 326-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11994885&dopt=Abstract
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Olanzapine induces remarkable weight gain in adolescent patients. Author(s): Haapasalo-Pesu KM, Saarijarvi S. Source: European Child & Adolescent Psychiatry. 2001 September; 10(3): 205-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11596822&dopt=Abstract
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Olanzapine-induced destabilization of diabetes in the absence of weight gain. Author(s): Ramankutty G. Source: Acta Psychiatrica Scandinavica. 2002 March; 105(3): 235-6; Discussion 236-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11939979&dopt=Abstract
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Olanzapine-induced weight gain in patients with first-episode schizophrenia: a double-blind, placebo-controlled study of fluoxetine addition. Author(s): Poyurovsky M, Pashinian A, Gil-Ad I, Maayan R, Schneidman M, Fuchs C, Weizman A. Source: The American Journal of Psychiatry. 2002 June; 159(6): 1058-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12042201&dopt=Abstract
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One- and two-year predictors of excess weight gain among elementary schoolchildren in multiethnic, low-income, inner-city neighborhoods. Author(s): O'Loughlin J, Gray-Donald K, Paradis G, Meshefedjian G. Source: American Journal of Epidemiology. 2000 October 15; 152(8): 739-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11052551&dopt=Abstract
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Orlistat in the treatment of psychopharmacologically induced weight gain. Author(s): Anghelescu I, Klawe C, Benkert O. Source: Journal of Clinical Psychopharmacology. 2000 December; 20(6): 716-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11106155&dopt=Abstract
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Overweight teens at increased risk for weight gain while using depot medroxyprogesterone acetate. Author(s): Mangan SA, Larsen PG, Hudson S. Source: Journal of Pediatric and Adolescent Gynecology. 2002 April; 15(2): 79-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12057528&dopt=Abstract
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Parent-offspring conflict theory, signaling of need, and weight gain in early life. Author(s): Wells JC. Source: The Quarterly Review of Biology. 2003 June; 78(2): 169-202. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825417&dopt=Abstract
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Pattern and cost of weight gain in previously obese women. Author(s): Votruba SB, Blanc S, Schoeller DA. Source: American Journal of Physiology. Endocrinology and Metabolism. 2002 April; 282(4): E923-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11882514&dopt=Abstract
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Pattern and predictors of weight gain during pregnancy among HIV-1-infected women from Tanzania. Author(s): Villamor E, Msamanga G, Spiegelman D, Peterson KE, Antelman G, Fawzi WW. Source: Journal of Acquired Immune Deficiency Syndromes (1999). 2003 April 15; 32(5): 560-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679710&dopt=Abstract
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Physical activity and its impact on health outcomes. Paper 2: Prevention of unhealthy weight gain and obesity by physical activity: an analysis of the evidence. Author(s): Erlichman J, Kerbey AL, James WP. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 November; 3(4): 273-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458973&dopt=Abstract
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Polymorphism of the promoter region of the serotonin 5-HT(2C) receptor gene and clozapine-induced weight gain. Author(s): Reynolds GP, Zhang Z, Zhang X. Source: The American Journal of Psychiatry. 2003 April; 160(4): 677-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668355&dopt=Abstract
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Predictors of weight gain: the biological-behavioural debate. Author(s): Filozof C, Gonzalez C. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 May; 1(1): 21-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119641&dopt=Abstract
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Preventive strategies against weight gain and obesity. Author(s): Swinburn B, Egger G. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 November; 3(4): 289-301. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458974&dopt=Abstract
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Pronounced early increase in circulating leptin predicts a lower weight gain during clozapine treatment. Author(s): Monteleone P, Fabrazzo M, Tortorella A, La Pia S, Maj M. Source: Journal of Clinical Psychopharmacology. 2002 August; 22(4): 424-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172344&dopt=Abstract
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Psychosocial influences on weight gain attitudes and behaviors during pregnancy. Author(s): Dipietro JA, Millet S, Costigan KA, Gurewitsch E, Caulfield LE. Source: Journal of the American Dietetic Association. 2003 October; 103(10): 1314-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520249&dopt=Abstract
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Psychosocial thriving during late pregnancy: relationship to ethnicity, gestational weight gain, and birth weight. Author(s): Walker LO, Kim M. Source: Journal of Obstetric, Gynecologic, and Neonatal Nursing : Jognn / Naacog. 2002 May-June; 31(3): 263-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12033539&dopt=Abstract
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Quality of life and stimulation of weight gain after treatment with megestrol acetate: correlation between cytokine levels and nutritional status, appetite in geriatric patients with wasting syndrome. Author(s): Yeh S, Wu SY, Levine DM, Parker TS, Olson JS, Stevens MR, Schuster MW. Source: J Nutr Health Aging. 2000; 4(4): 246-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11115810&dopt=Abstract
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Randomized controlled study of the effects of different durations of light exposure on weight gain by preterm infants in a neonatal intensive care unit. Author(s): Boo NY, Chee SC, Rohana J. Source: Acta Paediatrica (Oslo, Norway : 1992). 2002; 91(6): 674-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12162601&dopt=Abstract
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Randomized controlled trial to prevent excessive weight gain in pregnant women. Author(s): Polley BA, Wing RR, Sims CJ. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 November; 26(11): 1494-502. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439652&dopt=Abstract
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Rapid weight gain during infancy and obesity in young adulthood in a cohort of African Americans. Author(s): Stettler N, Kumanyika SK, Katz SH, Zemel BS, Stallings VA. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1374-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791612&dopt=Abstract
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Rapid weight gain during infancy as a predictor of adult obesity. Author(s): Yanovski JA. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1350-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791608&dopt=Abstract
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Relation between interdialytic weight gain, body weight and nutrition in hemodialysis patients. Author(s): Ifudu O, Uribarri J, Rajwani I, Vlacich V, Reydel K, Delosreyes G, Friedman EA. Source: American Journal of Nephrology. 2002 July-August; 22(4): 363-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12169869&dopt=Abstract
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Relationship between interdialytic weight gain and acid-base status in hemodialysis by bicarbonate. Author(s): Agroyannis B, Fourtounas C, Tzanatos H, Dalamangas A, Vlahakos DV. Source: Artificial Organs. 2002 April; 26(4): 385-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11952511&dopt=Abstract
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Relationship of family history of type 2 diabetes, hypoglycemia, and autoantibodies to weight gain and lipids with intensive and conventional therapy in the Diabetes Control and Complications Trial. Author(s): Purnell JQ, Dev RK, Steffes MW, Cleary PA, Palmer JP, Hirsch IB, Hokanson JE, Brunzell JD. Source: Diabetes. 2003 October; 52(10): 2623-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514648&dopt=Abstract
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Relationships between cigarette smoking during pregnancy, gestational age, maternal weight gain, and infant birthweight. Author(s): Secker-Walker RH, Vacek PM. Source: Addictive Behaviors. 2003 January-February; 28(1): 55-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507527&dopt=Abstract
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Reproductive function during weight gain in anorexia nervosa. Leptin represents a metabolic gate to gonadotropin secretion. Author(s): Holtkamp K, Mika C, Grzella I, Heer M, Pak H, Hebebrand J, HerpertzDahlmann B. Source: Journal of Neural Transmission (Vienna, Austria : 1996). 2003 April; 110(4): 42735. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12658369&dopt=Abstract
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Reversal of antipsychotic-associated weight gain. Author(s): O'Keefe CD, Noordsy DL, Liss TB, Weiss H. Source: The Journal of Clinical Psychiatry. 2003 August; 64(8): 907-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12927005&dopt=Abstract
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Safety of available agents used to treat bipolar disorder: focus on weight gain. Author(s): Nemeroff CB. Source: The Journal of Clinical Psychiatry. 2003 May; 64(5): 532-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755655&dopt=Abstract
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Serial body composition by bioimpedance analysis in a diabetic subject with rapid insulin-induced weight gain--a case report. Author(s): Lee IT, Lin SY, Sheu WH. Source: Kaohsiung J Med Sci. 2002 January; 18(1): 45-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12017983&dopt=Abstract
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Serum uric acid and plasma norepinephrine concentrations predict subsequent weight gain and blood pressure elevation. Author(s): Masuo K, Kawaguchi H, Mikami H, Ogihara T, Tuck ML. Source: Hypertension. 2003 October; 42(4): 474-80. Epub 2003 September 02. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953019&dopt=Abstract
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Severe weight gain induced by combination treatment with risperidone and paroxetine. Author(s): Fukui H, Murai T. Source: Clinical Neuropharmacology. 2002 September-October; 25(5): 269-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12410060&dopt=Abstract
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Short-term weight gain in abstaining women smokers. Author(s): Pomerleau CS, Pomerleau OF, Namenek RJ, Mehringer AM. Source: Journal of Substance Abuse Treatment. 2000 June; 18(4): 339-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10812306&dopt=Abstract
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Sociodemographic factors associated with long-term weight gain, current body fatness and central adiposity in Swedish women. Author(s): Lahmann PH, Lissner L, Gullberg B, Berglund G. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2000 June; 24(6): 685-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10878674&dopt=Abstract
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Sociodemographic, behavioral, and reproductive factors associated with weight gain in Chinese women. Author(s): Wen W, Gao YT, Shu XO, Yang G, Li HL, Jin F, Zheng W. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 933-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861234&dopt=Abstract
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Sodium, not fluid, controls interdialytic weight gain. Author(s): Rigby AJ, Scribner BH, Ahmad S. Source: Nephrol News Issues. 2000 August; 14(9): 21-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11933426&dopt=Abstract
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Symphysis-fundus height and weight gain pattern in Japanese women with twin pregnancies. Author(s): Ayustawati, Matsubara S, Minakami H, Ohkuchi A, Izumi A, Sato I. Source: J Reprod Med. 2003 April; 48(4): 277-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746992&dopt=Abstract
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Syndrome W: a new model of hyperinsulinemia, hypertension and midlife weight gain in healthy women with normal glucose tolerance. Author(s): Mogul HR, Weinstein BI, Mogul DB, Peterson SJ, Zhang S, Frey M, Gambert SR, Southren AL. Source: Heart Disease. 2002 March-April; 4(2): 78-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11975838&dopt=Abstract
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The effect of therapeutically induced weight gain on plasma leptin levels in patients with anorexia nervosa. Author(s): Holtkamp K, Hebebrand J, Mika C, Grzella I, Heer M, Heussen N, HerpertzDahlmann B. Source: Journal of Psychiatric Research. 2003 March-April; 37(2): 165-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842170&dopt=Abstract
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The effects of an educational intervention on antipsychotic-induced weight gain. Author(s): Littrell KH, Hilligoss NM, Kirshner CD, Petty RG, Johnson CG. Source: Journal of Nursing Scholarship : an Official Publication of Sigma Theta Tau International Honor Society of Nursing / Sigma Theta Tau. 2003; 35(3): 237-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14562491&dopt=Abstract
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The impact of body mass index and weight gain during pregnancy on puerperal complications after spontaneous vaginal delivery. Author(s): Giuliani A, Tamussino K, Basver A, Haas J, Petru E. Source: Wiener Klinische Wochenschrift. 2002 June 14; 114(10-11): 383-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12708091&dopt=Abstract
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The impact of weight gain on quality of life among persons with schizophrenia. Author(s): Allison DB, Mackell JA, McDonnell DD. Source: Psychiatric Services (Washington, D.C.). 2003 April; 54(4): 565-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663847&dopt=Abstract
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The relationship of changes in leptin, neuropeptide Y and reproductive hormones to antipsychotic induced weight gain. Author(s): Fitzgerald PB, Scaffidi A, Morris MJ, de Castella AR, Kulkarni J. Source: Human Psychopharmacology. 2003 October; 18(7): 551-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14533137&dopt=Abstract
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The relationship of rapid weight gain in infancy to obesity and skeletal maturity in childhood. Author(s): Cameron N, Pettifor J, De Wet T, Norris S. Source: Obesity Research. 2003 March; 11(3): 457-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634445&dopt=Abstract
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The role of physical activity in prevention and treatment of body weight gain in adults. Author(s): Jakicic JM. Source: The Journal of Nutrition. 2002 December; 132(12): 3826S-3829S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468633&dopt=Abstract
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Topiramate produced weight loss following olanzapine-induced weight gain in schizophrenia. Author(s): Levy E, Margolese HC, Chouinard G. Source: The Journal of Clinical Psychiatry. 2002 November; 63(11): 1045. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12469686&dopt=Abstract
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Treatment of weight gain with fluoxetine in olanzapine-treated schizophrenic outpatients. Author(s): Bustillo JR, Lauriello J, Parker K, Hammond R, Rowland L, Bogenschutz M, Keith S. Source: Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology. 2003 March; 28(3): 527-9. Epub 2002 October 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629532&dopt=Abstract
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Treatment with ursodeoxycholic acid is associated with weight gain in patients with primary biliary cirrhosis. Author(s): Siegel JL, Jorgensen R, Angulo P, Lindor KD. Source: Journal of Clinical Gastroenterology. 2003 August; 37(2): 183-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869893&dopt=Abstract
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Undesirable weight gain and psychotropic medications. Author(s): Beeber LS. Source: Journal of Psychosocial Nursing and Mental Health Services. 1988 October; 26(10): 38-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3193382&dopt=Abstract
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Use of beta-blockers in obesity hypertension: potential role of weight gain. Author(s): Pischon T, Sharma AM. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 November; 2(4): 275-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119998&dopt=Abstract
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Using early weight gain and other nutrition-related risk factors to predict pregnancy outcomes. Author(s): Springer NS, Bischoping K, Sampselle CM, Mayes FL, Petersen BA. Source: Journal of the American Dietetic Association. 1992 February; 92(2): 217-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1737905&dopt=Abstract
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Valproic acid modulates islet cell insulin secretion: a possible mechanism of weight gain in epilepsy patients. Author(s): Luef GJ, Lechleitner M, Bauer G, Trinka E, Hengster P. Source: Epilepsy Research. 2003 June-July; 55(1-2): 53-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12948616&dopt=Abstract
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Valproic acid-associated weight gain in older children and teens with epilepsy. Author(s): Wirrell EC. Source: Pediatric Neurology. 2003 February; 28(2): 126-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699863&dopt=Abstract
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Variables affecting weight gain in renal transplant recipients. Author(s): Clunk JM, Lin CY, Curtis JJ. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2001 August; 38(2): 349-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11479161&dopt=Abstract
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Visual disturbances and weight gain. Author(s): Sharma S, Granot R, Thomas N, Wilcsek GA, White C, Fitzsimons R, Tidmarsh J, Tuch BE. Source: Postgraduate Medical Journal. 2001 November; 77(913): 732-3, 736-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11677286&dopt=Abstract
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Vitamin D supplements enhance weight gain and nutritional status in pregnant Asians. Author(s): Maxwell JD, Ang L, Brooke OG, Brown IR. Source: British Journal of Obstetrics and Gynaecology. 1981 October; 88(10): 987-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6793058&dopt=Abstract
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Weight gain among women in the late reproductive years. Author(s): Sammel MD, Grisso JA, Freeman EW, Hollander L, Liu L, Liu S, Nelson DB, Battistini M. Source: Family Practice. 2003 August; 20(4): 401-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876110&dopt=Abstract
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Weight gain and quality of life among patients taking antipsychotics. Author(s): Fetter JC. Source: Psychiatric Services (Washington, D.C.). 2003 July; 54(7): 1041. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851449&dopt=Abstract
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Weight gain concerns in the breastfed infant. Essential strategies for assisting families. Author(s): Page-Goertz S. Source: Adv Nurse Pract. 2003 March; 11(3): 42-8, 91. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12683169&dopt=Abstract
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Weight gain during pregnancy. Author(s): Cox S. Source: Journal of Midwifery & Women's Health. 2003 May-June; 48(3): 229-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764310&dopt=Abstract
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Weight gain in breastfed infants of mothers taking antidepressant medications. Author(s): Hendrick V, Smith LM, Hwang S, Altshuler LL, Haynes D. Source: The Journal of Clinical Psychiatry. 2003 April; 64(4): 410-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716242&dopt=Abstract
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Weight gain in first-episode psychosis. Author(s): Addington J, Mansley C, Addington D. Source: Canadian Journal of Psychiatry. Revue Canadienne De Psychiatrie. 2003 May; 48(4): 272-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776395&dopt=Abstract
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Weight gain in patients after therapy for hyperthyroidism. Author(s): Brunova J, Bruna J, Joubert G, Koning M. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 2003 July; 93(7): 529-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939927&dopt=Abstract
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Weight gain in the treatment of mood disorders. Author(s): Aronne LJ, Segal KR. Source: The Journal of Clinical Psychiatry. 2003; 64 Suppl 8: 22-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892538&dopt=Abstract
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Weight gain profiles of new anti-psychotics: public health consequences. Author(s): Tardieu S, Micallef J, Gentile S, Blin O. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 August; 4(3): 129-38. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12916814&dopt=Abstract
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CHAPTER 2. NUTRITION AND WEIGHT GAIN Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and weight gain.
Finding Nutrition Studies on Weight Gain The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “weight gain” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
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Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following is a typical result when searching for recently indexed consumer information on weight gain: •
A longitudinal study of the effects of a gluten-free diet on glycemic control and weight gain in subjects with type 1 diabetes and celiac disease. Author(s): University Department of Paediatrics, Addenbrooke's Hospital, Cambridge, UK. Source: Amin, R Murphy, N Edge, J Ahmed, M L Acerini, C L Dunger, D B DiabetesCare. 2002 July; 25(7): 1117-22 0149-5992
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Are weight-loss diets recipes for weight gain. Source: Tufts-Univ-diet-nutr-lett. New York, N.Y. : Tufts University Diet and Nutrition Letter, 1983-c1997. November 1996. volume 14 (9) page 6. 0747-4105
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Ask the doctor. I've been fighting obesity all my life. I'm a 62-year-old woman and every five years or so I lose about 20 pounds, then slowly gain it back. I've heard that this “yo-yo” pattern of weight loss, weight gain, weight loss, may be more dangerous than just staying heavy. Should I give up trying to lose weight? Source: Lee, T H Harv-Heart-Lett. 2001 January; 11(5): 7-8 1051-5313
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Holiday weight gain: fact or fiction? Author(s): Energy Metabolism Lab, USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA. Source: Roberts, S B Mayer, J Nutr-Revolume 2000 December; 58(12): 378-9 0029-6643
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If you want to quit smoking but fear the weight gain. Source: Tufts-Univ-diet-nutr-lett. New York, N.Y. : Tufts University Diet and Nutrition Letter, 1983-c1997. January 1996. volume 13 (11) page 6-7. 0747-4105
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Improved glycemic control reduces the impact of weight gain on cardiovascular risk factors in type 1 diabetes. The Epidemiology of Diabetes Complications Study. Author(s): Division of Endocrinology and Metabolism, School of Medicine, Children's Hospital of Pittsburgh, Pennsylvania, USA.
[email protected] Source: Williams, K V Erbey, J R Becker, D Orchard, T J Diabetes-Care. 1999 July; 22(7): 1084-91 0149-5992
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Infant feeding, early weight gain, and risk of type 1 diabetes. Childhood Diabetes in Finland (DiMe) Study Group. Author(s): School of Public Health, University of Tampere, Finland.
[email protected] Source: Hypponen, E Kenward, M G Virtanen, S M Piitulainen, A Virta Autio, P Tuomilehto, J Knip, M Akerblom, H K Diabetes-Care. 1999 December; 22(12): 1961-5 0149-5992
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Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Author(s): Department of Nutrition, Harvard School of Public Health, Boston, MA 02115. Source: Chan, J M Rimm, E B Colditz, G A Stampfer, M J Willett, W C Diabetes-Care. 1994 September; 17(9): 961-9 0149-5992
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Physical inactivity and metabolic factors as predictors of weight gain. Author(s): University of Maastricht. Source: Saris, W H Nutr-Revolume 1996 April; 54(4 Pt 2): S110-5 0029-6643
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Resistance to weight gain during overfeeding: a NEAT explanation. Author(s): Columbia University College of Physicians and Surgeons, Boca Grande, FL 33921, USA. Source: Vanltallie, T B Nutr-Revolume 2001 February; 59(2): 48-51 0029-6643
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Weight gain and loss. Source: Anonymous Harv-Health-Lett. 2001 March; 26(5): 1-3 1052-1577
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Weight gain during pregnancy: current guidelines. Source: Abrams, B. Nutrition-and-the-M.D (USA). (October 1993). volume 19(10) page 13.
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Weight gain on the night shift. Source: Tufts-Univ-diet-nutr-lett. New York, N.Y. : Tufts University Diet and Nutrition Letter, 1983-c1997. October 1996. volume 14 (8) page 1-2. 0747-4105
The following information is typical of that found when using the “Full IBIDS Database” to search for “weight gain” (or a synonym): •
Combination-therapy with bedtime NPH insulin and sulphonylureas gives similar glycaemic control but lower weight gain than insulin twice daily in patients with type 2 diabetes. Author(s): Department of Medicine, Karlstad Central Hospital, Sweden. Source: Olsson, P O Lindstrom, T Diabetes-Metab. 2002 September; 28(4 Pt 1): 272-7 1262-3636
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Conjugated linoleic acid may be useful in treating diabetes by controlling body fat and weight gain. Author(s): Food Research Institute, Department of Food Microbiology and Toxicology, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
[email protected] Source: Pariza, M W Diabetes-Technol-Ther. 2002; 4(3): 335-8 1520-9156
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Dietary and genetic influences on susceptibility or resistance to weight gain on a high fat diet. Author(s): Molecular Neuroendocrinology Group, Aberdeen Centre for Energy Regulation and Obesity, Rowett Research Institute, Aberdeen AB21 9SB, UK.
[email protected] Source: Mercer, J G Nutr-Metab-Cardiovasc-Dis. 2001 August; 11(4 Suppl): 114-7 09394753
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Effect of gastrointestinal nematode and liver fluke infections on weight gain and reproductive performance of beef heifers. Author(s): Dean Lee Research Station, Louisiana State University AgCenter, 8105 Tom Bowman Dr., Alexandria, LA 71302, USA.
[email protected] Source: Loyacano, A F Williams, J C Gurie, J DeRosa, A A Vet-Parasitol. 2002 August 2; 107(3): 227-34 0304-4017
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Effect of nutrition education by paraprofessionals on dietary intake, maternal weight gain, and infant birth weight in pregnant Native American and Caucasian adolescents. Source: Hermann, J. Williams, G. Hunt, D. J-ext. United States : Extension Journal, Inc., [1987-. February 2001. volume 39 (1) page N/A. 1077-5315
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Metformin and carbohydrate-modified diet: a novel obesity treatment protocol: preliminary findings from a case series of nondiabetic women with midlife weight gain and hyperinsulinemia. Author(s): Division of Endocrinology, New York Medical College, Valhalla, New York, USA.
[email protected] Source: Mogul, H R Peterson, S J Weinstein, B I Zhang, S Southren, A L Heart-Dis. 2001 Sep-October; 3(5): 285-92 1521-737X
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Predictors of weight gain: the biological-behavioural debate. Author(s): Department of Biology, John F Kennedy University, Buenos Aires, Argentina.
[email protected] Source: Filozof, C Gonzalez, C Obes-Revolume 2000 May; 1(1): 21-6 1467-7881
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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The following is a specific Web list relating to weight gain; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Ascorbic Acid Source: Integrative Medicine Communications; www.drkoop.com Vitamin C (Ascorbic Acid) Source: Integrative Medicine Communications; www.drkoop.com
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Minerals Chromium Source: Prima Communications, Inc.www.personalhealthzone.com Creatine Source: Integrative Medicine Communications; www.drkoop.com Creatine Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10020,00.html Creatine Monohydrate Source: Healthnotes, Inc.; www.healthnotes.com Phosphocreatine Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Healthnotes, Inc.; www.healthnotes.com
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Food and Diet Atkins Diet Source: Healthnotes, Inc.; www.healthnotes.com Diabetes Source: Healthnotes, Inc.; www.healthnotes.com Gluten-free Diet Source: Healthnotes, Inc.; www.healthnotes.com High Cholesterol Source: Healthnotes, Inc.; www.healthnotes.com High-Fiber Diet Source: Healthnotes, Inc.; www.healthnotes.com
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Weight Loss and Obesity Source: Healthnotes, Inc.; www.healthnotes.com
The following is a specific Web list relating to weight gain; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Ascorbic Acid Source: Integrative Medicine Communications; www.drkoop.com Vitamin C (Ascorbic Acid) Source: Integrative Medicine Communications; www.drkoop.com
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Minerals Chromium Source: Prima Communications, Inc.www.personalhealthzone.com Creatine Source: Integrative Medicine Communications; www.drkoop.com Creatine Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10020,00.html Creatine Monohydrate Source: Healthnotes, Inc.; www.healthnotes.com Phosphocreatine Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Healthnotes, Inc.; www.healthnotes.com
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Food and Diet Atkins Diet Source: Healthnotes, Inc.; www.healthnotes.com Diabetes Source: Healthnotes, Inc.; www.healthnotes.com Gluten-Free Diet Source: Healthnotes, Inc.; www.healthnotes.com
Nutrition
High Cholesterol Source: Healthnotes, Inc.; www.healthnotes.com High-Fiber Diet Source: Healthnotes, Inc.; www.healthnotes.com Weight Loss and Obesity Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND WEIGHT GAIN Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to weight gain. At the conclusion of this chapter, we will provide additional sources.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to weight gain and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “weight gain” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to weight gain: •
7-monohydroxyethylrutoside protects against chronic doxorubicin-induced cardiotoxicity when administered only once per week. Author(s): van Acker FA, van Acker SA, Kramer K, Haenen GR, Bast A, van der Vijgh WJ. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2000 April; 6(4): 1337-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10778960&dopt=Abstract
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90-day oral toxicity study of a grape seed extract (IH636) in rats. Author(s): Wren AF, Cleary M, Frantz C, Melton S, Norris L. Source: Journal of Agricultural and Food Chemistry. 2002 March 27; 50(7): 2180-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11902976&dopt=Abstract
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A 13-week feeding study in the rat with shea oleine and hardened shea oleine. Author(s): Earl LK, Baldrick P, Hepburn PA.
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Source: International Journal of Toxicology. 2002 January-February; 21(1): 13-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11936895&dopt=Abstract •
A comparison of eight grades of fat as broiler feed ingredients. Author(s): Pesti GM, Bakalli RI, Qiao M, Sterling KG. Source: Poultry Science. 2002 March; 81(3): 382-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11902416&dopt=Abstract
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A pancreatic extract-enriched diet improves the nutritional status of aged rats. Author(s): Chambon-Savanovitch C, Felgines C, Walrand S, Raul F, Zarrabian S, Meunier MT, Farges MC, Cynober L, Vasson MP. Source: The Journal of Nutrition. 2001 March; 131(3): 813-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11238764&dopt=Abstract
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A randomized controlled trial of nerve stimulation for relief of nausea and vomiting in pregnancy. Author(s): Rosen T, de Veciana M, Miller HS, Stewart L, Rebarber A, Slotnick RN. Source: Obstetrics and Gynecology. 2003 July; 102(1): 129-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850618&dopt=Abstract
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A randomized study of nutritional support in patients with colorectal and gastric cancer. Author(s): Persson CR, Johansson BB, Sjoden PO, Glimelius BL. Source: Nutrition and Cancer. 2002; 42(1): 48-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12235650&dopt=Abstract
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A soy protein diet alters hepatic lipid metabolism gene expression and reduces serum lipids and renal fibrogenic cytokines in rats with chronic nephrotic syndrome. Author(s): Tovar AR, Murguia F, Cruz C, Hernandez-Pando R, Aguilar-Salinas CA, Pedraza-Chaverri J, Correa-Rotter R, Torres N. Source: The Journal of Nutrition. 2002 September; 132(9): 2562-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12221209&dopt=Abstract
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A sustained, non-insulin related, hypoglycaemic effect of electroacupuncture in diabetic Psammomys obesus. Author(s): Shapira MY, Appelbaum EY, Hirshberg B, Mizrahi Y, Bar-On H, Ziv E. Source: Diabetologia. 2000 June; 43(6): 809-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10907127&dopt=Abstract
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Accelerative effect of olive oil on liver glycogen synthesis in rats subjected to waterimmersion restraint stress. Author(s): Takeuchi H, Suzuki N, Tada M, He P.
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Source: Bioscience, Biotechnology, and Biochemistry. 2001 July; 65(7): 1489-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11515530&dopt=Abstract •
Activation of EGF receptors mediates pulmonary vasoconstriction induced by residual oil fly ash. Author(s): Huang YC, Wu W, Ghio AJ, Carter JD, Silbajoris R, Devlin RB, Samet JM. Source: Experimental Lung Research. 2002 January-February; 28(1): 19-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11792073&dopt=Abstract
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Acute and chronic toxicity of Nigella sativa fixed oil. Author(s): Zaoui A, Cherrah Y, Mahassini N, Alaoui K, Amarouch H, Hassar M. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2002 January; 9(1): 69-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11924767&dopt=Abstract
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Adaptation of Sprague Dawley rats to long-term feeding of high fat or high fructose diets. Author(s): Stark AH, Timar B, Madar Z. Source: European Journal of Nutrition. 2000 October; 39(5): 229-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11131370&dopt=Abstract
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Adrenalectomy-induced cell death in the dentate gyrus: further characterisation using TUNEL and effects of the Ginkgo biloba extract, EGb 761, and ginkgolide B. Author(s): Maclennan KM, Zheng Y, Sheard PW, Williams SM, Darlington CL, Smith PF. Source: Hippocampus. 2003; 13(2): 212-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699329&dopt=Abstract
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Age old remedy impacts HIV--MRC. Author(s): Bateman C. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 2003 May; 93(5): 322-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12830588&dopt=Abstract
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Alpha-amylase supplementation of broiler diets based on corn. Author(s): Gracia MI, Aranibar MJ, Lazaro R, Medel P, Mateos GG. Source: Poultry Science. 2003 March; 82(3): 436-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705405&dopt=Abstract
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Alternation of hepatic antioxidant enzyme activities and lipid profile in streptozotocin-induced diabetic rats by supplementation of dandelion water extract. Author(s): Cho SY, Park JY, Park EM, Choi MS, Lee MK, Jeon SM, Jang MK, Kim MJ, Park YB.
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Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2002 March; 317(1-2): 109-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11814465&dopt=Abstract •
American College of Sports Medicine roundtable. The physiological and health effects of oral creatine supplementation. Author(s): Terjung RL, Clarkson P, Eichner ER, Greenhaff PL, Hespel PJ, Israel RG, Kraemer WJ, Meyer RA, Spriet LL, Tarnopolsky MA, Wagenmakers AJ, Williams MH. Source: Medicine and Science in Sports and Exercise. 2000 March; 32(3): 706-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10731017&dopt=Abstract
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Cognitive behavior therapy for weight gain. Author(s): Umbricht D, Flury H, Bridler R. Source: The American Journal of Psychiatry. 2001 June; 158(6): 971. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11384925&dopt=Abstract
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Dance and reducing television viewing to prevent weight gain in African-American girls: the Stanford GEMS pilot study. Author(s): Robinson TN, Killen JD, Kraemer HC, Wilson DM, Matheson DM, Haskell WL, Pruitt LA, Powell TM, Owens AS, Thompson NS, Flint-Moore NM, Davis GJ, Emig KA, Brown RT, Rochon J, Green S, Varady A. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S65-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713212&dopt=Abstract
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Dietary alpha-linolenic acid-rich diacylglycerols reduce body weight gain accompanying the stimulation of intestinal beta-oxidation and related gene expressions in C57BL/KsJ-db/db mice. Author(s): Murase T, Nagasawa A, Suzuki J, Wakisaka T, Hase T, Tokimitsu I. Source: The Journal of Nutrition. 2002 October; 132(10): 3018-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368389&dopt=Abstract
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Dietary fiber, weight gain, and cardiovascular disease risk factors in young adults. Author(s): Ludwig DS, Pereira MA, Kroenke CH, Hilner JE, Van Horn L, Slattery ML, Jacobs DR Jr. Source: Jama : the Journal of the American Medical Association. 1999 October 27; 282(16): 1539-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10546693&dopt=Abstract
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Food supplementation with encouragement to feed it to infants from 4 to 12 months of age has a small impact on weight gain. Author(s): Bhandari N, Bahl R, Nayyar B, Khokhar P, Rohde JE, Bhan MK.
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Source: The Journal of Nutrition. 2001 July; 131(7): 1946-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11435512&dopt=Abstract •
High intake, but not low intake, of CLA impairs weight gain in growing mice. Author(s): Hayman A, MacGibbon A, Pack RJ, Rutherfurd K, Green JH. Source: Lipids. 2002 July; 37(7): 689-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12216840&dopt=Abstract
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Marijuana safety study completed: weight gain, no safety problems. Author(s): James JS. Source: Aids Treat News. 2000 August 4; (348): 3-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12170987&dopt=Abstract
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Massage therapy by mothers and trained professionals enhances weight gain in preterm infants. Author(s): Ferber SG, Kuint J, Weller A, Feldman R, Dollberg S, Arbel E, Kohelet D. Source: Early Human Development. 2002 April; 67(1-2): 37-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11893434&dopt=Abstract
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Nonpharmacologic and pharmacologic management of weight gain. Author(s): Greenberg I, Chan S, Blackburn GL. Source: The Journal of Clinical Psychiatry. 1999; 60 Suppl 21: 31-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10548140&dopt=Abstract
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Pre- and postnatal dietary conjugated linoleic acid alters adipose development, body weight gain and body composition in Sprague-Dawley rats. Author(s): Poulos SP, Sisk M, Hausman DB, Azain MJ, Hausman GJ. Source: The Journal of Nutrition. 2001 October; 131(10): 2722-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11584096&dopt=Abstract
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Preventive strategies against weight gain and obesity. Author(s): Swinburn B, Egger G. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 November; 3(4): 289-301. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458974&dopt=Abstract
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Psychosocial thriving during late pregnancy: relationship to ethnicity, gestational weight gain, and birth weight. Author(s): Walker LO, Kim M.
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Source: Journal of Obstetric, Gynecologic, and Neonatal Nursing : Jognn / Naacog. 2002 May-June; 31(3): 263-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12033539&dopt=Abstract •
The effects of an educational intervention on antipsychotic-induced weight gain. Author(s): Littrell KH, Hilligoss NM, Kirshner CD, Petty RG, Johnson CG. Source: Journal of Nursing Scholarship : an Official Publication of Sigma Theta Tau International Honor Society of Nursing / Sigma Theta Tau. 2003; 35(3): 237-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14562491&dopt=Abstract
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Weight gain and antipsychotic medication. Author(s): Blackburn GL. Source: The Journal of Clinical Psychiatry. 2000; 61 Suppl 8: 36-41; Discussion 42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10811242&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
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The following is a specific Web list relating to weight gain; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Angioedema Source: Integrative Medicine Communications; www.drkoop.com Anorexia Nervosa Source: Integrative Medicine Communications; www.drkoop.com Athletic Performance Source: Healthnotes, Inc.; www.healthnotes.com Bronchitis Source: Integrative Medicine Communications; www.drkoop.com Depression Source: Integrative Medicine Communications; www.drkoop.com Depression (Mild to Moderate) Source: Prima Communications, Inc.www.personalhealthzone.com Diabetes Mellitus Source: Integrative Medicine Communications; www.drkoop.com Eating Disorders Source: Healthnotes, Inc.; www.healthnotes.com Gastritis Source: Healthnotes, Inc.; www.healthnotes.com Heart Attack Source: Healthnotes, Inc.; www.healthnotes.com High Cholesterol Source: Integrative Medicine Communications; www.drkoop.com HIV and AIDS Support Source: Healthnotes, Inc.; www.healthnotes.com Hypercholesterolemia Source: Integrative Medicine Communications; www.drkoop.com Hypothyroidism Source: Healthnotes, Inc.; www.healthnotes.com Hypothyroidism Source: Integrative Medicine Communications; www.drkoop.com Insulin Resistance Syndrome Source: Healthnotes, Inc.; www.healthnotes.com
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Menopause Source: Integrative Medicine Communications; www.drkoop.com Obesity Source: Integrative Medicine Communications; www.drkoop.com Pms Source: Integrative Medicine Communications; www.drkoop.com Preeclampsia Source: Integrative Medicine Communications; www.drkoop.com Pregnancy and Postpartum Support Source: Healthnotes, Inc.; www.healthnotes.com Premenstrual Syndrome Source: Healthnotes, Inc.; www.healthnotes.com Premenstrual Syndrome Source: Integrative Medicine Communications; www.drkoop.com Prostate Cancer Source: Integrative Medicine Communications; www.drkoop.com Seasonal Affective Disorder Source: Healthnotes, Inc.; www.healthnotes.com Systemic Lupus Erythematosus Source: Healthnotes, Inc.; www.healthnotes.com Ulcerative Colitis Source: Healthnotes, Inc.; www.healthnotes.com •
Alternative Therapy Guided Imagery Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,699,00.html
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Herbs and Supplements Adrenal Extract Source: Healthnotes, Inc.; www.healthnotes.com Astragalus Mem Alternative names: Huang-Qi; Astragalus membranaceus Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Black Cohosh Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10009,00.html Borago Alternative names: Borage; Borago officinalis Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Coenzyme Q Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,768,00.html Curcuma Alternative names: Turmeric; Curcuma longa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Dehydroepiandrosterone (DHEA) Source: Healthnotes, Inc.; www.healthnotes.com Dehydroepiandrosterone (DHEA) Source: Integrative Medicine Communications; www.drkoop.com Fiber Source: Integrative Medicine Communications; www.drkoop.com Forskolin Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10025,00.html Glucomannan Source: Healthnotes, Inc.; www.healthnotes.com Glycyrrhiza Glabra Source: Integrative Medicine Communications; www.drkoop.com Ipecac Source: Healthnotes, Inc.; www.healthnotes.com Licorice Alternative names: Glycyrrhiza glabra, Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com Ornithine Source: Healthnotes, Inc.; www.healthnotes.com Ornithine Alpha-ketoglutarate Source: Healthnotes, Inc.; www.healthnotes.com
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Panax Alternative names: Ginseng; Panax ginseng Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Phytolacca Alternative names: Poke root, Endod; Phytolacca dodecandra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Pueraria Alternative names: Kudzu; Pueraria lobata Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Ribes Alternative names: Black Currant; Ribes nigrum L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON WEIGHT GAIN Overview In this chapter, we will give you a bibliography on recent dissertations relating to weight gain. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “weight gain” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on weight gain, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Weight Gain ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to weight gain. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
A Placebo-controlled Randomized Trial of the Effects of Ppa and Nicotine Gum on Cessation Rates and Post-cessation Weight Gain in Women by Cooper, Theodore V.; PhD from The University of Memphis, 2002, 39 pages http://wwwlib.umi.com/dissertations/fullcit/3054558
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Direct and Correlated Responses to Selection for Weight Gain in Mice by Urrutia, Maria Soledad; PhD from McGill University (Canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NL24052
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Effects of Selected Combinations of an Anabolic Steroid (Oxandrolone), Dl Amphetamine Sulphate, and Protein Supplementation upon Weight Gain and Endurance of Male Wistar Rats by Peterson, Franklin James, PhD from University of Maryland College Park, 1973, 138 pages http://wwwlib.umi.com/dissertations/fullcit/7328894
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Maternal Weight Relationships and Infant Outcomes in Women with Gestational Diabetes Mellitus As Compared to the Weight Gain Recommendations for Pregnancy
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of the Institutes of Medicine by Jonaitis, Mary Ann; EDD from Columbia University Teachers College, 2002, 136 pages http://wwwlib.umi.com/dissertations/fullcit/3052886 •
The Relationship between Learning, Health Beliefs, Weight Gain, Alcohol Consumption, and Tobacco Use of Pregnant Women by Strychar, Irene Mary-Ann, EDD from The University of British Columbia (Canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/f3825028
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The Relationship between Learning, Health Beliefs, Weight Gain, Alcohol Consumption, and Tobacco Use of Pregnant Women by Strychar, Irene; EDD from The University of British Columbia (Canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL44642
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Women's Experience of Weight and Shape Changes during Pregnancy (Prenatal Care, Eating Disorders, Weight Gain) by Robb-Todter, Gail Elisabeth, PhD from University of Virginia, 1996, 314 pages http://wwwlib.umi.com/dissertations/fullcit/9616020
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND WEIGHT GAIN Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning weight gain.
Recent Trials on Weight Gain The following is a list of recent trials dedicated to weight gain.8 Further information on a trial is available at the Web site indicated. •
Preterm Infants' Weight Gain Following Massage Therapy Condition(s): Premature Birth Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Complementary and Alternative Medicine (NCCAM) Purpose - Excerpt: Multiple investigations have demonstrated that preterm infants who received massage therapy for 5 to 10 days exhibited 28% to 47% greater daily weight gain. Findings have consistently shown that preterms receiving massage do not consume more formula or calories than control infants. The proposed research will examine possible underlying mechanisms for this enhanced weight gain following massage therapy. Phase(s): Phase III Study Type: Interventional Contact(s): Maria Hernandez-Reif, Ph.D. 305-243-6781
[email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00029198
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The Effects of Overfeeding on Obesity-Prone (OP) and Obesity-Resistant (OR) Women Condition(s): Obesity; Thinness; weight gain Study Status: This study is currently recruiting patients.
8
These are listed at www.ClinicalTrials.gov.
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Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This is a longitudinal cohort study of how the responses to a 3 day period of controlled overfeeding relate to subsequent weight gain. We hypothesize that thin individuals are resistant to weight gain because they respond to periods of overfeeding by increasing fat oxidation, reducing food intake, and increasing physical activity relative to those who gain weight over time. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00072917 •
A Prospective Study to Evaluate Potential Factors Affecting Weight Among Breast Cancer Patients Receiving Adjuvant Chemotherapy Condition(s): Breast Neoplasm; Weight Gain Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: An estimated 178,700 new cases of invasive breast cancer will be diagnosed in 1998, most with early stage disease requiring adjuvant chemotherapy. Significant weight gain is consistently reported among 50 to 96% of breast cancer patients who have received systemic adjuvant chemotherapy, the average weight increase ranging from 3 to 6 kg in these studies. Weight gain in breast cancer patients post-diagnosis and treatment is associated with decreased disease-free and overall survival, as well as poor quality of life. Mechanisms underlying this weight gain have not been delineated or studied. The primary objective of this investigation is to evaluate factors that may lead to weight gain among women with breast cancer who are treated with adjuvant chemotherapy, in order to assess and elucidate underlying physiologic mechanism(s). Plausible mechanisms that will be evaluated include alterations in: (a) hormonal and growth factor status, including ovarian/gonadotrophic hormones such as total, bound, and free estradiol, androgens, sex hormone binding globulin (SHBG), follicle stimulating hormone (FSH), thyroid hormones, prolactin, insulin-like growth factors I and II (IGF I and II), and plasma leptin; (b) factors affecting energy intake or expenditure including oral intake, physical activity, and resting metabolic rate, and (c) psychological factors such as depression and quality of life. We will conduct a prospective study of approximately 140 women (including pre- and post-menopausal patients) with newly diagnosed, stage I, II, and IIIA, primary breast cancer, who will undergo adjuvant chemotherapy with currently utilized stage appropriate chemotherapeutic regimens. Body weight, body composition by dual energy X-ray absorptiometry (DXA), and the mechanistic factors described above will be measured at 3 time points, (a) baseline (prior to the first cycle or dose of adjuvant chemotherapy); (b) 2 weeks after the final administration of adjuvant chemotherapy; and (c) 6 months after the final administration of adjuvant chemotherapy. Total energy expenditure will also be measured by the doubly-labeled water (DLW) method at the first and second timepoints. Data will be collected for other factors that may affect weight gain including the particular chemotherapeutic regimen, number of cytotoxic agents in the regimen, route of delivery, menopausal and nodal status, and baseline weight. Statistical analysis of the factors postulated as predictive of weight gain will involve paired t-tests, analysis of variance (ANOVA), and multivariate regression techniques. We believe that chemotherapy may induce significant changes in the hormonal milieu or growth factor status, leptin, energy intake or expenditure, and/or body composition among women who do gain weight during adjuvant chemotherapy or post treatment. Information
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obtained from this study will provide the insight and rationale needed for logical and optimal interventions to curb weight gain in breast cancer patients. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001796 •
Pharmacologic Intervention for Postcessation Weight Gain Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To test pharmacologic intervention for smoking postcessation weight gain using nicotine gum and phenylpropanolamine (PPA). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005704
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Prevention of weight gain Condition(s): Obesity; Body Weight Changes Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The purpose of this study is to test methods for preventing weight gain in normal-weight and overweight women aged 25 through 44. Participants will complete brief questionnaires about their health, eating and exercise habits, and use of weight control strategies. They will then be randomly assigned to 1 of 3 treatment conditions. All 3 treatments receive information on the importance of maintaining a healthy body weight, the components of a healthy diet, and ways to increase activity levels. The 3 treatment differ in how this information is delivered. At 12, 24 and 36 months after enrolling in the study, participants will attend assessment sessions. They will complete questionnaires and have body weight measured. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011102
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Weight Gain in CF Condition(s): Cystic Fibrosis Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The current study examines the efficacy of two treatments to help children with cystic fibrosis (CF) meet their dietary calorie requirements of 120% to 150% of the recommended daily allowance of energy and the effect of these treatments on weight gain and maintenance. One treatment provides children with CF and their parents nutrition education about the best foods for meeting their dietary needs. The second treatment gives children with CF and their families similar nutritional
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information plus behavioral parenting methods for motivating children to eat the recommended foods. Children with CF and their families are seen weekly for 7 treatment sessions across 9 weeks for the active phase of treatment. Families are then followed for 2 years after treatment in order to better understand how long the treatments are effective and to determine the health benefits of better nutrition status and weight gain. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006169
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “weight gain” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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•
For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON WEIGHT GAIN Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “weight gain” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on weight gain, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Weight Gain By performing a patent search focusing on weight gain, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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example of the type of information that you can expect to obtain from a patent search on weight gain: •
Chromium-carboxylic acid feed supplement Inventor(s): Thompson; Leif H. (Philo, IL) Assignee(s): Thompson Animal Systems, Inc. (Philo, IL) Patent Number: 6,139,881 Date filed: January 18, 2000 Abstract: The combination of a chromium ion and a carboxylic acid ion selected from the group consisting of a formate ion, a malate ion, and a fumarate ion is an effective feed supplement for ruminant animals and improves their weight gain, feed efficiency, body composition, and milk production. Excerpt(s): This invention relates to feed supplements for ruminant animals. Ruminants are hoofed, even-toed mammals of the suborder Ruminantia that have a stomach divided into four compartments and that chew a cud consisting of regurgitated, partially digested food. Well known ruminants include cattle, sheep, goats, deer, and giraffes. Of this group, the most important to man are cattle, sheep, and goats because they are raised as livestock for home use and profit around the world. The diet fed to ruminant livestock is important because it has a major effect on the animal's growth rate, body composition, and, in the case of mature females, milk production. Within the past several decades, the supplementation of plant feed with various micronutrients has become more common. A large number of feed supplements for ruminants have been disclosed. Web site: http://www.delphion.com/details?pn=US06139881__
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Corticotropin releasing factor receptor 2 deficient mice and uses thereof Inventor(s): Bale; Tracy L. (San Diego, CA), Lee; Kuo-Fen (Del Mar, CA), Smith; George W. (Mason, MI), Vale; Wylie W. (La Jolla, CA) Assignee(s): Research Development Foundation (Carson City, NV) Patent Number: 6,353,152 Date filed: July 14, 2000 Abstract: The present invention provides transgenic mice deficient in corticotropin releasing factor receptor 2. Corticotropin releasing factor is a critical integrator of the hypothalamic-pituitary-adrenal axis in response to stress. CRF and its related molecule urocortin bind CRF receptor 1 and CRFR2 with distinct affinities. CRFR2 mutant mice were hypersensitive to stress and displayed increased anxiety-like behavior. Mutant mice had normal basal feeding and weight gain, but exhibited decreased food intake following food deprivation. Intravenous UCN dramatically decreased the mean arterial pressure in the controls but had no effect in the mutants. A deficiency of CRFR2 results in a significant increase in urocortin mRNA in the rostral region of the Edinger Westphal and a significant increase in CRF mRNA in central nucleus of the amygdala. These results demonstrate that the CRFR2 mutant mice, opposed to CRFR1 mutant mice, have an increased sensitivity to stress and display anxiety-like behavior. These mice are useful for the study of anxiety, depression, and the physiology of the HPA axis.
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Excerpt(s): The present invention relates generally to the fields of neurobiology, endocrinology, and psychiatry. More specifically, the present invention relates to the study of anxiety and to mice deficient for corticotropin releasing factor receptor 2. Corticotropin releasing factor (CRF) is a critical coordinator of the hypothalamicpituitary-adrenal (HPA) axis. In response to stress, corticotropin releasing factor released from the paraventricular nucleus of the hypothalamus (PVN) activates corticotropin releasing factor receptors on anterior pituitary corticotropes, resulting in release of adrenocorticotropic hormone (ACTH) into the bloodstream. ACTH in turn activates ACTH receptors in the adrenal cortex to increase synthesis and release of glucocorticoids (1). The receptors for CRF, CRFR1 and CRFR2 are localized throughout the CNS and periphery. While CRF has a higher affinity for CRFR1 than for CRFR2, urocortin (UCN), a CRF-related peptide, is thought to be the endogenous ligand for CRFR2 since it binds with almost 40-fold higher affinity than does CRF (2). CRFR1 and CRFR2 share approximately 71% amino acid sequence similarity and are distinct in their localization within the brain and peripheral tissues (3-6). CRFR1 is expressed mainly in the pituitary gland, cortex, cerebellum, hindbrain, and olfactory bulb, whereas CRFR2 is found in the lateral septum, ventral medial hypothalamus (VMH), choroid plexus, and many peripheral sites (5, 7, 8). CRFR2 has several isoforms, one of which has been shown to not bind any known ligand (9). Web site: http://www.delphion.com/details?pn=US06353152__ •
Delivery system for antimethanogenic agents Inventor(s): Edgar; John Alexander (Carlten, AU), May; Christopher (Heidelberg Heights, AU), Payne; Alan Lindsay (Beaumarls, AU), Stewart; Philip Laurence (Eltham, AU) Assignee(s): Commonwealth Scientific and Industrial Research Organisation (Campbell, AU) Patent Number: 5,972,910 Date filed: July 23, 1997 Abstract: A delivery system is provided to reduce methane production in animals or to improve the weight gain of an animal. Embodiments include a delivery system comprising a volatile and/or water soluble antimethanogenic agent with cyclodextrin or a cyclodextrin-like compound. Excerpt(s): The present invention relates to a delivery system for delivering a volatile and/or water soluble antimethanogenic agent to an animal, a composition comprising the agent and methods of treatment of an animal. Microorganisms capable of generating methane are commonly found in the gut flora of animals including ruminants. The microorganisms which produce methane in ruminants result in the loss of energy available to the animal and are also believed to contribute significantly to greenhouse gases. Specifically, it has been known for many years that suppression of methane production in ruminants can theoretically lead to increased production and much work has been undertaken to reduce methane biosynthesis and achieve production gains in domestic animals. This has been most successfully achieved by modifications to the diet of animals. Diet manipulation is only possible in a limited number of animal production systems and is generally only able to reduce and not completely suppress methane production. A number of approaches to methane suppression in animals are being explored, not only to increase animal production but also to reduce the level of methane in the environment because of its contribution to the "greenhouse" effect.
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Web site: http://www.delphion.com/details?pn=US05972910__ •
Derivatives of (+)-venlafaxine and methods of preparing and using the same Inventor(s): Jerussi; Thomas P. (Framingham, MA), Senanayake; Chrisantha H. (Shrewsbury, MA) Assignee(s): Sepracor, Inc. (Marlborough, MA) Patent Number: 6,197,828 Date filed: November 30, 1999 Abstract: Methods of preparing, and compositions comprising, derivatives of (+)venlafaxine are disclosed. Also disclosed are methods of treating and preventing diseases and disorders including, but not limited to, affective disorders such as depression, bipolar and manic disorders, attention deficit disorder, attention deficit disorder with hyperactivity, Parkinson's disease, epilepsy, cerebral function disorders, obesity and weight gain, incontinence, dementia and related disorders. Excerpt(s): The invention relates to optically pure derivatives of (+)-venlafaxine, methods of their synthesis, compositions comprising them, and methods of their use. A number of nontricyclic antidepressants have recently been developed that diminish the cardiovascular and anticholinergic liability characteristic of tricyclic antidepressants. Some of these compounds are used as anti-obesity agents and have shown promise in the treatment of cerebral function disorders such as Parkinson's disease and senile dementia. See e.g., WO 94/00047 and WO 94/00114. The nontricyclic compound venlafaxine, chemically named (.+-.)-1-[2-(dimethylamino)-1-(4-methoxyphenyl)ethyl]cyclohexanol, is an antidepressant which has been studied extensively and which is described in, for example, U.S. Pat. No. 4,761,501 and Pento, J. T. Drugs of the Future 13(9):839-840 (1988). Its hydrochloride salt is currently commercially available in the United States under the trade name Effexor.RTM. Effexor.RTM., which is a racemic mixture of the (+) and (-) enantiomers of venlafaxine, is indicated for the treatment of depression. Klamerus, K. J. et al. J. Clin. Pharmacol. 32:716-724 (1992). All of these metabolites are racemic. In vitro studies suggest that O-desmethylvenlafaxine is a more potent inhibitor of norepinephrine and dopamine uptake than the parent compound racemic venlafaxine. Muth, E. A. et al. Drug Develop. Res. 23:191-199 (1991). Odesmethylvenlafaxine has also been reported to have a half-life (t1/2) of about 10 hours, which is approximately 2.5 times as long as that of venlafaxine. Klamerus, K. J. et al. J. Clin. Pharmacol. 32:716-724 (1992). Studies directed at understanding the activity of Odesmethylvenlafaxine as compared to its parent have been hampered, however, by the metabolic difference between laboratory animals and man in their exposure to venlafaxine. Howell, S. R. et al. Xenobiotica 24(4):315-327 (1994). Web site: http://www.delphion.com/details?pn=US06197828__
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Dietary compositions and methods Inventor(s): Bruckner; Geza (222 E. Eagle, Versailles, KY 40383), Szabo; Joseph (Ordogorom lejfo 11/B., Budapest, HU) Assignee(s): none reported Patent Number: 6,359,017 Date filed: February 24, 2000
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Abstract: Dietary compositions and methods employ a mammal food base and a component comprising estrogen, androgen or a mixture thereof in an amount sufficient to reduce weight gain normally incurred in the mammal type subsequent to neutering, castration, spaying, ovariectomy or ovariohysterectomy, or post menopause. Preferably, the component comprises phytoestrogen, phytoandrogen or a mixture thereof. The compositions are adapted for administration to the mammal on a regular, preferably daily, basis. Excerpt(s): The present invention is directed to dietary compositions, particularly for mammals, including humans, dogs, cats and horses, and to methods for reducing weight gain normally incurred in mammals subsequent to neutering, castration, spaying, ovariectomy or ovariohysterectomy, or post menopause. Procedures including neutering, castration, spaying, ovariectomy or ovariohysterectomy are increasingly performed on dogs and cats for health related reasons and/or for population control. It is not uncommon for dogs or cats having undergone one of the aforementioned procedures to gain a significant amount of weight thereafter, and often exceed target healthy weight limits. Weight gain incurred subsequent to ovariectomy or ovariohysterectomy procedures in other mammals, including humans, is not uncommon. Additionally, post menopausal weight gain often occurs in humans even when ovariectomy or ovariohysterectomy procedures are not performed. Web site: http://www.delphion.com/details?pn=US06359017__ •
Enhancing milk production by adding to feed a nonionic surfactant coated on a carrier Inventor(s): Kamande; George (Abbotsford, CA), Shelford; James A. (Vancouver, CA) Assignee(s): The University of British Columbia (Vancouver, CA) Patent Number: 6,221,381 Date filed: September 24, 1999 Abstract: Methods and compositions are provided for enhancing feed utilization efficiency in a ruminant animal by adding to the feed a sufficient amount of a nonionic surfactant to enhance the utilization of the feed by the animal. The methods and compositions result in enhanced weight gain and/or milk production by the animal. Preferred nonionic surfactants include polyoxyethylenesorbitan monooleate and polyoxyethylenesorbitan trioleate at a concentration range of from about 0.01 to 1% (w/w) of the dry weight of the feed. A digestion enhancing enzyme and lactic acid bacteria inoculum may also be added to the feed. The surfactant is added to the feed by spraying a dilute solution of the surfactant onto the feed, or by coating the surfactant onto a particulate carrier such as celite, diatomaceous earth or silica and adding the carrier to the feed. Excerpt(s): The present invention relates generally to ruminant feed compositions containing nonionic surfactants, either alone or in combination with digestion enhancing agents, and to methods for enhancing feedstock utilization efficiency in ruminant livestock. More particularly, this invention relates to the addition of nonionic surfactants to ruminant feed, with or without added digestion enhancing agents, and feeding the resulting product to the animal. Anaerobic fermentation occurs during ruminant digestion, during which proteins and carbohydrates are degraded. It is desirable in ruminant digestion to be able to control protease and carbohydrase activity to optimize the digestive process. Since feed is a major cost in ruminant production,
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enhancing digestive efficiency remains a driving objective in the industry. Although forages remain the major feed source, it is widely believed that the efficiency of feed utilization by ruminants has remained relatively unchanged during the last two decades. New innovations that enhance the digestive efficiency provide a compromise to emerging environmental concerns regarding ground water pollution in most dairying areas. Nevertheless, an in depth understanding of the roles of feed processing and bacterial digestion are required to fully manipulate the digestive processes of the rumen. Cheng et al. ("Microbial ecology and physiology of feed degradation within the rumen," in Physiological aspects of digestion and metabolism in ruminants: Proceedings of the seventh international symposium on ruminant physiology, Tsuda, Ed., 1991) has identified the following three general factors as influencing microbial digestion of feeds: (a) plant structures that regulate bacterial access to nutrients; (b) microbial factors that control adhesion and the development of digestive microbial consortia; and (c) complexes of oriented hydrolytic enzymes of the adherent microorganisms. Feed processing practices, e.g., grinding, normally attempt to increase enzyme-substrate interaction by the exposition of susceptible substrate binding sites. Web site: http://www.delphion.com/details?pn=US06221381__ •
Extended release growth promoting two component composition Inventor(s): Cady; Susan Mancini (Yardley, PA), Gibson; John W. (Springville, AL), Macar; Claude (Paris, FR) Assignee(s): Akzo Nobel N.V. (Amhem, NL), Southern BioSystems (Birmingham, AL) Patent Number: 6,498,153 Date filed: March 22, 1999 Abstract: An extended release composition comprising a first composition comprising growth promoters and a second composition comprising growth promoters and a biodegradable polymer is described. A method of increasing weight gain in food animals utilizing the composition, a pharmaceutical dosage form containing the composition and a method of preparing the pharmaceutical dosage form are also described, as are pellets of the composition for implantation in food animals. Excerpt(s): Sustained release pharmaceutical compositions containing growth promoters for use in food animals are described in U.S. Pat. No. 3,939,265 issued to J. A. Grandadam on Feb. 17, 1976 and U.S. Pat. No. 5,288,496 issued to D. H. Lewis on Feb. 22, 1994. The rate of release of the growth promoters of these compositions, however, generally does not comport with the growth periods of food animals in feedlots, the rate of release of the promoters declining over the growth period and becoming markedly reduced before the expiration of the period. To overcome this deficiency in feedlot growth promotion, it would be desirable to provide an extended release composition, from which the growth promoters are uniformly released over the growth period of the food animal in the feedlot, thereby enhancing the weight gain of the animal and improving the feed efficiency of the formulation. It has now been found that a composition comprising a first composition comprising growth promoters and a second composition comprising growth promoters and a biodegradable polymer releases the promoters over an extended period of time corresponding to the growth period of feedlot animals. wherein R.sub.6 is loweralkyl; the ester derivatives, geometric isomers, stereoisomers, or optical isomers thereof; and a biodegradable polymer selected from the group consisting of homopolymers and copolymers of.gamma.butyrolactone,.delta.-valerolactone,.epsilon.-caprolactone, glycolide, DL-lactide, L-
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lactide, glycolic acid, DL-lactic acid, L-lactic acid, and combinations thereof, polydioxanones, polyorthesters, polyanhydrides, polycarbonates, polyesteramides, and polyphosphazines, useful for the promotion of weight gain in food animals. The present invention also relates to a pharmaceutical dosage form containing the composition, a method of preparing the dosage form utilizing the composition, as well as pellets of the composition for implantation in food animals. Preferred compositions of growth promoters are those wherein R, R.sub.1, R.sub.2, R.sub.3, and R4, R.sub.5 and R.sub.6 are methyl and the aroyl or alkanoyl ester derivatives thereof, where applicable. Web site: http://www.delphion.com/details?pn=US06498153__ •
Hormone replacement therapy Inventor(s): Henley; Edna C. (St. Louis, MO), Potter; Susan M. (Ellisville, MO), Taylor; Richard B. (Valley Park, MO) Assignee(s): Protein Technologies International (St. Louis, MO) Patent Number: 6,326,366 Date filed: August 22, 2000 Abstract: The present invention relates to a hormone replacement therapy, and a composition useful therein, for women having reduced levels of endogenous estrogen. A mammalian estrogen and an isoflavone which is incapable of being metabolized to equol are co-administered to a woman having a reduced level of endogenous estrogen. The hormone replacement therapy is effective to inhibit or prevent diseases or conditions resulting from, or exacerbated by, a reduction in endogenous estrogen including: coronary heart disease, cardiovascular disease, osteoporosis, loss of cognitive function, urinary incontinence, weight gain, fat mass gain, and vasomotor symptoms. A composition for use in the hormone replacement therapy of the present invention contains a mammalian estrogen and at least one isoflavone, where the isoflavone is incapable of being metabolized to equol by a human, and where the composition contains less than 10% by weight of isoflavones and phytoestrogens capable of being metabolized to equol by a human. Excerpt(s): The present invention relates to a composition and a method for reducing the risk of coronary heart disease, osteoporosis, loss of cognitive function, urinary incontinence, weight and fat mass gain, and vasomotor symptoms in women having a reduced level of endogenous estrogen. In particular, a combination of a mammalian estrogen and an isoflavone are used in a hormone replacement therapy regimen, where the isoflavone is incapable of being metabolized to equol by a human. Estrogen plays an important role in protecting the health of women. It has been implicated as a significant factor in protecting and maintaining cardiovascular health, bone mass, and mental cognition. The health protective effects of estrogen for women have been proposed as one of the reasons that women in the United States live an average of 71/2 years longer than men. Women form 59% of the U.S. population over age 65 and 72% of the population over age 85. A woman's endogenous level of estrogen is significantly reduced upon entering menopause or upon premature surgical menopause induced by removal of the uterus and/or ovaries. The amount of a woman's endogenous estrogen is typically reduced to less than 10% of premenopausal levels following natural or surgical menopause. This reduction of endogenous estrogen levels results in the loss of estrogen's health protective effects, particularly with respect to cardiovascular health, bone health, and mental cognition.
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Web site: http://www.delphion.com/details?pn=US06326366__ •
Interactions between genotype and diet in swine that prevent E. coli associated intestinal disease Inventor(s): Bosworth; Brad (Cambride, GB), Ridpath; Julia (Gilbert, IA), Wiseman; Barry (Belle Mead, NJ) Assignee(s): Biotechnology Research and Development Corporation (Peoria, IL), The United States of America as represented by the Department of (Washington, DC) Patent Number: 6,355,859 Date filed: September 18, 1998 Abstract: The present invention relates interactions between genotype and diet that are useful in the dietary control of intestinal disease. Compositions are related that are useful to differentiate, with a high level of sensitivity and specificity, swine that are genetically resistant to a reduced rate of weight gain when fed diets containing high levels of SBM. The reduced rate of gain can be prevented by reducing the levels of SBM in nursery diets and replacing a majority of the soy bean meal with animal-based protein sources, fish meal, plasma or milk. Genetically resistant swine fed either the diet low in SBM, or a diet high in SBM, and susceptible swine fed a diet low in SBM, were not colonized by F18+E. coli and gained weight at an acceptable rate. Excerpt(s): This invention relates interactions between genotype and diet in swine that prevent E. coli associated intestinal disease. Methods and compositions are provided for identifying swine which are genetically able to utilize low cost feed stuffs and feed compositions to prevent intestinal disorders after weaning. Disease caused by F18+E. coli can be prevented by reducing the amount of soy bean meal (SBM) and total protein in the diet; however, this decrease in the total protein content of the pig's diet results in decreased quality e.g. weight (Bosworth et al., 1996; Bertschinger et al., 1979). Therefore, this treatment for F18+E. coli is not economical. Diets that prevent disease due to F18+E. coli but still contain high enough protein levels to allow swine to gain weight rapidly after weaning would be desirable. Reduction of costs in swine production is a goal of breeders. Two of the most significant costs associated with swine production relate to food and disease, especially in the postweaning period. Intestinal diseases reduce weight gain, hence decrease the value of the swine. Treatment costs also occur. Swine weaned early require a high amount of protein in their diet in order to gain weight adequately, and the source of the protein is a major food diet cost. Plant-based sources high in protein content, typically soy bean meal (SBM), are common ingredients in most swine diets and are cheaper than animal-based sources, such as fish meal and blood meal. However, swine fed diets with high levels of SBM frequently have a reduced rate of weight gain relative to swine fed nursery diets postweaning in which a portion of the SBM is replaced with animal byproducts, such as whey and plasma (Li et al., 1991). The mechanisms responsible for this reduced rate of gain in recently weaned swine are not defined, but it could be that SBM acts as a food allergen in recently weaned swine who have just been removed from a diet high in animal protein (i.e., sows' milk). Web site: http://www.delphion.com/details?pn=US06355859__
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Limiting weight gain of cats by feeding carbohydrate source that excludes rice Inventor(s): Sunvold; Gregory D. (Eaton, OH) Assignee(s): The Procter & Gamble Company (Cincinnati, OH) Patent Number: 6,630,159 Date filed: March 27, 2001 Abstract: A process is provided for limiting weight gain in cats. The process includes feeding the cat a pet food composition that includes a source of protein, a source of fat, and a source of carbohydrates from a grain source that excludes rice. Use of preferred low glycemic index grain sources that comprise a blend of corn and sorghum; a blend of corn, sorghum, and barley; or a blend of corn, sorghum, and oats, has the effect of decreasing the postprandial blood glucose and insulin response of the cat as compared to when feeding a rice-based diet. The result is that the animal becomes satiated and voluntarily decreases its intake of food, causing less weight gain. This effect is even more marked when the composition is fed to male cats. Excerpt(s): This invention relates to a process of administering a pet food composition to prevent obesity in companion animals, such as cats and dogs. More particularly, the invention relates to a process for limiting weight gain in cats. The invention is further directed to a process for decreasing the postprandial blood glucose and insulin response in cats to promote satiety and a voluntary decrease in food intake. Obesity is a significant health concern in companion animals. Veterinary care professionals have reported that approximately 20-40% of the pets in their care are overweight. These animals bear a greater risk for health problems associated with the respiratory, cardiovascular, and skeletal systems. More particularly, obese feline patients have demonstrated greater susceptibility to diseases such as diabetes mellitus, osteoarthritis, ligament injuries, perineal dermatitis, cardiomyopathy, and hepatic lipidosis. Accordingly, new technologies meeting the health needs of obese feline patients are in high demand by pet owners and veterinarians alike. The causes of feline obesity include sedentary lifestyle and confinement indoors, as well as improper nutrition, genetic predisposition, and hormonal disorders such as thyroid and pituitary gland dysfunction. Moreover, spayed and neutered cats often exhibit a decrease in their physical activity and metabolism and therefore, have a greater tendency to gain weight. Web site: http://www.delphion.com/details?pn=US06630159__
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Measurement of intramuscular fat in cattle Inventor(s): Brethour; John R. (Hays, KS) Assignee(s): Kansas State University Research Foundation (Manhattan, KS) Patent Number: 5,960,105 Date filed: August 4, 1997 Abstract: A system determines the number of days livestock should be maintained on feed for maximum profit. In the preferred embodiment, current attributes such as marbling and backfat thickness are used to predict what these attributes, as predicted attribute values, will be at various times in the future. These predicted attributes along with other factors such as projected rate of weight gain, costs of feed and livestock prices are used to determine how many days the livestock should be maintained on feed in order to maximize profit.
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Excerpt(s): The present invention concerns the measurement of intramuscular fat, i.e., marbling, in cattle using ultrasound to produce an image of an interior portion of a muscle and then to analyze data representative of that image to produce a measurement of marbling. The grading systems for beef carcasses emphasize leanness in terms of yield grades and palatability in terms of quality grades, ice. intramuscular fat or marbling. Marbling is considered an indicator of favorable ogano-leptic properties such as juiciness, flavor and tenderness. The yield and quality grades of beef are determined after slaughter. If these grades could be determined accurately in live cattle, producers would have the ability to cluster live cattle during the feedlot phases on the basis of anticipated grades to satisfy packer and consumer specifications. Additionally, this would enable cattle breeders to select breeding stock on the basis of the desirable grading traits. Ultrasound techniques have been used with some success for determining anticipated yield grades in cattle. A smooth tissue boundary such as that between subcutaneous fat and muscle results in a specular reflection of the ultrasound that produces a congruent image on the ultrasound monitor. Because of this, ultrasound produces a fairly accurate image of backfat and other attributes predictive of yield grade. Web site: http://www.delphion.com/details?pn=US05960105__ •
Method for selectively altering body fat level, feed efficiently, or weight gain Inventor(s): Cook; Mark E. (Madison, WI), Jerome; Daria (Detroit Lakes, MN), Pariza; Michael W. (Madison, WI) Assignee(s): Wisconsin Alumni Research Foundation (Madison, WI) Patent Number: 6,020,378 Date filed: March 30, 1999 Abstract: A method for treating an animal to reduce body fat while the animal exhibits improved feed efficiency and either continued weight gain or an increase in lean body mass includes the steps of administering to the animal a combination of CLA isomers in a ratio selected to retain a desirable benefit attributable to one isomer while counteracting an undesirable effect of the same isomer. Excerpt(s): Not applicable. To be determined. The present application generally relates to methods of treating animals, including humans. More particularly, it relates to methods of treating animals to selectively alter body fat, feed efficiency, or weight gain (which can also be measured as growth rate). Web site: http://www.delphion.com/details?pn=US06020378__
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Method of monitoring and controlling electroless plating in real time Inventor(s): Smith; Richard (65 St. Mark's Pl., New York, NY 10003), Wasserman; Arthur (35 E. 35th St., Box 6E, New York, NY 10016) Assignee(s): none reported Patent Number: 5,993,892 Date filed: September 12, 1996 Abstract: A sample coupon of known dimensions is immersed in the electroless plating bath. Immersion time can extend for the life of the bath. The coupon is attached to a
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load-cell which incorporates strain-gauge technology. The millivolt output of the loadcell to galvanometer displays weight gain at chosen intervals (e.g., 1 minute), and can signal operator if weight gain is less than the chart contained in engineering specifications to make replenishment additions defined in specification. The galvanometer output, with specialized software to computer traces weight gain profile providing data for actuating valves (e.g., proportionating pump) and provides hardcopy quality control record. Control of this one chemical replenishment parameter is sufficient to give real time process optimization and minimizes auto-catalytic breakdown. Instruments can be positioned in controlled environment. Excerpt(s): Electroless plating is an auto-catalytic chemical process that deposits a metal or an alloy. As employed in industry, it is characterized by enhancing corrosion resistance, wear properties and providing electrical conductivity to defined areas. It has the ability of depositing an exact thickness of metal on parts regardless of the parts' shape or their position in the electroless plating tank. Web site: http://www.delphion.com/details?pn=US05993892__ •
Methods and reagents for regulating obesity Inventor(s): Bernfield; Merton (Boston, MA), Reizes; Ofer (Newton, MA) Assignee(s): Children's Medical Center Corporation (Boston, MA) Patent Number: 6,284,729 Date filed: May 6, 1998 Abstract: It has now been demonstrated that syndecan binds to and interacts with MC4R, and thereby modulates neuropeptide regulation of body weight, via the agouti/MC4R signaling pathway. Transgenic animals were made initially using a construct including a cytomegalovirus promoter and the 3' untranslated region, including the polyadenylation site, of the bovine growth hormone gene, as well as cDNA encoding syndecan-1. The mice express the syndecan-1 transgene in many tissues, with expression in the brain occurring preferentially in their hypothalamus. These mice are characterized by elevated levels of circulating syndecan-1 ectodomain and exhibit enormous weight gain after reaching sexual maturity, but have a relatively normal distribution of fat, are completely healthy and heterozygotes reproduce, and show other indicators associated with obesity in humans. Agouti mice which are transgenic for syndecan-1 ectodomain demonstrate that syndecan-1 and agouti interact, potentiating obesity. The double heterozygote shows both an earlier onset, and greater extent, of obesity than either normal agouti or the original transgenic syndecan-1 mice.Based on these studies and animal models, one can design and test compounds regulating obesity. These mice are also useful in understanding the factors involved in weight regulation and in designing and screening for drugs which are involved in weight regulation and that can either enhance or reduce appetite and activity. Excerpt(s): Obesity is a well established risk factor for a number of potentially lifethreatening diseases such as atherosclerosis, hypertension, diabetes, stroke, pulmonary embolism, and cancer. Furthermore, it complicates numerous chronic conditions such as respiratory diseases, osteoarthritis, osteoporosis, gall bladder disease, and dyslipidemias. The enormity of this problem is best reflected in the fact that death rates escalate with increasing body weight. More than 50% of all-cause mortality is attributable to obesity-related conditions once the body mass index (BMI) exceeds 30 kg/m.sup.2, as seen in 35 million Americans. (Lee1992. JAMA. 268:2045-2049). By
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contributing to greater than 300,000 deaths per year, obesity ranks second only to tobacco smoking as the most common cause of potentially preventable death. (McGinnis 1993 MA.270:2207-2212). Accompanying the devastating medical consequences of this problem is the severe financial burden placed on the health care system in the United States. The estimated economic impact of obesity and its associated illnesses from medical expenses and loss of income are reported to be in excess of $68 billion/year. (Colditz G. 1992. Am J Clin Nutr. 55:503S-507S). This does not include the greater than $30 billion per year spent on weight loss foods, products, and programs. (Wolf 1994. Pharmacoeconomics. 5:34-37). A major reason for the long-term failure of established approaches is their basis on misconceptions and a poor understanding of the mechanisms of obesity. Conventional wisdom maintained that obesity is a self-inflicted disease of gluttony. Comprehensive treatment programs, therefore, focused on behavior modifications to reduce caloric intake and increase physical activity using a myriad of systems. These methods have limited efficacy and are associated with recidivism rates exceeding 95%. (NIH Technology Assessment Conference Panel. 1993. Ann Intern Med. 119:764-770). Failure of short-term approaches, together with the recent progress made in elucidating the pathophysiology of obesity, have lead to a reappraisal of pharmacotherapy as a potential long-term, adjuvant treatment. (National Task Force on Obesity. 1996. JAMA. 276:1907-1915). The premise is that body weight is a physiologically controlled parameter similar to blood pressure and obesity is a chronic disease similar to hypertension. The goal of long-term (perhaps life long) medical therapy would be to facilitate both weight loss and subsequent weight maintenance in conjunction with a healthy diet and exercise. To assess this approach, the long-term efficacy of currently available drugs must be judged against that of nonpharmacological interventions alone. Currently, no single drug regimen emerges as superior in either promoting or sustaining weight loss. Although promising, the success of this approach is limited by the efficacy of currently available anorexiant drugs. Surgical interventions, such as gastric partitioning procedures, jejunoileal bypass, and vagotomy, have also been developed to treat severe obesity. (Greenway 1996. Endo Metab Clin N Amer. 25:1005-1027). Although these procedures induce similar rates of early weight loss as nonsurgical interventions, they have been shown to maintain a weight loss of up to 33% for more than 10 years. (Long 1994. Diabetes Care. 17:372-375). While still far from optimal, this is a substantial improvement over that achieved with behavioral and medical management alone. The superior long-term outcome with surgical procedures in attributed to the inherent permanence of the intervention which addresses the chronic nature of the disease. Although advantageous in the long run, the acute risk benefit ratio has reserved these invasive procedures for morbidly obese patients according to the NIH consensus conference on obesity surgery (BMI>40 kg/m.sup.2). (NIH Conference. 1991. Ann Intern Med. 115:956-961). Therefore, this is not an alternative for the majority of overweight patients unless and until they become profoundly obese and are suffering the attendant complications. No one knows all of the mechanisms involved in regulation of weight gain, although it is believed that many genetic as well as environmental factors, including diet and exercise, play major, interrelated roles. A number of publications have reported the discovery of genes that have been "knocked out" or overexpressed in transgenic mice, resulting in affected animals becoming incredibly obese, or vice versa. See, for example, Ezzell, "Fat Times for Obesity Research: Tons of New Information, but How Does It All Fit Together" J. NIH Res. 7, 39-43 (October 1995). Researchers have reported the cloning of at least two distinct genes, Ob which encodes a protein "leptin" believed to cause weight reduction in obese animals, and Db, which is believed to cause weight gain in animals. Other genes which have been reported include the fat, tub, agouti, and melanocortin 4 receptor genes. Recent reviews relating to the insights regarding the mechanisms involved in
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obesity help to understand these complex pathways. See, for example, Trish Gura, Science 275, 752-753 (Feb. 7, 1997) and Jeffrey S. Flier, Proc. Natl. Acad. Sci. USA 94, 4242-4245 (April 1997). Leptin, discovered in 1994 by Jeffrey Friedman's team at Rockefeller University, NY, is a 16 kD protein produced by the obesity (ob) gene of mice. Homozygotes with defective ob genes are unable to reproduce, stay warm, or grow normally, and become grossly overweight. The receptor for leptin has now been identified and cloned. Defects in the receptor also result in grossly obese animals. The receptor is expressed in the brain primarily in four regions, including the arcuate nucleus. In humans, however, the linkage between obesity and overexpression of leptin does not seem to be closely correlated, and no individuals have been identified that have a mutated Ob receptor or gene. Another molecule which appears to be important in weight control is the appetite-stimulating neurotransmitter referred to as neuropeptide Y or "NPY". NPY levels are elevated in animals with decreased levels of leptin. Genetic studies with knockout NPY and ob/ob animals indicate that NPY plays a role in, but is not a controlling factor, in obesity. Another line of research has implicated a role in obesity for the melanocortin receptor ("MCR"). Two MCRs, MCR3 and MCR4, are produced in the arcuate nucleus of the hypothalamus, a prime target of leptin action as well as of NPY production. Synthetic peptides mimicking melanocortins which bind to MCR-4 suppress feeding. Animals in which the gene encoding MCR-4 has been knocked out show the opposite behavior, exhibiting high weight gain and high NPY expression. Web site: http://www.delphion.com/details?pn=US06284729__ •
Methods for raising rabbits Inventor(s): Barclay; William R. (Boulder, CO), Mordenti; Archimede (Bologna, IT), Tassinari; Marco (Bologna, IT), Zotti; Alessandro (Lazzanochi Saurna, IT) Assignee(s): Martek Biosciences Boulder Corporation (Boulder, CO) Patent Number: 6,568,351 Date filed: July 19, 2002 Abstract: The present invention provides a method for raising rabbits, in particular by feeding the rabbit with a feed containing a source of long-chain fatty acid. In this manner, mortality and the feed conversion rates are decreased while average daily weight gain and long-chain fatty acid content of rabbit meat are increased compared to a rabbit raised in the absence of the long-chain fatty acid source. Excerpt(s): The present invention is related to a method for raising rabbits, in particular by feeding the rabbit with a feed containing a source of long-chain fatty acid. Rabbits are grown commercially as a source of meat in many areas of the world including Italy, Spain, France, and China. Typically, the total production period is about 80-85 days divided into 3 phases: (1) weaning period--day 1 to day 30; (2) adaptation period--day 31 to day 50; and (3) grower/finishing period--day 51 to day 85. During the adaptation period the rabbits may be fed antibiotics in the feed to help maintain their health and improve weight gain and in some regions growth promoters are also used. The use of antibiotics in animal production is falling out of favor due to the development of antibiotic-resistant bacteria, as well as the movement to more natural production techniques. These compounds are generally not used in the grower/finishing period and there is a continuing need to find ways to help improve both the health and nutritional content of the rabbits especially during the grower/finisher period of production. There is a need for a method for raising rabbits that decreases the mortality rate of the rabbits. There is also a need for a method for decreasing the feed conversion
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rate of rabbits. There is also a need for a method for increasing the average daily weight gain of rabbits. And there is a need for a method for increasing long-chain fatty acid (e.g., omega-3 fatty acid such as docosahexaenoic acid or DHA) content of rabbit meat. Web site: http://www.delphion.com/details?pn=US06568351__ •
Methods for treating obesity and weight gain using optically pure (-)-bupropion Inventor(s): Young; James W. (Palo Alto, CA) Assignee(s): Sepracor (Marlborough, MA) Patent Number: 6,110,973 Date filed: January 28, 1999 Abstract: Methods are disclosed utilizing the optically pure (-)-isomer of bupropion, which is a potent drug for treating obesity and weight gain. Excerpt(s): This invention relates to methods of treatment and pharmaceutical compositions employing the compound (-)-bupropion. Many organic compounds exist in optically active forms, i.e., they have the ability to rotate the plane of plane-polarized light. In describing an optically active compound, the prefixes D and L or R and S are used to denote the absolute configuration of the molecule about its chiral center(s). The prefixes (+) and (-) or d and l are employed to designate the sign of rotation of planepolarized light by the compound, with (-) or l meaning that the compound is levorotatory. A compound prefixed with (+) or d is dextrorotatory. For a given chemical structure, these compounds, called stereoisomers, are identical except that they are mirror images of one another. A specific stereoisomer may also be referred to as an enantiomer, and a mixture of such isomers is often called an enantiomeric or racemic mixture. Stereochemical purity is of importance in the field of pharmaceuticals, where 16 of the 20 most prescribed drugs exhibit chirality. A case in point is provided by the Lform of the.beta.-adrenergic blocking agent, propranolol, which is known to be 100 times more potent than the D-enantiomer. Web site: http://www.delphion.com/details?pn=US06110973__
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Methods of treating or preventing weight gain, obesity, and related disorders Inventor(s): Fang; Qun K. (35 Atwood St., Wellesley, MA 02181), Jerussi; Thomas P. (19 Garvey Rd., Framingham, MA 01701), Senanayake; Chrisantha H. (11 Old Farm Cir., Shrewsbury, MA 01545) Assignee(s): none reported Patent Number: 6,538,034 Date filed: December 4, 2001 Abstract: Methods are disclosed for the treatment and prevention of obesity, weight gain, and eating disorders. The methods comprise the administration of racemic or optically pure sibutramine metabolites and pharmaceutically acceptable salts, solvates, and clathrates thereof. Excerpt(s): The invention relates to methods of using, and compositions comprising, dopamine reuptake inhibitors and, in particular, racemic and optically pure metabolites of sibutramine. Sibutramine, chemically named [N-1-[1-(4-chlorophenyl)cyclobutyl]-3-
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methylbutyl]-N,N-dimethylamine, is a neuronal monoamine reuptake inhibitor which was originally disclosed in U.S. Pat. Nos. 4,746,680 and 4,806,570. Sibutramine inhibits the reuptake of norepinephrine and, to a lesser extent, serotonin and dopamine. See, e.g., Buckett et al., Prog. Neuro-psychopharm. & Biol. Psychiat., 12:575-584, 1988; King et al., J. Clin. Pharm., 26:607-611 (1989). Racemic sibutramine is sold as a hydrochloride monohydrate under the tradename MERIDIA.RTM., and is indicated for the treatment of obesity. Physician's Desk Reference.RTM. 1494-1498 (53.sup.rd ed., 1999). The treatment of obesity using racemic sibutramine is disclosed, for example, in U.S. Pat. No. 5,436,272. Web site: http://www.delphion.com/details?pn=US06538034__ •
Milk replacer composition and method Inventor(s): Claycamp; Robert M. (Seymour, IN), Hayes; Robin L. (Rensselaer, IN) Assignee(s): Rose Acre Farms, Inc. (Seymour, IN) Patent Number: 6,348,223 Date filed: June 29, 1999 Abstract: Improved milk replacer and dry feed compositions for young mammals are provided that employ a high quality inedible egg product to minimize or eliminate the need for milk source ingredients. These improved compositions include one or more high quality inedible egg products in an amount from about 1% to 100% of the total weight of the composition. The balance of these improved compositions may consist of any ingredient(s) in any combination when such composition is capable of meeting or exceeding the nutritional requirements of the species to be fed. One aspect of the present invention provides a method for producing a high quality inedible egg product. This invention also provides an improved diet program wherein a young mammal is initially fed a milk replacer according to the present invention, and then when it is time to wean the animal of the milk replacer, a dry feed according to the present invention is introduced. This improved diet program allows a caretaker to wean the young mammal quickly with no deleterious effects in terms of the health or growth of the mammal. Animals fed these improved compositions benefit from a significant reduction in the incidence of disease and a significant increase in the rate of weight gain compared to young mammals fed prior art milk replacer formulations. Excerpt(s): This invention relates generally to synthesized foodstuffs for young mammals and more particularly to milk replacer and dry feed compositions containing high quality inedible egg products as the main ingredient and to the method of producing such milk replacer and dry feed compositions. It is well known that in the early stages of life for a mammal, mother's milk is the ideal source of nutrition. Unfortunately for many young mammals, whether by tragedy or by economic necessity, as in the case of animals whose milk is commercially valuable, mother's milk is not always available. In these instances, the use of a milk replacing composition is required. There exist many formulations for foodstuffs for neo-natal animals that incorporate dried milk products and vitamin and mineral supplements. The common feature of these prior art compositions is that they derive most of their protein content from a milk source ingredient such as skim milk, buttermilk, whole whey, delactosed whey, casein, milk albumin, and/or whey protein concentrate. Milk source ingredients are used extensively in traditional milk replacers because the existing health data relating to young mammals fed milk replacer diets based on non-milk source ingredients is poor. That is, animals fed with prior art milk replacers having protein sources other than milk
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proteins are known to suffer from protein deficiencies that can potentially result in debilitating illnesses. This data suggests that only milk-based milk replacers can be used to obtain a healthy young animal. Web site: http://www.delphion.com/details?pn=US06348223__ •
Nutrient formulation and process for enhancing the health, livability, cumulative weight gain or feed efficiency in poultry and other animals Inventor(s): Dibner; Julia J. (Chesterfield, MO), Ivey; Francis J. (Creve Coeur, MO), Knight; Christopher D. (St. Louis, MO) Assignee(s): Novus International, Inc. (St. Louis, MO) Patent Number: 5,976,580 Date filed: December 6, 1996 Abstract: A nutrient formulation including moisture, a coloring agent, a palatability modifier, and/or an adjuvant which is designed for use in poultry and other animals, and a method of feeding it which improves subsequent livability, cumulative feed efficiency, weight gain, and resistance to disease challenge or other stresses is disclosed. Excerpt(s): The present invention is directed to a high moisture material for providing nutrients, drugs, vitamins, minerals, bile salts, surfactants, probiotics, enzymes, peptides, hormones, prostaglandins, antioxidants, living cells, and immunoactive agents to poultry and other animals, and more particularly, a high moisture material and process which may be used to improve the health and enhance the livability, cumulative weight gain and feed conversion efficiency of poultry and other animals. For economic reasons, the management of chick hatching in commercial facilities places high importance on percent chicks hatched of eggs set. To achieve hatch rates of 90%, earlyhatching birds are often left in the hatch incubator for a period of time to allow the laterhatching chicks to emerge and dry. By the time the chicks are removed from the incubator tray, therefore, they will range in age from several hours up to about 2 days in age (as measured from hatching for each bird). This period is referred to as the posthatch holding period. After the chicks are removed from the incubator trays in a commercial hatchery, they are processed (inoculated and sexed) and then placed in boxes commonly referred to as chick boxes for shipping to the production farm. The processing period typically requires several hours and the chicks may reside in the chick boxes for several more hours before transit to the production farm actually begins. Web site: http://www.delphion.com/details?pn=US05976580__
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Peptide, a method for its preparation and a pharmaceutical composition containing the peptide Inventor(s): Deigin; Vladislav I. (North York, CA), Yarova; Yelena (Toronto, CA) Assignee(s): Immunotech Developments Inc. (Toronto, CA) Patent Number: 6,184,208 Date filed: July 22, 1996 Abstract: A peptide of the formula IX-Tyr-Y-Phe-Z-A Iwherein X is hydrogen, arginine, D-arginine, ornithine, D-ornithine, lysine, D-lysine, homoarginine, D-homoarginine, citrulline, D-citrulline; Tyr is tyrosine; Y is D-alanine, D-valine, D-leucine, D-isoleucine,
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D-phenylalanine, D-asparagine, D-tryptophan, D-proline, D-serine, D-threonine, Dtyrosine, D-hydroxyproline, D-cysteine, D-cysteyl-cysteine, D-methionine, D-lysine, Dhomoarginine, D-arginine, D-histidine, D-aspartic acid, D-glutamic acid, D-.beta.alanine, or D-ornithine; Phe is phenylalanine; Z is alanine, D-alanine, valine, D-valine, leucine, D-leucine, isoleucine, D-isoleucine, phenylalanine, D-phenylalanine, asparagine, D-asparagine, glycine, glutamine, D-glutamine, tryptophan, D-tryptophan, proline, D-proline, serine, D-serine, threonine, D-threonine, tyrosine, D-tyrosine, hydroxyproline, D-hydroxyproline, cysteine, D-cysteine, cysteyl-cysteine, cysteine-Dcysteine, D-cysteyl-cysteine, D-cysteine-D-cysteine, methionine, D-methionine, lysine, D-lysine, arginine, D-arginine, histidine, D-histidine, aspartic acid, D-aspartic acid, glutamic acid, D-glutamic acid,.beta.-alanine, D-.beta.-alanine, ornithine, or D-ornithine; and A is hydroxyl or substituted amide (C.sub.1 -C.sub.3); compositions containing same and its use in modulating physiological processes such as weight gain, activities of the epithelium growth zone, hair growth, wound healing, and to stimulate reparative and anabolic processes, and exert analgesic effects. Excerpt(s): The invention relates to a biologically active peptide; a novel pharmaceutical composition containing the peptide; a method for preparing the peptide; and, uses of the peptide. Hormones are known to control the metabolic processes both in growing and mature organisms. Peptides often act as hormones. They are not only hormonally active themselves but regulate the action of other hormones, which control the vital activity of the organism. However, the potential of such natural compounds is limited. Therefore, many scientific laboratories have tried to develop methods for preparing synthetic derivatives of natural peptides, which are more active than their natural analogues (EP 0136720, 1984; EP 0137904, 1984). Moreover, new peptides have been synthesized, which are absent in the organism but have unique properties. Among them there is a special group of physiologically active peptides directly or indirectly controlling the action of hormones such as the growth hormone. Some of these active peptides increase the growth hormone level in blood (PCT 89/07111, 1989; PCT 91/16923, 1991) while others suppress the hormone (FR 2235701, 1978; FR 2532308, 1982). A peptide which activates the growth of the epidermal layer in man (PCT 90/13570, 1990), and a metal-containing peptide, which has a significant stimulating effect on hair growth in warm-blooded animals (PCT 91/07431, 1991) have been synthesized. Another peptide analogue has been reported to facilitate hair removal in animals (FR 2487677, 1982). Web site: http://www.delphion.com/details?pn=US06184208__ •
Pig appeasing pheromones for enhancing weight gain in a mammal Inventor(s): Pageat; Patrick (Apt, FR) Assignee(s): Fideline (Saint Saturnin d'Apt, FR) Patent Number: 6,054,481 Date filed: July 16, 1999 Abstract: A composition comprising a mixture of fatty acids such as oleic, palmitic and linoleic acids and derivatives thereof which are used for enhancing weight gain in a mammal. Methods to enhance weight gain using the fatty acid compositions are also described. Excerpt(s): The present invention relates to a composition comprising a mixture of fatty acids or derivatives thereof derived from secretions of mammalian mammary glands.
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This composition can be utilized to decrease stress, anxiety and aggressiveness in mammals. Stress, by definition, is the reaction of an animal body to forces of deleterious nature, infections and various abnormal states that tend to disturb homeostasis. Animals exposed to stress respond with changes in the activity of the autonomic and neuroendocrine systems and in behavior. The activation of these biological systems is a prerequisite for the animal to cope with stress and thus is the principal resource that will provide the adequate biological defense against a threat that challenges the homeostasis of the animal. Moberg, G. P. Animal Stress, pp. 27-49 (1985); Vogel, W. H. Neuropsychobiology, 13 pp. 1290135 (1985). Web site: http://www.delphion.com/details?pn=US06054481__ •
Protein tyrosine phosphate-1B (PTP-1B) deficient mice and uses thereof Inventor(s): Elchebly; Mounib (Montreal, CA), Gresser; Michael (Les Cedres, CA), Kennedy; Brian (Kirkland, CA), Payette; Paul (St. Laurent, CA), Ramachandran; Chidambaram (Pierrefonds, CA), Tremblay; Michel (Dorval, CA) Assignee(s): McGill University (Quebec, CA), Merck & Co., Inc. (Rahway, NJ) Patent Number: 6,605,753 Date filed: January 23, 2001 Abstract: The present invention provides mice that have had their PTP-1B genes disrupted by targeted homologous recombination. The mice have no detectable PTP-1B protein, yet appear to be physiologically normal. However, in the fed state on a normal diet, the mice have half the level of circulating insulin as their wild-type littermates. In glucose and insulin tolerance tests, the mice show an increased insulin sensitivity. When fed a high fat, high carbohydrate diet, the mice show a resistance to weight gain as compared to their wild-type littermates. Methods making the mice and cell lines derived from the mice are also provided. The present invention also provides methods of identifying inhibitors of the enzymatic activity of PTP-1B as well as inhibitors identified by such methods. Excerpt(s): The invention is directed to the field of transgenic mice containing a disrupted PTP-1B gene. The mice may contain a disruption in either one or both copies of the PTP-1B gene. In the case of mice containing a disruption in both copies of the PTP-1B gene, such mice lack detectable expression of PTP-1B protein. Protein tyrosine phosphatases (PTPases) are a large family of transmembrane or intracellular enzymes that dephosphorylate substrates involved in a variety of regulatory processes (Fischer et al., 1991, Science 253:401-406). Protein tyrosine phosphatase-1B (PTP-1B) is a.about.50 kd intracellular protein present in abundant amounts in various human tissues (Charbonneau et al., 1989, Proc. Natl. Acad. Sci. USA 86:5252-5256; Goldstein, 1993, Receptor 3:1-15). Like other PTPases, PTP-1B has a catalytic domain characterized by the sequence motif (I/V)HCXAGXXR(S/T)G (SEQ.ID.NO.:1), containing arginine and cysteine residues that are critical to the enzyme's activity (Streuli et al., 1990, EMBO J. 9:2399-2407; Guan et al., 1990, Proc. Natl. Acad. Sci. USA 87:1501-1505; Guan & Dixon, 1991, J. Biol. Chem. 266:17026-17030). The amino terminal 35 amino acid residues of PTP-1B localize the protein to the endoplasmic reticulum (Frangioni et al., 1992, Cell 68:545-560). Determining which proteins are substrates of PTP-1B has been of considerable interest. One substrate which has aroused special interest is the insulin receptor. The binding of insulin to the insulin receptor results in autophosphorylation of the receptor, most notably on tyrosines 1146, 1150, and 1151 in the kinase catalytic domain (White & Kahn, 1994, J. Biol. Chem. 269:1-4). This causes activation of the
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insulin receptor tyrosine kinase, which phosphorylates the various insulin receptor substrate (IRS) proteins that propagate the insulin signaling event further downstream to mediate insulin's various biological effects. Web site: http://www.delphion.com/details?pn=US06605753__ •
Sarcospan-deficient mouse as a model for clinical disorders associated with sarcospan mutations Inventor(s): Campbell; Kevin P. (Iowa City, IA), Crosbie; Rachelle (Iowa City, IA), Lebakken; Connie (Iowa City, IA), Williamson; Roger (Iowa City, IA) Assignee(s): University of Iowa Research Foundation (Iowa City, IA) Patent Number: 6,207,878 Date filed: October 21, 1999 Abstract: Disclosed is a transgenic knockout mouse whose genome has a homozygous disruption in its endogenous sarcospan gene, wherein the disruption prevents the synthesis of functional sarcospan in cells of the mouse. The mouse is characterized as exhibiting from 1.4 to 6.8 fold larger epididymal fat pad deposits as compared to the epididymal fat pad deposits of a wild type mouse. Methods for production of the mouse are presented. Also disclosed are cells derived from the transgenic knockout mouse. The mouse can be used in a method for identifying therapeutic agents for the treatment of an individual diagnosed with a metabolic disorder associated with a reduction or loss of expression of wild-type sarcospan. An example of such a disorder is weight gain in the individual associated with a reduction or loss of expression of wild-type sarcospan. These specific methods are also provided. Excerpt(s): The dystrophin-glycoprotein complex (DGC) is a multi-subunit protein complex expressed at the sarcolemma of skeletal, cardiac, and smooth muscle fibers (reviewed in Campbell, Cell 80: 675-679 (1995), and Straub and Campbell, Curr. Opin. Neurol. 10: 169-175 (1997)). The DGC is currently known to be composed of at least nine proteins including dystrophin, the syntrophins,.alpha.- and.beta.-dystroglycan,.alpha.,.beta.-,.gamma.-, and.delta.-sarcoglycans and sarcospan. One of the functions of the DGC is likely to provide a structural link between the extracellular matrix and the actin cytoskeleton through interactions of dystrophin with filamentous actin, and.alpha.dystroglycan with the extracellular matrix component laminin, thereby maintaining the stability of the sarcolemma under contractile forces (Ervasti and Campbell, J. Cell Biol. 122(4): 809-823 (1993); and Campbell, Cell 80: 675-679 (1995). Recent evidence suggests that the DGC may play other roles in normal muscle physiology through interactions with cell signaling molecules or other proteins at the sarcolemma. Sarcospan is the most recently cloned component of the DGC (Crosbie et al., J. Biol. Chem. 272: 31221-31224 (1997). Hydropathy plots predict that the protein has four transmembrane domains with an extracellular loop extending between transmembrane domains 3 and 4 (Scott et al., Genomics 20: 227-230 (1994); Crosbie et al., J. Biol. Chem. 272: 31221-31224 (1997). Dendogram analysis designates sarcospan as a member of the tetraspan superfamily, also known as the transmembrane-4 superfamily or the tetraspanins (Heighway et al., Genomics 35: 227-230 (1996); Wright and Tomlinson, Immunol. Today 15: 588-594 (1994). Tetraspan proteins are thought to function as molecular facilitators, mediating interaction between proteins at the plasma membrane. The tetraspans have also been implicated in cell adhesion, migration, and proliferation (Wright et al., Immunol. Today 15: 588-594 (1994); Maecher et al., FASEB 11: 428-442 (1997). Sarcospan is tightly associated with the sarcoglycans to form a subcomplex of the DGC (Crosbie et al., J. Cell
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Biol. 145: 153-165 (1999). The function of the sarcoglycan-sarcospan complex is currently unknown. One hypothesis is that it stabilizes.alpha.-dystroglycan at the membrane. Another hypothesis is that the sarcoglycan-sarcospan complex may be important in the signaling functions of the DGC, a possibility which remains relatively unexplored. Defects in components of the DGC have been implicated in muscle disorders manifested by muscle weakness and wasting. Currently, it is known that six forms of muscular dystrophies are caused by primary genetic defects within components of the DGC. These include Duchenne and Becker muscular dystrophies, the most prevalent forms of muscular dystrophies that are caused by mutations in the dystrophin gene and four forms of autosomal recessive limb-girdle muscular dystrophies (LGMD2-C, -D, -E and F) caused by primary mutations in each of the four sarcoglycan genes (Straub and Campbell, Curr. Opin. Neurol. 10: 169-175 (1997). Additionally, mutations in the laminin-.alpha.2 chain cause a severe form of congenital muscular dystrophy. Recent data suggests that dystroglycan is important in basement membrane formation (Henry and Campbell, Cell 95: 859-870 (1998) and dystroglycan-null mice die at a very early embryonic stage (Williamson et al., Hum. Mol. Genet. 6: 831-841 (1997). It is likely that human-null mutations in the dystroglycans would also lead to an early embryonic lethality. In contrast, disruption of the.alpha.1-syntrophin gene in mice was not lethal, and also did not result in muscle degeneration (Kameya et al., J. Biol. Chem. 274: 21932200 (1999). However, neuronal nitric oxide synthase, which is usually localized at the sarcolemma through.alpha.1-syntrophin, was not found at the sarcolemma in these animals (Kameya et al., J. Biol. Chem. 274: 2193-2200 (1999). Web site: http://www.delphion.com/details?pn=US06207878__ •
Seaweed supplement diet for enhancing immune response in mammals and poultry Inventor(s): Allen; Vivien Gore (Lubbock, TX), Fontenot; Joseph P. (Blacksburg, VA), Pond; Kevin R. (Wolfforth, TX), Saker; Korinn E. (Blacksburg, VA) Assignee(s): Texas Tech University (Lubbock, TX), Virginia Tech Intellectual Properties, Inc. (Blacksburg, VA) Patent Number: 6,342,242 Date filed: February 27, 1998 Abstract: Seaweed harvested from the ocean when ground as an intact meal or exposed to alkaline hydrolsis extraction procedure resulting in a water soluble form provides a feed ingredient with mineral composition and plant growth regulating activity when included as a pasture treatment or feed ingredient for mammals and poultry, resulting in enhanced immune function, enhanced health, weight gain, and meat grade quality. Steers grazing seaweed extract treated forage continued to exhibit enhanced immune function after entering feedlot phase finishin with no seaweed extract diet supplement. Excerpt(s): The invention relates to seaweed and treated seaweed feed supplements for mammals and poultry wherein the host exhibits enhanced immune response. In another aspect, the invention relates to the introduction of seaweed supplement directly to mammal and poultry feed as well as introduction of grazing animals to plants and grasses, which have been pre-treated with seaweed extract. In still another aspect, the invention relates to seaweed feed supplement, which enhances the host immune system for periods beyond cessation of seaweed supplement introduction to the host diet. Seaweeds have been used through antiquity in crop production and as early as the 1950's, evidence of plant growth hormones in seaweed was reported. Seaweed is now recognized as a source of plant growth regulators and has been demonstrated to have
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activity that includes cytokinin, auxin, gibberellin, and idole acidic acid. Seaweed has also long served as feed for domestic and wild animals. Some even graze on seaweed growing on rocky beaches and floating in the ocean water. Seaweeds have been dried and sold as a meal product to be mixed with other feed stuffs. The value of seaweed has been generally attributed to the fact that it is low in carbohydrate and proteins and rich in trace elements; including B,D,E and other vitamin precursors including beta-carotene; and various growth hormones. Previous seaweed products are not always uniformly effective because of various contents of the trace elements and vitamins in other compounds due to the time and location of harvest and the method of processing. Therefore, seaweed products have not always provided significant reliable benefit to the host being fed the product. Bacterial, fungal, viral and other disease causing agents inflict mammals including man, other mammals, plants, insects and poultry. The prevention and control of, for example, diseases have important health and economic implications. Diseases contribute to infections in humans and other mammals including common colds, herpes and cancer and the importance of their control is obvious. Also important is control of agent diseases in mammals and poultry for economic reasons as well as the ability of such mammals and poultry to become disease reservoirs or carriers, which facilitates the spreading of diseases to other host including humans. Plant diseases have been known to have a disruptive effect on the cultivation of fruit trees, tobacco and various vegetables as well as the utilization of plant leaves and grasses by grazing animals. Web site: http://www.delphion.com/details?pn=US06342242__ •
Small molecules that increase the conversion of food to body weight gain Inventor(s): Taub; Floyd E. (Silver Spring, MD) Assignee(s): Dovetail Technologies, Inc. (College Park, MD) Patent Number: 6,166,086 Date filed: February 24, 1999 Abstract: The present invention relates to peptide-like compounds, eg aminocarboxylic acid amide derivatives, and to methods of using same in the field of general health care, for example, to improve resistance to stress, improve production of desired characteristics or useful products in animals, to increase weight gain, and to decrease feed efficiency. The invention has applications in the field of animal husbandry. It also relates to administering beta-alethine to improve feed efficiency in an animal, comprising administering to animal an amount of.beta.-alethine sufficient to reduce the amount of food required to increase a unit of weight in the animal. Excerpt(s): In the area of animal husbandry, antimicrobials, including antibacterials, are used routinely for prophylaxis, chemotherapy and growth promotion. Animals receiving antibiotics in their feed, gain four to five percent more body weight than animals that do not receive antibiotics. They are important for sustainable livestock production ad for the control of animal infections that could be passed on to humans. However, microbiological and clinical evidence is mounting that resistant bacteria or resistance determinants might be passed from animals to humans, resulting in human infections that are more difficult to treat. With a marked increase in the prevalence and distribution of antimicrobial-resistant infections in hospitals and the community the question has been raised as to how this escalation of resistance could have been influenced by the use of antimicrobials in livestock production. Antimicrobials are used extensively in livestock, fish and plant production. Most are administered to livestock
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animals in subtherapeutic doses as growth promoters which boost the utilization of the genetic potential for growth of pigs and poultry, improve feed conversion and reduce waste production output from intensive livestock production. They are also used prophylactically to prevent diseases, for example, after commingling of animals from different farms, or among animals raised in crowded conditions with thousands of animals living under confinement on a single premises. Web site: http://www.delphion.com/details?pn=US06166086__ •
Smoking cessation treatments using naltrexone and related compounds Inventor(s): Krishnan-Sarin; Suchitra (Durham, CT), Meandzija; Boris (Hamden, CT), O'Connor; Patrick G. (Woodbridge, CT), O'Malley; Stephanie (New Haven, CT) Assignee(s): Yale University (New Haven, CT) Patent Number: 6,004,970 Date filed: November 12, 1997 Abstract: Nicotine dependency is treated by administration of an opioid antagonist. In some embodiments, rapid or ultra rapid detoxification techniques include using a combination of an effective amount of an opioid antagonist such as nalmefene, naloxone or naltrexone or a mixture of any one of these, and either clonidine or related compounds either while awake, or while under sedation or anesthesia, followed by continued administration of an effective amount of an opioid antagonist with or without agents that enhance nicotine dependency treatment. Persons are also treated for nicotine dependency with more gradual detoxification methods using administration of a combination of an effective amount of an opioid antagonist such as nalmefene, naloxone, naltrexone, or a mixture of any of these, and an effective amount of agents used to treat nicotine withdrawal including nicotine, such as that delivered by a nicotine patch, nicotine chewing gum, nicotine inhaler or other methods for delivering nicotine, antidepressants and antianxiety agents, and/or clonidine and related compounds. Administration of an effective amount of an opioid antagonist to prevent relapse, attenuate craving, and reduce weight gain during and after treatment for nicotine dependency is continued in some embodiments. Excerpt(s): This invention relates to the use of opioid antagonists such as naltrexone, naloxone or nalmephene alone or with either nicotine replacement therapy or with other withdrawal attenuating agents, to increase smoking abstinence rates, to decrease craving for cigarettes, reduce relapse to heavy smoking during detoxification or once smoking abstinence has been achieved, and to reduce weight gain associated with smoking cessation. Tobacco dependence continues to be a major health hazard for millions of Americans, and because smoking may pose a health risk for non-smokers as well, smoking cessation treatments are of great public interest. Dependence is an adaptive biological state induced by chronic drug exposure which manifests itself in various behavioral and physiological responses when drug exposure ceases. Withdrawal from nicotine following chronic use of tobacco products results in the emergence of an abstinence syndrome which reaches its peak intensity within the first day. Cessation of smoking has been shown to result in a number of signs and symptoms of withdrawal such as increases in irritability, anxiety, restlessness, impatience, somatic complaints, cigarette craving, hunger, insomnia, tremulousness and heart rate as well as difficulty concentrating, all of which are collectively called the tobacco withdrawal syndrome.
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Web site: http://www.delphion.com/details?pn=US06004970__ •
Therapeutic uses for an aminosterol compound Inventor(s): Zasloff; Michael (Merion Station, PA) Assignee(s): Magainin Pharmaceuticals, Inc. (Plymouth, PA) Patent Number: 6,143,738 Date filed: May 16, 1997 Abstract: A pharmaceutical composition includes, as an active ingredient, a compound according to formula 1436 as shown in FIG. 1, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier or excipient. Various pharmaceutical products may be produced including this pharmaceutical composition. Such pharmaceutical products may be used for the treatment of cancers, such as leukemia; inflammation; arthritis; and viruses, such as HSV. Methods for using the pharmaceutical compositions also are described. In these methods, various diseases are treated or other body functions are activated or inhibited by administering an effective amount of the pharmaceutical composition. For example, inflammation, arthritis, herpes simplex virus, melanoma, and leukemia may be treated by administering an effective amount of the pharmaceutical compositions. Viral replication, weight gain, and growth factor production can be inhibited by administering an effective amount of these pharmaceutical compositions. Appetite can be suppressed by administering an effective amount of the pharmaceutical compositions, and a diuretic effect can be produced. Excerpt(s): Several aminosterol compositions have been isolated from the liver and stomach of the dogfish shark, Squalus acanthias. One important aminosterol, squalamine, is the subject of U.S. Pat. No. 5,192,756 to Zasloff, et al., which patent is entirely incorporated herein by reference. That patent describes the antibiotic properties of squalamine. Since the discovery of squalamine, several interesting properties of this compound have been discovered. For example, as described in U.S. patent appl. Ser. No. 08/416,883 (filed Apr. 20, 1995) and U.S. patent application Ser. No. 08/478,763 (filed Jun. 7, 1995), squalamine may function as an antiangiogenic agent. These patent applications are entirely incorporated herein by reference. Additional uses of squalamine (e.g., as an NHE3 inhibiting agent and as an agent for inhibiting the growth of endothelial cells) are disclosed in U.S. patent appl. Ser. No. 08/474,799 (filed Jun. 7, 1995) and U.S. patent appl. Ser. No. 08/840,706 (filed Apr. 25, 1997, entitled "Treatment of Carcinomas Using Squalamine in Combination with Other Anti-cancer Agents," in the names of Michael Zasloff and Jon Williams). These applications also are entirely incorporated herein by reference. Methods for synthesizing squalamine have been devised, such as the methods described in WO 94/19366 (published Sep. 1, 1994) and in U.S. patent appl. Ser. No. 60/032,378. This PCT publication and the U.S. patent application are entirely incorporated herein by reference. The PCT application relates to U.S. patent appl. Ser. No. 08/023,347, which application also is entirely incorporated herein by reference. Additionally, U.S. patent appl. Ser. No. 08/474,799 also discloses squalamine isolation and synthesis techniques. Compound 1436 previously has been described in U.S. patent appl. Ser. Nos. 08/483,057; 08/479,457; and 08/487,443, each filed Jun. 7, 1995. Each of these U.S. patent applications is entirely incorporated herein by reference. These U.S. patent applications describe the structure of compound 1436 and other aminosterols, as well as processes for synthesizing and isolating compound 1436 and other aminosterols. For example, compound 1436 may be prepared from a squalamine starting material. Additional methods for synthesizing compound 1436 (as
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well as squalamine) are described in U.S. Provisional patent appl. Ser. No. 60/032,378, filed Dec. 6, 1996, which application is entirely incorporated herein by reference. Web site: http://www.delphion.com/details?pn=US06143738__ •
Transgenic mouse model for fatty acid transport Inventor(s): Abumrad; Nada (Cold Spring Harbor, NY), Ibrahimi; Azeddine (Setauket, NY), Picken; Christopher M. (Sayville, NY) Assignee(s): The Research Foundation of the State University of New York (Stony Brook, NY) Patent Number: 6,316,693 Date filed: September 28, 1998 Abstract: The present invention is directed toward a transgenic mouse comprised of germ cells and somatic cells which contain a recombinant CD36 gene operatively linked to a muscle creatine kinase promoter. Overexpression of the reconbinant CD36 gene in muscle tissue promotes localized (tissue-specific) and systemic changes in fatty acid metabolism, overall body fat and weight gain in the animal. Excerpt(s): This invention relates to transgenic animals which overexpress a fatty acid transporter molecule in tissues active in fatty acid utilization. Long-chain fatty acids (FA) have multiple properties and functions. FA are important substrates for phospholipids, which are essential membrane components. FA are also substrates for prostaglandins, which have a variety of regulatory effects. For most cells FA constitute a main source of energy. FA also directly regulate a variety of biological processes. For example, FA modulate ion channel activation, enzyme function and synaptic transmission. More recently FA have been shown to have regulatory effects on the expression of various genes, especially those encoding proteins active in lipid metabolism. In view of the diverse functionality of FA, researchers believe that FA play a central role in the pathophysiology of multiple conditions, such as diabetes and obesity, for example. FA also contribute to insulin insensitivity and to the prevalence of vascular and coronary diseases. High levels of circulating blood FA are also associated with diabetes, many forms of obesity and hyperlipidemias. High levels of blood FA are believed to contribute to an increased production of low-density lipoproteins by the liver. Cholesterol from lipoproteins is esterified with free FA by macrophages in the vascular wall yielding cholesteryl ester which accumulates and leads to the formation of lipid-filled macrophages, precursors of atherosclerotic lesions. Web site: http://www.delphion.com/details?pn=US06316693__
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Treatment and system for nicotine withdrawal Inventor(s): Reynolds; Mark (4 Sidehill Rd., Westport, CT 06880) Assignee(s): none reported Patent Number: 6,409,991 Date filed: December 15, 1999 Abstract: A kit and associated method in which symptoms of nicotine withdrawal syndrome are relieved as well as addressing the associated weight gain issues and
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craving for sweets by combining nicotine replacement therapy with complementary dosages of xylitol. Excerpt(s): The present invention relates to a method for relieving nicotine addiction and in particular to a kit and associated method in which symptoms of nicotine withdrawal syndrome are relieved while addressing the associated oral cravings for sweets. Cigarette smoking continues to be the major preventable cause of death in the United States resulting in nearly 400,000 deaths per year due to cancer and cardiovascular disease. Despite the potential adverse health effects, the vast majority of cigarette smokers are unable to cease smoking. The lack of smoking cessation success is thought to be related to the tobacco withdrawal syndrome or tobacco abstinence syndrome that most smokers experience during their attempts to quit. As many as one third of heavy smokers who are now 35 years old will die before age 85 of diseases caused by their smoking. The estimated cost of health problems associated with smoking, including medical care, absenteeism, decreased work productivity, and accidents is estimated to be $56 billion per year. Web site: http://www.delphion.com/details?pn=US06409991__ •
Treatment of stressed animals with dihydroxyquinoline compounds Inventor(s): Owens; Fredric Newell (Stillwater, OK), Samuels; Winston A. (Chesterfield, MO) Assignee(s): Solutia Inc. (St. Louis, MO) Patent Number: 6,017,564 Date filed: August 21, 1998 Abstract: The collective health, feed efficiency, weight gain and fecal odors of stressed ruminant mammals can be improved by feeding them a diet of feed comprising a substituted 1,2-dihydroquinoline compound. Excerpt(s): The present invention relates to treatment of animals with dihydroxyquinoline compounds, and more particularly to such treatment by application of such compounds to the feed of the animal. Due to the stress of shipment, receiving cattle tend to shrink during the shipment and perhaps 85% are sick when they arrive at the feedlot, or become sick, particularly with respiratory disease, soon after arrival. The receiving cattle tend to drink large quantities of water, but often tend not to get up and eat. Many require medication such as vaccines. Some even fail to recover from the sickness induced by the shipping stress, which sometimes results in death of calves. Thus, shipping produces undesirable stress and morbidity in the calves and contributes to higher medical costs and other costs associated with delays in return to health, loss of useable cattle due to disease and death, and reduced rate of weight gain and feed efficiency in the feed yard (i.e., weight gain per pound of feed). Accordingly, a treatment or other technique for accelerating restoration to health, increasing rate of weight gain, and reducing morbidity of the receiving cattle, and for reducing medical costs and improving feed efficiency would be highly desirable. In sum, the morbid cattle tend to require greater medical expense, to grow slower throughout the feedlot phase, are less efficient in converting feed to weight gain, and their carcasses tend to be graded lower after slaughter. Other ruminant mammals, such as sheep, suffer similarly from stress. In addition, many meat products derived from ruminant mammals (such as, cattle and sheep), swine and fish have very limited shelf lives. After a relatively short period of time, the meat may turn color and become rancid (that is, develop an
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unacceptable smell or flavor or both). In short, it spoils. Shelf life for beef is typically measured as the length of time for the meat, in plastic trays, overwrapped with an oxygen-permeable polyvinyl chloride film, and displayed under fluorescent lighting (150 foot candles) at 4.degree. C., to discolor; to turn brown or grey. This definition will be used herein to apply to other meat products as well. Web site: http://www.delphion.com/details?pn=US06017564__ •
Use for drug acarbose precose for weight control prevention of weight gain for weight loss for treatment and prevention of obesity Inventor(s): Rosner; Harvey (530F Grand St. Apt. 3F, New York, NY 10002) Assignee(s): none reported Patent Number: 6,387,361 Date filed: August 2, 1999 Abstract: Control of weight gain has long been a problem for many people who if they lose weight by dieting often gain it back in a short period of time. Therefore, there has been much research to find a simple means to control weight in humans.Acarbose, an oligosaccharide, is an oral alpha glucosidase inhibitor. The mechanism of action of acarbose results from a competitive inhibition of pancreatic amylase and membrane bound intestinal aplpha-glucoside hydrolase enzymes. Pancreatic alpha amylase hydrolizes complex starches in the lumen of the small intestine. The membrane bound intestinal alpha glucosidases hydrolyze oligo saccharides, trissaccharides and disaccharides to glucose and other monosaccharides in the brush boarder of the small intestines. It has no inhibitory effect against lactase and would therefore not be expected to induce the symptoms of lactose intolerance. The weight gain or loss for an individual is essentially the difference between the calories absorbed and the calories burned. Excerpt(s): It is an object of the invention to control weight in humans by ingesting acarbose with meals with food containing carbohydrates. This and other objects and advantages will become obvious from the following detailed description. The invention is directed to a method of controlling weight in human beings by ingesting acarbose at meals with food containing carbohydrates. Acarbose is known to be an oral.varies.glucosidase inhibitor, which acts by a reversible inhibitor of membrane-bound intestinal.varies.-glucoside hydraslase enzymes. Membrane intestinal.varies.glucosidases hydrolize oligosaccharides and disaccharides to glucose and other monosaccharides in the brush border of the small intestine. Web site: http://www.delphion.com/details?pn=US06387361__
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Use of metformin to counteract weight gain associated with valproate and other psychotropic medications Inventor(s): Cottingham; Elizabeth Marie (300 Warren Ave., Cincinnati, OH 45219), Morrison; John Ainslie (3740 Clifton Ave., Cincinnati, OH 45220) Assignee(s): none reported Patent Number: 6,194,466 Date filed: October 12, 1999
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Abstract: A method for minimizing the weight gain side effect associated with Valproate treatment is disclosed. In this method, Metformin, a biguanide compound, is concurrently administered to a patient taking the Valproate therapy. A pharmaceutical composition containing the combination of Valproate and Metformin is also disclosed. Excerpt(s): The present invention relates to improvements in the treatment of patients for seizure, bipolar disorders and psychoses. Clinical experience and published studies indicate the effectiveness of Valproate (depakote) in the treatment of seizure disorders and bipolar disorders. See, for example, Mattson, et al., Department of Veterans Affairs Epilepsy Cooperative Study No. 264: A Comparison of Valproate with Carbazapine for the Treatment of Complex Partial Seizures and Secondarily Generalized Tonic-Chronic Seizures In Adults. N. Eng. J. Med., 327: 765-771 (1992); Freeman, et al., Mood Stabilizer Combinations: A Review of Safety and Efficacy. Am. J. Psychiatry, 155: 12-21 (1998); and Verity, et al., A Multi-Center Comparative Trial Of Sodium Valproate And Carbamazepine In Pediatric Epilepsy. Developmental Medicine And Child Neurology, 37: 97-108 (1993). Use of Valproate, however, is also associated with side effects in as many as 50% of the patients taking it; these side effects include marked weight gain. Isojarvi et al., Polycystic Ovaries And Hyperandrogenism In Women Taking Valproate For Epilepsy, N. Eng. J. Med., 329: 1383-1388 (1993). Although not all patients experience this weight gain side effect, in those that do, the weight gain can be considerable, as much as 40-50 pounds. This side effect presents a number of patient issues, both medical and psychological, for the treating physician to consider. Such a marked weight gain can place a significant burden on the heart and circulatory system of the patient. In addition, particularly in-patients suffering from depression, such weight gain can hurt self-image and adversely impact the depressed state. Finally, and perhaps most importantly, such side effects can reduce patient compliance with the therapy regimen, thereby resulting in ineffective treatment for the primary disorder. Identification of a means to counteract these side effects partially or completely is, therefore, important. There is at present no way to prevent or treat obesity associated with the use of Valproate, except through behavioral changes such as increased physical activity or decreased caloric intake. Metformin is a biguanide drug which is known to improve insulin action at the cellular level, but not affect insulin secretion. Metformin is used to treat patients with non-insulin dependent diabetes and has recently been used to treat women with polycystic ovary syndrome, a syndrome characterized by hirsutism, hyperandrogenism, and polycystic ovaries. It has not, however, been suggested for use in controlling the weight gain caused by Valproate or other psychotropic actives. See, for example, Valazquez, et al, Metformin Therapy Is Associated With A Decrease In Plasma Plasminogen Activator Inhibitor-1, Lipoprotein (a) and Immunoreactive Insulin Levels In-Patients With Polycystic Ovary Syndrome. Metabolism, 46: 454-457 (1997); Valazquez, et al, Metformin Therapy In Polycystic Ovary Syndrome Reduces Hyperinsulinemia, Insulin Resistance, Hyperandrogenism, And Systolic Blood Pressure, While Facilitating Normal Menses And Pregnancy. Metabolism, 43: 647-654 (1994); Jackson, et al., Mechanism of Metformin Action In Non-Insulin Dependent Diabetes. Diabetes; 36: 632-640 (1987); Landin, et al., Treating Insulin Resistance in Hypertension With Metformin Reduces Both Blood Pressure And Metabolic Risk Factors. J. Intern. Med.; 229: 181-187 (1991); and Nestler, et al., Effects of Metformin on Spontaneous and Clomiphene-Induced Ovulation in the Polycystic Ovary Syndrome. N. Engl. J. Med. 338: 1876-1880 (1998). Web site: http://www.delphion.com/details?pn=US06194466__
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Use of thermally treated clays in animal feeds Inventor(s): Alonso-Debolt; Maria (Kingwood, TX) Assignee(s): Milwhite, Inc. (Houston, TX) Patent Number: 5,935,623 Date filed: January 15, 1998 Abstract: A method of promoting weight gain in an animal by feeding the animal calcined attapulgite which reduces adverse effects of a mycotoxin present in an animal food formulation. The calcined attapulgite is obtained by heating an attapulgite clay at or above 300.degree. F. The calcined attapulgite can be fed to an animal in any form either before, after, or during intake of food by the animal. Furthermore, a mixture of calcined attapulgite and bentonite may be used, instead of calcined attapulgite itself. Also provided is an animal feed composition for promoting weight gain including calcined attapulgite. Such a composition reduces adverse effects of a mycotoxincontaminated animal feed. The composition may further contain a bentonite clay. Excerpt(s): The present invention relates generally to methods and compositions of promoting weight gain in an animal by reducing adverse effects of a mycotoxin present in animal feeds. Mycotoxins are a group of structurally diverse, mold elaborated compounds that induce diseases known as mycotoxicosis in humans and animals. As much as twenty-five percent of the world's food crops are estimated to be contaminated with mycotoxins. Ingestion of sufficient quantities of mycotoxin-contaminated material leads to acute, and more commonly, chronic intoxication. As secondary mold metabolites, mycotoxins may contaminate animal feeds and human food ingredients in the absence of intact fungal elements. In many instances, processing of feed stuff may mask the presence of mold growth without concomitant destruction of mycotoxins. Mycotoxin-contaminated animal feeds and human foods are consumed worldwide, although their adverse health effects are not fully recognized. When a mycotoxicosis occurs in animals, it affects their health and reduces production efficiency because of increased susceptibility to infectious agents as a result of immune suppression. This has grave economic consequences. Furthermore, ingestion of such animals may have subtle health effects on humans which are not currently understood. Although it is known that fungi are capable of producing mycotoxins that frequently contaminate the food consumed by humans and animals, precise factors that initiate mycotoxin production are not well defined. The exact type and extent of the mycotoxin contamination is a function of mold types, growth conditions during the crop season, and storage practices. Mycotoxins of major concern include aflatoxin, zearalenone, fumonosin, ochratoxin, vomitoxin, etc. Web site: http://www.delphion.com/details?pn=US05935623__
Patent Applications on Weight Gain As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to weight gain: 10
This has been a common practice outside the United States prior to December 2000.
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Administering bacilus laterosporus to increase poultry feed conversion and weight gain Inventor(s): Porubcan, Randolph S.; (Shakopee, MN) Correspondence: Jeffrey L. Wendt; 600 Town Center One; 1450 Lake Robbins Drive; The Woodlands; TX; 77380; US Patent Application Number: 20030099624 Date filed: April 23, 2002 Abstract: Disclosed is a process for improving feed conversion and weight gain in poultry, including chickens, wherein Bacillus laterosporus, or any microorganism with a similarity index, based on its cellular fatty acid profile, of greater than 0.5 to Bacillus laterosporus (including Bacillus laterosporus strain CM-33 (ATCC Accession No. PTA3952)) is administered to poultry. Strain CM-33 of Bacillus laterosporus was isolated from soil and has a similarity index of 76% to Bacillus laterosporus. The administration of strain CM-33 is preferably divided into daily doses of about 2.0 million colony forming units (cfu)/day and continued for about 40 days of the growth cycle. The cells or spores can be administered through the bird's drinking water or by other methods, including spraying them onto the bird's feed. Excerpt(s): The present application claims priority priority under 35 U.S.C. 120 to Provisional Patent Application Serial No. 60/303,196 filed in the United States Patent and Trademark Office on Jul. 5, 2001 of which is incorporated herein by reference in its entirety. Beneficial microorganisms can be fed to animals raised for human consumption, for the purpose of suppressing deleterious organisms or directly promoting the animal's growth. The Association of American Feed Control Officials (AAFCO) lists 41 probiotic microorganisms that are recommended for direct-feeding to animals. Official Publication (1989), Association of American Feed Control Officials Incorporated. 27 of these microorganisms (65% of the total) are classified as lactic acidproducing bacteria. Lactic acid-producing bacteria had been previously mentioned as having probiotic activity. However, only five species of Bacillus bacteria were on the list, and Bacillus laterosporus was not mentioned. U.S. Pat. No. 5,045,314 discusses that certain strains of Bacillus laterosporus may control nematodes in ruminant animals, including goats. But such use was not mentioned for poultry, as they are not generally affected by nematode parasites. Twenty-seven strains of B. laterosporus are discussed, but only four, including strain ATCC 64, possessed nematicidal effect, and such effect was enhanced significantly by heat or enzyme treatment of the B. laterosporus, which caused activation of a specific toxin compound. There is, therefore, no suggestion or motivation to use any strain of Bacillus laterosporus for growth promotion in poultry, where nematodes are not considered a problem. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Animals expressing exogenous IGF-I in their milk Inventor(s): Bleck, Gregory T.; (Baraboo, WI), Donovan, Sharon M.; (Champaign, IL), Monaco-Seigel, Marcia; (Sidney, IL), Wheeler, Matthew B.; (Tolono, IL) Correspondence: Greenlee Winner And Sullivan P C; 5370 Manhattan Circle; Suite 201; Boulder; CO; 80303; US Patent Application Number: 20020144296 Date filed: August 15, 2001
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Excerpt(s): This application claims priority to United States Provisional Application No. 60/255,474, filed Aug. 15, 2000, which is incorporated by reference in its entirety to the extent not inconsistent with the disclosure herewith. The present invention relates to animals that express exogenous growth factors in their milk, and in particular to pigs that express exogenous IGF-I in their milk. The present invention also relates to methods for increasing piglet weight gain and intestinal lactase enzyme activity. The early neonatal period is the time of greatest animal loss for pork producers. The 1991 USDA National Swine Survey on Morbidity/Mortality and Heath Management of Swine in the U.S. estimated that overall pre-weaning mortality was 15% and that nearly all cases of morbidity and mortality occurred in piglets less than 7 days of age (USDA, 1991). Importantly, 58% of the cases of morbidity were reportedly due to scours and 30% of the mortality was attributed to scours or starvation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Composition of multipurpose high functional alkaline solution composition, preparation thereof, and for the use of nonspecific immunostimulator Inventor(s): Choi, Hyun-Suk; (Ansung, KR), Choi, Soo-Il; (Ansung, KR), Jeon, KyungSoo; (Ansung, KR), Park, Yong-Ho; (Seoul, KR), Yoo, Byung-Woo; (Seoul, KR) Correspondence: Jacobson Holman Pllc; 400 Seventh Street N.W.; Suite 600; Washington; DC; 20004; US Patent Application Number: 20020098205 Date filed: January 14, 2002 Abstract: Disclosed are a multipurpose, high-functional, alkaline solution composition, preparation therefor and use thereof as a nonspecific immunostimulator. The composition comprises 1-25 parts by weight of borax (Na.sub.2B.sub.4O.sub.7.10H.sub.2O), 10.sup.-5-10.sup.-4 parts by weight of sodium thiosulfate (Na.sub.2S.sub.2O.sub.3.5H.sub.2O), 30-150 parts by weight of potassium carbonate, 30-200 parts by weight of refined sugar (C.sub.12H.sub.22O.sub.11), and 100200 parts by weight of water, based on 100 parts by weight of sodium metasilicate (Na.sub.2SiO.sub.3.5H.sub.2- O). In addition to bringing about an improvement in disease resistance, weight gain rate, crop yield, crop quality, harvest time, the composition shows nonspecific immunostimulating activities, including antibody production and immune enhancement, by activating immune cells, thereby maximizing vaccination effects on malignant viral diseases. Excerpt(s): The present invention relates to a multi-purpose, high-functional, alkaline solution composition, a preparation method therefor, and use thereof as an nonspecific immunostimulator. More particularly, the present invention relates to an alkaline solution composition which mostly comprises sodium metasilicate (pentahydrate) and shows nonspecific immunostimulating activities, including antibody production and immune enhancement, by activating immune cells, thereby maximizing vaccination effects versus malignant virus diseases, preparation therefor, and use thereof as an immunostimulator. The functionality of alkaline mass in the body has been of great interest since the early 20.sup.th century. Extensive research has recently revealed that alkaline mass in the body increases ionization ratios of potassium and sodium to heighten the purification capability of blood, resulting in blood clearance, fatiguereduction, and aging retardation. One alkaline solution composition is disclosed in Korean Pat. No. 128,110, yielded to the present inventor, which comprises 10-18 parts by weight of sodium silicate, 0.1-0.5 parts by weight of sodium hyperoxide, 5-10 parts by
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weight of potassium carbonate, 1 part by weight of sodium carbonate, 10-18 parts by weight of refined sugar and 0.1-3.0 parts by weight of silver thiosulfate in water. The said composition is now used for the post-treatment of fiber products and the fermentation of feedstuff and in the agricultural industry by virtue of its high far infrared radiation efficiency, antibacterial activity and deodorizing activity. The composition, however, is disadvantageous in that its preparation is complicated and it is difficult to store for a long period of time. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Compositions and methods for treatment of body weight conditions Inventor(s): Bastian, Eric Douglas; (Twin Falls, ID), Paulsen, Starla Joyce; (Twin Falls, ID), Ward, Loren Spencer; (Twin Falls, ID) Correspondence: Banner & Witcoff, LTD.; Ten South Wacker Drive; Suite 3000; Chicago; IL; 60606; US Patent Application Number: 20030165574 Date filed: February 21, 2003 Abstract: A nutritional supplement composition having therapeutically effective amounts of milk minerals including calcium, a protein source including.kappa.-casein fragment 106-169, and enzyme-inhibiting peptides is provided for the treatment of body weight conditions. The nutritional supplement composition is administered in amounts effective for limiting weight gain and/or enhancing weight loss, as well as promoting overall good health, in the treatment of body weight conditions, including overweight and obesity. Excerpt(s): This application is based on, and claims the benefit of co-pending U.S. Provisional Application Serial No. 60/360,709, filed on Mar. 1, 2002, the disclosure of which is incorporated herein by reference. The present invention is directed to compositions and methods for treatment of body weight conditions by administering a therapeutically effective nutritional supplement composition. More particularly, the nutritional composition, which includes a milk mineral blend and protein components, is effective for enhancing weight loss and/or limiting weight gain. In 2000, almost 20% of the population fell into the obese category as defined by a BMI of greater than or equal to 30. Problems associated with obesity include cardiovascular disease, diabetes mellitus, certain types of cancer, osteoarthritis and sleeping disorders. Obesity and related disorders account for almost 10% of US health care expenditures. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Compositions and methods of use for extracts of magnoliaceae plants Inventor(s): Garrison, Robert JR.; (Carlsbad, CA), Stogniew, Martin; (Blue Bell, PA) Correspondence: Pennie And Edmonds; 1155 Avenue OF The Americas; New York; NY; 100362711 Patent Application Number: 20020076456 Date filed: November 29, 2001 Abstract: The invention relates to compositions and methods for preventing, treating, or managing sleeplessness, restlessness, weight gain including weight gain due to stress
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or lack of sleep, or all three comprising the administration of a prophylactically and therapeutically effective amount of Magnoliaceae plant or extracts thereof to a mammal in need of such therapy. Preferably the mammal is human and the compositions have comprise at least two compounds selected from magnolol, honokiol, and magnoflorine. Alternatively, the compositions may also comprise about 2% honokiol by weight of the composition. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/255,402 filed Dec. 15, 2000, which is incorporated by reference herein in its entirety. The present invention relates to novel methods and compositions for the treatment, prevention, or management of sleeplessness, restlessness and weight gain. The methods and compositions utilize plants, portions thereof or extracts therefrom belonging to the Magnoliaceae family. In addition, the methods and compositions utilize mixtures of specific small molecules extracted from the plants belonging to the family Magnoliaceae, such as, but not limited to, magnolol, honokiol, and magnoflorine. The unique compositions of the invention may also comprise various amounts of the Magnoliaceae plant, plant extract, plant extracts combined with different amounts of biologically active small molecules or other therapeutic agents. These compositions are particularly useful for the treatment of sleeplessness, restlessness and weight gain in humans. The invention also encompasses various modes of administration of the therapeutic extracts or other compositions of the invention. The recent growth in sales of natural products labeled as dietary supplements in the United States has renewed scientific interest in the study of the prophylactic and therapeutic effects of multi-component botanical products. Unlike single entity pharmaceutical products, botanical products comprise a large number of diverse chemical constituents that often act synergistically to exert a desired biological effect. The type of extraction process utilized and the manner in which the formulation is standardized have dramatic effects on the pharmacological activity of the final product. The development of new botanical products requires multidisciplinary effort consisting of expertise in ethnobotany, natural product chemistry, analytical chemistry, pharmacology, and natural product extraction. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Computer system for determining a customized animal feed Inventor(s): Burghardi, Steve R.; (Eden Prairie, MN), Cook, David A.; (Coon Rapids, MN), Knudson, Brian J.; (Chanhassen, MN), Oedekoven, Mark A.; (Minneapolis, MN), Peterson, Loren; (Loretto, MN) Correspondence: Charles G. Carter; Foley & Lardner; Firstar Center; 777 East Wisconsin Avenue; Milwaukee; WI; 53202-5367; US Patent Application Number: 20020120402 Date filed: December 15, 2000 Abstract: A method and system for creating a customized animal feed is disclosed. The method and system include having ingredient data from more than one location, animal data, and evaluation data. The specifications for a customized feed are generated using ingredient data representative of the mix of ingredients available at one or more locations. A customized feed is generated which is designed to fulfill the nutritional requirements for the animal's diet. The nutritional requirements are derived from the animal data. Furthermore, the feed is optimized to fulfil the requirements of the evaluation criteria. Evaluation criteria such as (i) animal production rate, (ii) the cost of feed per unit animal weight gain, and (iii) the feed weight per unit animal weight gain,
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are then utilized together with the feed data and animal data to provide a customized feed which has been generated based upon evaluation data which is representative of one or more of the evaluation criteria. Excerpt(s): The present invention relates to a computerized system for determining a customized feed for animals, such as cattle, swine, poultry, fish, crustaceans and the like. In particular, the system determines a feed mix based upon data relating to information such as animal characteristics, available ingredients, speed of product production, and cost of production. In food production, and specifically producing animal products such as milk, beef, pork, eggs, chicken, fish etc., there is need to improve production efficiency. Production efficiency, i.e. producing the maximum quantity of animal products while minimizing the time and cost of production for those products, is important in maintaining a competitive advantage. A producer (i.e. a farmer, rancher, pork producer, and the like) generally wants to maximize the amount of animal product produced (e.g. gallons of milk, pounds of beef or pork produced) while keeping the costs associated with feed at a low level in order to achieve maximum animal productivity. The maximized amount of animal product should be produced at a minimized cost to the producer. Costs to the producer include the cost of feed needed to produce the animal products, as well as the costs of related equipment and facilities needed in the production of animal products. In order to minimize the effect of fixed costs associated with equipment and facilities, the maximum amount of animal product should preferably be produced in a minimum time period. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Decreasing adipose mass by altering RSK2 activity Inventor(s): Bjorbaek, Christian; (Boston, MA), Flier, Jeffrey S.; (West Newton, MA), Goodyear, Laurie J.; (Brewster, MA) Correspondence: Hamilton, Brook, Smith & Reynolds, P.C.; 530 Virginia Road; P.O. Box 9133; Concord; MA; 01742-9133; US Patent Application Number: 20030158139 Date filed: September 27, 2002 Abstract: Deletion of the rsk2 gene in mice results in reduced body weight, reduced body fat and reduced sensitivity to diet-induced weight gain, as well as lower levels of leptin in the serum of rsk2 deficient mice and lower levels of oxygen consumption, as compared to wild type littermates. Thus, altering RSK2 activity provides a means for modulating RSK2-mediated signaling and therefore modulating the above described physiological parameters. The present invention encompasses methods and compositions for altering, or modulating in a mammal, body weight, fat content, leptin levels by altering, or modulating, RSK2 activity. Specifically encompassed in the present invention are methods and compositions to alter activity of the RSK2. The present invention is drawn to a model for the study of Coffin-Lowry syndrome as well as an in vivo model to screen and test therapeutic agents for the treatment of Coffin-Lowry syndrome. The present invention is further drawn to use of the rsk2 knockout mouse as a model to study and treatment of lipodystrophy and impaired glucose tolerance in mammals. Excerpt(s): This application is a continuation of U.S. application Ser. No. 10/016,692, filed Oct. 30, 2001, which is a continuation of International Application No. PCT/US00/11679, which designated the United States and was filed on May 1, 2000,
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which claims the benefit of U.S. Provisional Application No: 60/131,762, filed Apr. 30, 1999. The entire teachings of the above applications are incorporated by reference. Ribosomal-S6-kinases (p90.sup.rsk or RSK) are intracellular serine/threonine protein kinases that are activated by perturbations including stimulation with insulin and other growth factors. Three members of the RSK family have been identified (RSK1, RSK2, RSK3). RSK proteins are expressed in many tissues. RSK2 is highly expressed in brain, muscle and fat tissue. RSK2 is activated, for example, in response to the growth factors via the MAPK pathway and possibly other pathways. Studies in mammalian cell lines show that RSK isoforms, upon activation, translocate to the nucleus where they may be involved in phosphorylation of transcription factors. Putative RSK substrates include histones as well as transcription factors like c-Fos, c-Jun, Elk-1 and serum response factor. RSK2 acts as a CREB (cAMP-responsive binding-element protein) kinase in response to the growth factors via the MAPK pathway. These results implicate a role of RSK proteins as mediators of cellular proliferation. Mutations in the rsk2 gene have recently been demonstrated to cause Coffin-Lowry syndrome, an X-linked disorder characterized by mental retardation, short stature and digital dysmorphisms. Yet the function of RSK2 in vivo remains largely unknown. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
DELIQUESCENT SALT ADDITION TO ALUM USED TO TREAT ANIMAL WASTE PRODUCTS Inventor(s): Barnes, Russell Hayden; (Salisbury, MD), Hurd, Joseph Lewis; (Sandy Creek, NY), Lind, Christopher Bruce; (Syracuse, NY) Correspondence: Arthur J. Plantamura, ESQ.; General Chemical Corporation; 90 East Halsey Road; Parsippany; NJ; 07954; US Patent Application Number: 20020106344 Date filed: February 8, 2001 Abstract: Animal enclosures such as poultry houses generate high amounts of ammonia that adversely affect weight gain and mortality or the animals, particularly among young chicks. The addition of a deliquescent salt, such as calcium chloride, to alum to treat animal waste products rapidly activates the alum to remove ammonia from the atmosphere. The ammonia sulfate by-product is useful as a nitrogen fertilizer. Excerpt(s): This invention relates to improvements in the treatment of animal litter with alum to reduce the generation of ammonia in the litter. More particularly, this invention relates to the addition of a deliquescent salt to alum to increase the absorption of water by the alum to speed the reaction of alum with ammonia. Moore, Jr., in a series of U.S. patents, has explained that animal litter or manure, particularly from farm animals such as poultry and pigs, contains ammonia and phosphates. The amounts of ammonia given off into the atmosphere adversely affects farm workers, and even the animals themselves. When large amounts of ammonia are present in the atmosphere of animal enclosures, the result is lower weight gain and higher mortality rates for the animals. Thus alum (aluminum sulfate), having the formula Al.sub.2(SO.sub.4).sub.3.nH.sub.2O wherein n above 1 and typically is about 14-18, has been used to reduce the pH, and thus the ammonia generation, of manure and animal bedding material. Alum, either in solid or liquid form, will lower the pH of the manure by hydrolysis and will convert ammonia to ammonium ions. Ammonium ions will react with sulfates to form ammonium sulfate; the latter is a water soluble nitrogen fertilizer and can be used as such. Desirably, the amount of ammonia present in the atmosphere of an animal
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enclosure should be held below about 25 ppm. The use of alum for this purpose has an added advantage in that the soluble phosphates present precipitate in the presence of aluminum and thus the soluble phosphate content of manure is also reduced by this treatment. Soluble phosphates are known to seep into ground water or are carried in surface runoff water. In either case, this presents a substantial environmental problem. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Dietary compositions Inventor(s): Bruckner, Geza; (Versailles, KY), Szabo, Joseph; (Budapest, HU) Correspondence: Dinsmore & Shohl, Llp; 1900 Chemed Center; 255 East Fifth Street; Cincinnati; OH; 45202; US Patent Application Number: 20020091110 Date filed: January 9, 2002 Abstract: Dietary compositions and methods employ a mammal food base and a component comprising estrogen, androgen or a mixture thereof in an amount sufficient to reduce weight gain normally incurred in the mammal type subsequent to neutering, castration, spaying, ovariectomy or ovariohysterectomy, or post menopause. Preferably, the component comprises phytoestrogen, phytoandrogen or a mixture thereof. The compositions are adapted for administration to the mammal on a regular, preferably daily, basis. Excerpt(s): The present invention is directed to dietary compositions, particularly for mammals, including humans, dogs, cats and horses, and to methods for reducing weight gain normally incurred in mammals subsequent to neutering, castration, spaying, ovariectomy or ovariohysterectomy, or post menopause. Procedures including neutering, castration, spaying, ovariectomy or ovariohysterectomy are increasingly performed on dogs and cats for health related reasons and/or for population control. It is not uncommon for dogs or cats having undergone one of the aforementioned procedures to gain a significant amount of weight thereafter, and often exceed target healthy weight limits. Weight gain incurred subsequent to ovariectomy or ovariohysterectomy procedures in other mammals, including humans, is not uncommon. Additionally, post menopausal weight gain often occurs in humans even when ovariectomy or ovariohysterectomy procedures are not performed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Herbal composition and method for controlling body weight and composition Inventor(s): Hong, Wei; (Beijing, CN), Jing, Wei; (Beijing, CN), Wei, Kaiyuan; (US), Xian, Wei; (Beijing, CN), Xu, Xiurong; (Beijing, CN) Correspondence: Lyon & Lyon Llp; 633 West Fifth Street; Suite 4700; Los Angeles; CA; 90071; US Patent Application Number: 20020164387 Date filed: January 17, 2002 Abstract: The present invention relates to a dietary supplement for the treatment of obesity, including both weight loss and reduction of weight gain. Pursuant to the invention, a decoction of a herbal mixture, comprising rhubarb, red saga root,
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astragalus, turmeric, and dried ginger and various combinations thereof, provides therapeutic weight loss as well as lipid reduction and change body composition. The invention includes methods of manufacture and administration and also includes the herbal decoction in various forms of administration and in combination with food. Excerpt(s): This application claims priority to Chinese Patent Application No. 01103777.6 filed Feb. 12, 2001, entitled "COMPOSITION AND METHOD FOR EFFECTING WEIGHT REDUCTION" and the disclosure is hereby incorporated by reference. The present invention generally relates to dietary supplements and foods for reducing weight gain, effecting weight loss and causing favorable changes in body composition. More specifically, the invention relates to the field of herbal compositions, especially decoctions for oral administration containing rhubarb and other herbal ingredients. Body weight and body composition is determined by the competing balance of food intake and energy expenditure. Although both genetic and environmental factors can contribute to obesity, the most common cause of weight gain and an overweight body composition is excessively high caloric intake accompanied by a lack of physical activity. The resulting accumulation of surplus fat places overweight or obese individuals at increased risk of illness from hypertension, lipid disorders, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, osteoarthritis, sleep apnea and respiratory problems, certain cancers, and a wide variety of other diseases and undesired physiological conditions, as well as overall mortality. According to a study, the proportion of overweight individuals in the United States increased from 25% in 1980 to 33% in 1991. (Third National Health and Nutrition Examination Survey, 1991). In 1998 the National Institutes of Health reported that over 55 percent of the U.S. population are now considered overweight or obese. (Obesity Clinical Guidelines: NIH Statement Jun. 3, 1998, press release). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for improving body weight gain and feed conversion efficiency in animals Inventor(s): Pimentel, Julio; (Buford, GA) Correspondence: Patent Adminstrator; Katten Muchin Zavis Rosenman; 525 West Monroe Street; Suite 1600; Chicago; IL; 60661-3693; US Patent Application Number: 20030228313 Date filed: June 6, 2002 Abstract: A method for improving body weight gain and increasing feed conversion efficiency of in animals by feeding the animals a diet containing antibodies against antinutritional factors in food. Excerpt(s): The invention relates to a method for improving body weight gain and increasing the efficiency of converting feed into body weight gain in animals, by feeding to animals an effective dose of antibodies against anti-nutritional factors commonly found in feedstuffs or produced by microorganisms present in the gastro-intestinal tract. In the animal industry, the feed accounts for 50% to 70% of the overall production cost. Therefore any improvement in the ability of the animal to convert feed into marketable products, e.g., animal body weight, can markedly improve profitability for the animal producer. Various methods for improving feed conversion are known in the animal industry. One of the most common methods is adding sub-therapeutic levels of antibiotics to the feed, in order to improve animal performance. Antibiotics decrease the animal's exposure to bacterial infection and decrease the number of bacteria in the
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gastrointestinal tract, thereby allowing the animal to utilize nutrients more efficiently since the animal and the microflora are competing for the same nutrients. However continuous use of antibiotics as growth promoters causes several problems, including the introduction of drug residues in animal produce, promoting the growth of antibiotic resistant bacteria, and increasing the risk of environmental pollution. Due to the seriousness of these problems the use of antibiotics as growth promoters in the animal industry may soon be completely prohibited. The European Union has already banned the use of five different growth promoting antibiotics in animals raised for human consumption and others may follow. In the United States, three growth promoting antibiotics have been banned in recent years. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of controlling weight gain associated with therapeutic drugs Inventor(s): Mendel, Carl M.; (Short Hills, NJ), Seaton, Timothy B.; (Far Hills, NJ), Weinstein, Steve P.; (Hartsdale, NY) Correspondence: John D. Conway; Abbott Bioresearch Center; 100 Research Drive; Worcester; MA; 01605-4314; US Patent Application Number: 20030008897 Date filed: March 17, 2000 Abstract: A compound of formula I 1or a pharmaceutically acceptable salt thereof in which R.sub.1 and R.sub.2 are independently H or methyl (for example N,N-dimethyl-1[1-(4-chlorophe- nyl)cyclobutyl]-3-methylbutyl amine hydrochloride optionally in the form of its monohydrate) is used for treating weight gain associated with treatment with certain drug therapy, including the use of tricyclic antidepressants, lithium, sulphonylureas, beta-adrenergic blockers, certain steroid contraceptives, corticosteroids, insulin, cyproheptadine, sodium valproate, neuroleptics, phenothiazine or piztifen. Excerpt(s): This invention relates to a method of controlling weight gain associated with treatment with medicines. including enantiomers and pharmaceutically acceptable salts thereof, in which R.sub.1 and R.sub.2 are independently H or methyl, is administered in conjunction with a pharmaceutically acceptable diluent or carrier to a human in need thereof. The use of certain therapeutic drugs can promote weight gain. These drugs include tricyclic antidepressants, lithium, sulphonylureas, beta-adrenergic blockers, certain steroid contraceptives, corticosteroids, insulin, cyproheptadine, sodium valproate, piztifen, neuroleptics including typical neuroleptics for example phenothiazine and phenothiazine derivatives such as chlorpromazine, thioridazine, fluphenazine and trifluoperazine; butyrophenones such as haloperidol; thioxanthenes such as flupentixol and substituted benzamides such as sulpiride, atypical neuroleptics including clozapine, olanzapine, zotepine, risperidone, quetiapine and ziprasidone. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of decreasing fasting sugars and weight gains in diabetic patients Inventor(s): Landschulz, William H.; (East Lyme, CT) Correspondence: Pfizer INC.; Patent Department, Ms8260-1611; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20030079747 Date filed: June 19, 2002 Abstract: Inhaled insulin, relative to subcutaneously and/or transdermally administered insulin, can be used to prevent the rate of weight gain and to lower the levels of fasting glucose in diabetic patients. Excerpt(s): This invention is directed to a method of reducing the rate of weight gain and/or to lowering fasting blood sugars in a diabetic patient who is using exogenous insulin to control blood sugars, and who is taking said insulin by other than a pulmonary route of administration, comprising administering said insulin to said patient by the pulmonary route, i.e. as inhaled insulin. Additionally, the invention relates to starting a patient on inhaled insulin who is at risk for gaining weight or developing high fasting blood sugars. Diabetes mellitus is a serious metabolic disease that is defined by the presence of chronically elevated levels of blood glucose. Classic symptoms of diabetes mellitus in adults are polyuria and polydipsia together with elevated levels of plasma glucose. Normal fasting plasma glucose concentrations are less than 110 milligrams per deciliter. In diabetic patients, fasting concentrations are found to be at or above 126 milligrams per deciliter. In general, diabetes mellitus develops in response to damage to, or to defects in, the beta cells of the pancreas. Primary diabetes mellitus is classified as Type 1 diabetes (also called insulin-dependent diabetes mellitus or IDDM) and Type 2 diabetes mellitus (also called non-insulin dependent diabetes mellitus or IDDM). Type I (juvenile onset or insulin-dependent) diabetes is a wellknown hormone deficient state, in which the pancreatic beta cells appear to have been destroyed by the body's own immune defense mechanisms. Patients with Type I diabetes mellitus have little or no endogenous insulin secretory capacity. These patients develop extreme hyperglycemia. Type I diabetes was fatal until the introduction of insulin replacement therapy some 70 years ago--first using insulins from animal sources, and more recently, using human insulin made by recombinant DNA technology. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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METHOD TO SUPPRESS APPETITE AND REDUCE WEIGHT GAIN Inventor(s): COOK, MARK E.; (MADISON, WI), STRANSKY, DARIA L.; (OWATONNA, MN) Correspondence: Quarles & Brady Llp; Firstar Plaza, One South Pinckney Street; P.O. Box 2113 Suite 600; Madison; WI; 53701-2113; US Patent Application Number: 20020150575 Date filed: January 7, 2000 Abstract: A method of suppressing appetite and reducing weight gain in animals and human beings includes the step of administering to the animal a high dose of an antibody to a gut peptide. Excerpt(s): Not applicable. This invention relates to controlling appetite and weight gain in animals and human beings by using antibodies to gut peptides. Specifically, this
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invention relates to suppressing appetite and reducing weight gain in animals and humans by feeding animals or humans a substance that contains sufficiently high doses of anti-cholecystokinin (CCK) antibodies for a sufficient long period of time. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods and compositions for treating depression and other disorders using optically pure (-) -bupropion Inventor(s): Young, James W.; (Palo Alto, CA) Correspondence: Pennie & Edmonds Llp; 1667 K Street NW; Suite 1000; Washington; DC; 20006 Patent Application Number: 20020115726 Date filed: February 19, 2002 Abstract: Methods and compositions are disclosed utilizing the optically pure (-)-isomer of bupropion, which is a potent drug for treating depression, Parkinson's disease, obesity, weight gain and other disorders. Excerpt(s): This invention relates to methods of treatment and pharmaceutical compositions employing the compound (-)-bupropion. Many organic compounds exist in optically active forms, i.e., they have the ability to rotate the plane of plane-polarized light. In describing an optically active compound, the prefixes D and L or R and S are used to denote the absolute configuration of the molecule about its chiral center(s). The prefixes (+) and (-) or d and 1 are employed to designate the sign of rotation of planepolarized light by the compound, with (-) or 1 meaning that the compound is. levorotatory. A compound prefixed with (+) or d is dextrorotatory. For a given chemical structure, these compounds, called stereoisomers, are identical except that they are mirror images of one another. A specific stereoisomer may also be referred to as an enantiomer, and a mixture of such isomers is often called an enantiomeric or racemic mixture. Stereochemical purity is of importance in the field of pharmaceuticals, where 16 of the 20 most prescribed drugs exhibit chirality. A case in point is provided by the Lform of the.beta.-adrenergic blocking agent, propranolol, which is known to be 100 times more potent than the D-enantiomer. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for preventing antipsychotic-induced weight gain Inventor(s): Belanoff, Joseph K.; (Woodside, CA), Schatzberg, Alan F.; (Los Altos, CA) Correspondence: Townsend And Townsend And Crew, Llp; Two Embarcadero Center; Eighth Floor; San Francisco; CA; 94111-3834; US Patent Application Number: 20030027802 Date filed: July 22, 2002 Abstract: This invention generally pertains to the field of psychiatry. In particular, this invention pertains to the discovery that agents capable of inhibiting the binding of cortisol to its receptors can be used in methods for preventing antipsychotic-induced weight gain. Mifepristone, a potent specific glucocorticoid receptor antagonist, can be used in these methods. The invention also provides a kit for preventing AP-induced weight gain in a human including a glucocorticoid receptor antagonist and instructional
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material teaching the indications, dosage and schedule of administration of the glucocorticoid receptor antagonist. Excerpt(s): The present application claims priority to U.S. Ser. No. 60/307,693 filed Jul. 23, 2001 herein incorporated by reference in its entirety. This invention relates to the discovery that agents capable of inhibiting the biological action of the glucocorticoid receptor can be used in the methods for preventing weight gain induced by antipsychotic medications. Antipsychotic (AP) medications are among the most important therapeutic tools for treating various psychotic disorders. For these medications to be maximally beneficial, their adverse side effects, especially those associated with long-term administration, must be minimized. Numerous reports based on extensive clinical studies have, however, indicated that 40-80% of patients who are under chronic AP administration experience substantial weight gain, ultimately exceeding their ideal body weight by 20% or more (see, e.g., Umbricht et al., J Clin. Psychiatry 55 (Suppl. B):157-160, 1994; Baptista, Acta Psychiatr. Scand. 100:3-16, 1999). Such undesirable weight gain can significantly compromise the effectiveness of treatment for psychotic disorders. First of all, a person whose body weight significantly exceeds the healthful range is exposed to a dramatically increased risk in many serious health problems associated with obesity, such as cardiovascular disease, stroke, hypertension, type II diabetes, and certain types of cancer. Secondly, unwanted weight gain is one of the most common reasons for a patient's non-compliance of AP administration schedule, which necessarily leads to the failure of the treatment for the psychotic disorder. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods for reducing fat by administration of adiponectin Inventor(s): Kincade, Paul W.; (Nichols Hill, OK), Yokuta, Takafumi; (Norman, OK) Correspondence: Patrea L. Pabst; Holland & Knight Llp; Suite 2000, One Atlantic Center; 1201 West Peachtree Street, N.E.; Atlanta; GA; 30309-3400; US Patent Application Number: 20020132773 Date filed: March 14, 2002 Abstract: The stromal cells that support blood cell production within bone marrow are pre-adipocytes and functional interactions with marrow fat cells have long been suspected. Adiponectin was recently isolated as an adipocyte product and shown to have structural similarities to Clq as well as members of the TNF superfamily. It suppresses myeloid differentiation in short term bone marrow cultures and also inhibits macrophage functions. These observations raised the possibility that precursors of other blood cell lineages interact with fat cells in marrow via adiponectin. It has now been determined that the factor blocks B lymphopoiesis in Whitlock-Witte type bone marrow cultures, but not the production of myeloid cells in Dexter cultures. Several observations suggest that non-lymphoid cells represent the target of this new mediator, and the B lymphoid lineage is only indirectly influenced. Highly purified lymphocyte precursors in stromal cell-free, serum-free cultures were unaffected by adiponectin. Similarly, there was no influence on IL-7 responding pro-B cells in clonal assays. However, the cytokine dramatically inhibited adipogenesis in culture, suggesting that it may normally be a feedback inhibitor of this process. PCR analyses revealed that COX-2 is induced on exposure of cloned preadipocytes to adiponectin, resulting in prostaglandin release. This is critical to the inhibition of adipogenesis, because a COX-2 inhibitor, DUP-697 blocked the response of preadipocytes to adiponectin. Furthermore, fat cell formation in
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response to adiponectin was defective in mice with disruption of the COX-2 gene. In contrast, expression of TNF-.alpha., TGF-.beta., interferons and a new interferon-like cytokine known as limitin are not up-regulated by adiponectin. These results also demonstrate that COX-2 inducers can be used to cause weight loss, and that COX-2 inhibitors will cause weight gain. Excerpt(s): This application claims prioity to U.S. S. No. 60/275,755 filed Mar. 14, 2001. The present invention is generally in the field of causing weight loss, specifically by administration of adiponectin. The prevalence of obesity has reached epidemic proportions in most developed countries and carries with it staggering mortality and morbidity statistics. Obesity is a well established risk factor for a number of potentially life-threatening diseases such as atherosclerosis, hypertension, diabetes, stroke, pulmonary embolism, and cancer. (Meisler J., St. Jeor S. 1996. Am J Clin Nutr. 63:409S411S; Bray G. 1996. Endocrin Metab Clin North Aimer. 25:907-919). Furthermore, it complicates numerous chronic conditions such as respiratory diseases, osteoarthritis, osteoporosis, gall bladder disease, and dyslipidemias. The enormity of this problem is best reflected in the fact that death rates escalate with increasing body weight. More than 50% of all-cause mortality is attributable to obesity-related conditions once the body mass index (BMI) exceeds 30 kg/m.sup.2, as seen in 35 million Americans. (Lee L., Paffenbarger R. 1992. JAMA. 268:2045-2049). By contributing to greater than 300,000 deaths per year, obesity ranks second only to tobacco smoking as the most common cause of potentially preventable death. (McGinnis J., Foege W. 1993. MA.270:2207-2212). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods of treating affective disorders using derivatives of (-)- venlafaxine Inventor(s): Bhongle, Nandkumar N.; (Shrewsbury, MA), Jerussi, Thomas P.; (Framingham, MA), Senanayake, Chrisantha H.; (Shrewsbury, MA) Correspondence: Pennie & Edmonds Llp; 1667 K Street NW; Suite 1000; Washington; DC; 20006 Patent Application Number: 20020086904 Date filed: December 14, 2001 Abstract: Methods of preparing, and compositions comprising, derivatives of (-)venlafaxine are disclosed. Also disclosed are methods of treating and preventing diseases and disorders including, but not limited to, affective disorders such as depression, bipolar and manic disorders, attention deficit disorder, attention deficit disorder with hyperactivity, Parkinson's disease, epilepsy, cerebral function disorders, obesity and weight gain, incontinence, dementia and related disorders. Excerpt(s): The invention relates to optically pure derivatives of (-)-venlafaxine, methods of their synthesis, compositions comprising them, and methods of their use. A number of nontricyclic antidepressants have recently been developed that diminish the cardiovascular and anticholinergic liability characteristic of tricyclic antidepressants. Some of these compounds are used as anti-obesity agents and have shown promise in the treatment of cerebral function disorders such as Parkinson's disease and senile dementia. See, e.g., WO 94/00047 and WO 94/00114. The nontricyclic compound venlafaxine, chemically named (.+-.)-1-[2-(dimethylamino)-1-(4-m- ethoxyphenyl)ethyl]cyclohexanol, is an antidepressant which has been studied extensively and which is described in, for example, U.S. Pat. No. 4,761,501 and Pento, J. T. Drugs of the Future 13(9):839-840 (1988). Its hydrochloride salt is currently commercially available in the
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United States under the trade name Effexor.RTM. Effexor.RTM., which is a racemic mixture of the (+) and (-) enantiomers of venlafaxine, is indicated for the treatment of depression. Klamerus, K. J. et al. J. Clin. Pharmacol. 32:716-724 (1992). All of these metabolites are racemic. In vitro studies suggest that O-desmethylvenlafaxine is a more potent inhibitor of norepinephrine and dopamine uptake than the parent compound racemic venlafaxine. Muth, E. A. et al. Drug Develop. Res. 23:191-199 (1991). Odesmethylvenlafaxine has also been reported to have a half-life (t{fraction (1/2)}) of about 10 hours, which is approximately 2.5 times as long as that of venlafaxine. Klamerus, K. J. et al. J. Clin. Pharmacol. 32:716-724 (1992). Studies directed at understanding the activity of O-desmethylvenlafaxine as compared to its parent have been hampered, however, by the metabolic difference between laboratory animals and man in their exposure to venlafaxine. Howell, S. R. et al. Xenobiotica 24(4):315-327 (1994). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods of treating and preventing sexual dysfunction using (+) sibutramine in combination with phosphodiesterase inhibitors Inventor(s): Jerussi, Thomas P.; (Framingham, MA), Young, James W.; (Palo Alto, CA) Correspondence: Pennie & Edmonds Llp; 1155 Avenue OF The Americas; New York; NY; 10036; US Patent Application Number: 20030078303 Date filed: November 18, 2002 Abstract: This invention encompasses methods for the treatment and prevention of disorders that include, but are not limited to, eating disorders; weight gain; obesity; irritable bowel syndrome; obsessive-compulsive disorders; platelet adhesion; apnea; affective disorders such as attention deficit disorders, depression, and anxiety; male and female sexual function disorders; restless leg syndrome; osteoarthritis; substance abuse including nicotine and cocaine addiction; narcolepsy; pain such as neuropathic pain, diabetic neuropathy, and chronic pain; migraines; cerebral function disorders; chronic disorders such as premenstrual syndrome; and incontinence.The invention further encompasses pharmaceutical compositions and dosage forms which comprise optically pure (+) sibutramine, optionally in combination with a phosphodiesterase inhibitor or a lipase inhibitor. Excerpt(s): This is a continuation-in-part of U.S. patent application Ser. No. 08/442,263, filed May 16, 1995, the entire contents of which are incorporated herein by reference. This invention is directed to methods and compositions for the treatment or prevention of conditions using optically pure (+) sibutramine, optionally in combination with other pharmacologically active compounds. Sibutramine, chemically named [N-1-[1-(4chlorophenyl)cyclobutyl]-3- -methylbutyl]-N,N-dimethylamine, is a neuronal monoamine reuptake inhibitor which was originally disclosed in U.S. Pat. Nos. 4,746,680 and 4,806,570. Sibutramine inhibits the reuptake of norepinephrine and, to a lesser extent, serotonin and dopamine. See, e.g., Buckett et al., Prog. Neuro-psychopharm. & Biol. Psychiat., 12:575-584, 1988; King et al., J Clin. Pharm., 26:607-611 (1989). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Minimising body gain in insulin treatment Inventor(s): Axelsen, Mads; (Virum, DK), Bayer, Thomas; (Lyngby, DK), Sogaard, Birgitte; (Gilleleje, DK) Correspondence: Reza Green, ESQ.; Novo Nordisk Pharmaceuticals, INC.; 100 College Road West; Princeton; NJ; 08540; US Patent Application Number: 20030224973 Date filed: March 12, 2003 Abstract: A method for minimising weight gain, preventing weight gain or inducing weight loss in a mammal, said method involving a treatment regimen which comprises administration of an insulin derivative having a substituent containing from 6 to 40 carbon atoms attached to one of its amino acid residues. Excerpt(s): This application claims priority under 35 U.S.C. of Danish application no. PA 2002 00395 filed Mar. 13, 2002, and U.S. application No. 60/366,327 filed Mar. 14, 2002, the contents of which are fully incorporated herein by reference. This invention relates to a method for minimising weight gain in the treatment of diabetes mellitus, either type 1 diabetes or type 2 diabetes and conditions associated with diabetes mellitus. For several years it has been known that when treatment of diabetic patients with insulin is initiated the body weight of the patients generally starts to increase (see, for example, the results of the Diabetes Control and Complications Trial (DCCT) Research Group: Influence of Intensive Diabetes Treatment on Body Weight and Composition of Adults With Type 1 Diabetes in the Diabetes Control and Complications Trial. Diabetes Care 24:1711-1721, 2001). The body weight continues to increase for many years after the intensive insulin treatment is initiated. The problem is most pronounced in intensive insulin treatment but also known with conventional treatment. Since intensive insulin treatment significantly reduces the risk of development and progression of late complications such as retinopathy, nephropathy, and neuropathy compared with conventional therapy, intensive diabetes therapy is much preferred over conventional therapy. The major adverse effect of intensive treatment is an increase in severe hypoglycemia. After the increased rate of hypoglycemia, weight gain and increased risk of obesity are the most evident side effects of intensive treatment. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Neuromedin u receptor nmur2 and nucleotides encoding it Inventor(s): Howard, Andrew D.; (Park Ridge, NJ), Jiang, Qingping; (Midland Park, NJ), Liu, Qingyun; (The Woodlands, TX), Lynch, Kevin R.; (Charlottesville, VA), Mellin, Theodore N.; (Annadale, NJ), Strack, Alison; (Scotch Plains, NJ), Van Der Ploeg, Leonardus H.T.; (Scotch Plains, NJ), Wang, Ruiping; (Maple Glen, PA), Williams, David; (Telford, PA) Correspondence: Merck And CO Inc; P O Box 2000; Rahway; NJ; 070650907 Patent Application Number: 20030211968 Date filed: April 8, 2003 Abstract: A new neuromedin U receptor, designated NMUR2 has been found, which is involved in modulation of feeding behavior in mammals. Ligands of this receptor are able to modulate eating, and weight gain. Amino acid sequences of the human and rat forms, as well as their nucleic acid sequences are given.
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Excerpt(s): This invention relates to new human and rat neuromedin U receptors, designated hNMUR2, and rNMUR2, to nucleic acids encoding them, and to use of them in various assays. Neuromedin U (NMU) is a neuropeptide that is widely distributed in the gut and central nervous system, particularly in brain regions implicated in the control of feeding behavior. NMU belongs to the broad class of neuropeptides first isolated from porcine spinal cord and later from other species with potent activity on smooth muscle. One orphan receptor designated FM-3 (now NMUR1) was previously identified as a high affinity receptor of NMU, which is the subject of U.S. Provisional Patent Application Serial No. 60/092,623 (filed Jul. 13, 1998) and International Patent Application No. PCT/US99/15941 (filed Jul. 13, 1999). NMU, when injected into the rat brain, caused a marked suppression of food intake. Thus it appears that ligands of neuromedin receptors have potential as drugs which modulate feeding and regulate weight. However, it is equally clear that NMUR1 is not the only receptor whose activity is responsible for eating behaviors. It would be desirable to further identify and characterize other receptors whose ligands are potential drugs for eating disorders. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Nutritional supplement for the management of weight Inventor(s): Bell, Stacey J.; (Belmont, MA) Correspondence: Hamilton, Brook, Smith & Reynolds, P.C.; 530 Virginia Road; P.O. Box 9133; Concord; MA; 01742-9133; US Patent Application Number: 20030143287 Date filed: February 6, 2003 Abstract: Described herein is a nutritional supplement to be incorporated into the diet of an overweight or obese patient comprising a low glycemic index carbohydrate source, a source of protein, and a source of fat, and further comprising a source of green tea extract, a source of 5-hydroxytryptophan (5-HTP), and a source of chromium. The supplement provides active food-grade ingredients to improve the management weight loss, prevention of weight gain, and a feeling of satiety. Excerpt(s): This application is a continuation of International Application No. PCT/US01/24465, which designated the United States and was filed on Aug. 2, 2001, published in English, which is a continuation-in-part of U.S. application Ser. Nos. 09/634,246, filed Aug. 8, 2000 (now abandoned) and 09/783,724, filed Feb. 14, 2001, the entire teachings of which are incorporated herein by reference. The prevalence of obesity in adults, children and adolescents has increased rapidly over the past 30 years in the United States and globally and continues to rise. Obesity is classically defined based on the percentage of body fat or, more recently, the body mass index (BMI), also called Quetlet index (National Task Force on the Prevention and Treatment of Obesity, Arch. Intern. Med., 160: 898-904 (2000); Khaodhiar, L. et al., Clin. Cornerstone, 2: 17-31 (1999)). The BMI is defined as the ratio of weight (kg) divided by height (in meters) squared. Overweight and obesity are associated with increasing the risk of developing many chronic diseases of aging seen in the U.S. (Must, A. et al., JAMA, 282: 1523-9 (1999)). Such co-morbidities include type 2 diabetes mellitus, hypertension, coronary heart diseases and dyslipidemia, gallstones and cholecystectomy, osteoarthritis, cancer (of the breast, colon, endometrial, prostate, and gallbladder), and sleep apnea. It is estimated that there are around 325,00 deaths annually that are attributable to obesity. The key to reducing the severity of the diseases is to lose weight effectively. Although about 30 to 40% claim to be trying to lose weight or maintain lost weight, current
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therapies appear not to be working. Besides dietary manipulation, pharmacological management and in extreme cases, surgery, are sanctioned adjunctive therapies to treat overweight and obese patients (Expert Panel, National Institute of Health, Heart, Lung, and Blood Institute, 1-42 (June 1998); Bray, G. A., Contemporary Diagnosis and Management of Obesity, 246-273 (1998)). Drugs have side effects, and surgery, although effective, is a drastic measure and reserved for morbidly obese. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
OBG3 globular head and uses thereof for decreasing body mass Inventor(s): Bihain, Bernard; (Encinitas, CA), Erickson, Mary Ruth; (San Diego, CA), Fruebis, Joachim; (Cardiff, CA), Yen-Potin, Frances; (San Diego, CA) Correspondence: John Lucas, PH.D., J.D.; Genset CORP.; 10665 Sorrento Valley Road; San Diego; CA; 92121-1609; US Patent Application Number: 20020091080 Date filed: July 19, 2001 Abstract: The present invention relates to the field of obesity research. Obesity is a public health problem that is serious and widespread. A compound, globular OBG3, has been identified that reduces weight gain in animals. This compound should be effective for reducing body mass and for treating obesity-related diseases and disorders. These obesity-related diseases and disorders include hyperlipidemias, atherosclerosis, diabetes, and hypertension. Excerpt(s): The present invention relates to the field of metabolic research, in particular the discovery of compounds effective for reducing body mass and useful for treating obesity-related diseases and disorders. The obesity-related diseases or disorders envisioned to be treated by the methods of the invention include, but are not limited to, hyperlipidemia, atherosclerosis, diabetes, and hypertension. The following discussion is intended to facilitate the understanding of the invention, but is not intended nor admitted to be prior art to the invention. Obesity is a public health problem that is serious, widespread, and increasing. In the United States, 20 percent of the population is obese; in Europe, a slightly lower percentage is obese [Friedman (2000) Nature 404:632634]. Obesity is associated with increased risk of hypertension, cardiovascular disease, diabetes, and cancer as well as respiratory complications and osteoarthritis [Kopelman (2000) Nature 404:635-643]. Even modest weight loss ameliorates these associated conditions. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Phytase-containing animal food and method Inventor(s): Orr, Donald E. JR.; (Noblesville, IN), Ruch, Frank E. JR.; (Falmouth, ME), Webel, Douglas M.; (Noblesville, IN) Correspondence: Barnes & Thornburg; 11 South Meridian; Indianapolis; IN; 46204 Patent Application Number: 20030206913 Date filed: October 31, 2002 Abstract: A method is described for improving the nutritional value of a foodstuff comprising a source of myo-inositol hexakisphosphate by feeding the foodstuff in
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combination with a phytase expressed in yeast. The method comprises the step of feeding the animal the foodstuff in combination with a phytase expressed in yeast wherein the phytase can be selected from the group consisting of AppA1, AppA2 and a site-directed mutant of AppA. The invention also enables reduction of the feed to weight gain ratio and an increase bone mass and mineral content of an animal. A foodstuff and a feed additive comprising AppA2 or a site-directed mutant of AppA are also described. Excerpt(s): This application claims priority under 35 U.S.C.sctn. 11 9(e) to U.S. Provisional Application Serial No. 60/335,303, filed on Oct. 31, 2001. The present invention is related to a method of improving the nutritional value of a foodstuff and to an improved foodstuff. More particularly, the invention relates to a method of improving the nutritional value of a foodstuff comprising myo-inositol hexakisphosphate by feeding the foodstuff to an animal in combination with a phytase expressed in yeast. Phytases are myo-inositol hexakisphosphate phosphohydrolases that catalyze the stepwise removal of inorganic orthophosphate from phytate (myo-inositol hexakisphosphate). Phytate is the major storage form of phosphate in plant feeds, including cereals and legumes. Because monogastric animals such as pigs, poultry, and humans have little phytase in their gastrointestinal tracts nearly all of the ingested phytate phosphate is indigestible. Accordingly, these animals require supplementation of their diets with phytase or inorganic phosphate. In contrast, ruminants have microorganisms in the rumen that produce phytases and these animals do not require phytase supplementation of their diets. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Position demodulating method and circuit of disk apparatus Inventor(s): Hara, Takeyori; (Kawasaki, JP), Okamura, Eiji; (Kawasaki, JP), Takaishi, Kazuhiko; (Kawasaki, JP) Correspondence: Patrick G. Burns, ESQ.; Greer, Burns & Crain, LTD.; Suite 2500; 300 South Wacker DR.; Chicago; IL; 60606; US Patent Application Number: 20030063404 Date filed: January 11, 2002 Abstract: Position information PosN and PosQ are compared and position information Pos1 and Pos2 in which influences of an error of a position sensitivity gain appear oppositely are calculated. Subsequently, a weight gain G1=M and a weight gain G2=(1M) are obtained from the position information Pos1. A multiplication value obtained by multiplying the third position information Pos1 by the weight gain G1 and a multiplication value obtained by multiplying the fourth position information Pos2 by the weight gain G2 are added and synthesized, thereby calculating a decoded position. Excerpt(s): The invention relates to position demodulating method and circuit of a disk apparatus, for demodulating a position of a head in order to position the head to a target position. More particularly, the invention relates to position demodulating method and circuit of a disk apparatus, for calculating a decoded position from a position signal of a disk which was read by a head. A disk apparatus for reading a disk medium by a head comprises: a disk on which data is recorded; a motor for rotating the disk; the head for recording ad reproducing information on the disk; and an actuator for moving the head to a target position. As typical apparatuses, there are a magnetic disk apparatus known as a hard disk drive (HDD) and an optical disk apparatus known as a
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DVD-ROM or an MO. According to the invention, there are provided position demodulating method and circuit of a disk apparatus, in which a stairway at a switching boundary of position signals can be eliminated and, even if an error of position sensitivity occurs, a more accurate position can be demodulated. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Protein tyrosine phosphatase-1B (PTP-1B) deficient mice and assays for PTP-1B modulators Inventor(s): Elchebly, Mounib; (Montreal, CA), Gresser, Michael; (Les Cedres, CA), Kennedy, Brian; (Kirkland, CA), Payette, Paul; (St. Laurent, CA), Ramachandran, Chidambaram; (Pierrefonds, CA), Tremblay, Michel; (Dorval, CA) Correspondence: Merck & CO., INC.; Patent Department; P.O. Box 2000 - Ry60-30; Rahway; NJ; 07065-0907; US Patent Application Number: 20020138862 Date filed: July 30, 2001 Abstract: The present invention provides mice that have had their PTP-1B genes disrupted by targeted homologous recombination. The mice have no detectable PTP-1B protein, yet appear to be physiologically normal. However, in the fed state on a normal diet, the mice have half the level of circulating insulin as their wild-type littermates. In glucose and insulin tolerance tests, the mice show an increased insulin sensitivity. When fed a high fat, high carbohydrate diet, the mice show a resistance to weight gain as compared to their wild-type littermates.Methods of making the mice and cell lines derived from the mice are also provided.The present invention also provides methods of identifying inhibitors of the enzymatic activity of PTP-1B as well as inhibitors identified by such methods. Excerpt(s): The invention is directed to the field of transgenic mice containing a disrupted PTP-1B gene. The mice may contain a disruption in either one or both copies of the PTP-1B gene. In the case of mice containing a disruption in both copies of the PTP-1B gene, such mice lack detectable expression of PTP-1B protein. Protein tyrosine phosphatases (PTPases) are a large family of transmembrane or intracellular enzymes that dephosphorylate substrates involved in a variety of regulatory processes (Fischer et al., 1991, Science 253:401-406). Protein tyrosine phosphatase-1B (PTP-1B) is a.about.-50 kd intracellular protein present in abundant amounts in various human tissues (Charbonneau et al., 1989, Proc. Natl. Acad. Sci. USA 86:5252-5256; Goldstein, 1993, Receptor 3:1-15). Like other PTPases, PTP-1B has a catalytic domain characterized by the sequence motif (I/V)HCXAGXXR(S/T)G (SEQ.ID.NO.:1), containing arginine and cysteine residues that are critical to the enzyme's activity (Streuli et al., 1990, EMBO J. 9:2399-2407; Guan et al., 1990, Proc. Natl. Acad. Sci. USA 87:1501-1505; Guan & Dixon, 1991, J. Biol. Chem. 266:17026-17030). The amino terminal 35 amino acid residues of PTP-1B localize the protein to the endoplasmic reticulum (Frangioni et al., 1992, Cell 68:545-560). Determining which proteins are substrates of PTP-1B has been of considerable interest. One substrate which has aroused special interest is the insulin receptor. The binding of insulin to the insulin receptor results in autophosphorylation of the receptor, most notably on tyrosines 1146, 1150, and 1151 in the kinase catalytic domain (White & Kahn, 1994, J. Biol. Chem. 269:1-4). This causes activation of the insulin receptor tyrosine kinase, which phosphorylates the various insulin receptor substrate (IRS) proteins that propagate the insulin signaling event further downstream to mediate insulin's various biological effects.
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Regulation of weight Inventor(s): Alexi, Tajrena; (Auckland, NZ) Correspondence: Heller Ehrman White & Mcauliffe Llp; 275 Middlefield Road; Menlo Park; CA; 94025-3506; US Patent Application Number: 20020151522 Date filed: March 13, 2002 Abstract: Weight gain in a mammal, especially a human, having a condition that leads to decreased weight gain or weight loss, such as AIDS, brain trauma, a chronic neurodegenerative disease such as Alzheimer's disease, Parkinson's disease, Huntington's disease, or multiple sclerosis, or other condition, is promoted by increasing the effective concentration of a GPE-related compound (GPE or a GPE analog) in the central nervous system of the mammal. This increase may be achieved by administration to the mammal of an effective amount of a GPE-related compound, a prodrug thereof, or an implant containing cells that express the GPE-related compound or prodrug. Excerpt(s): This application claims the priority under 35 USC 119(e) of U.S. Provisional Application No. 60/278,562, filed Mar. 23, 2001, the disclosure of which is incorporated by reference into this application. This invention relates to methods of promoting weight gain. Weight loss after head injury is a common side effect (Pepe et al. (1999), The metabolic response to acute traumatic brain injury and implications for nutritional support, Journal of Head Trauma and Rehabilitation, 5: 462-474; Borzotta et al. (1994), Enteral versus parenteral nutrition after severe closed head injury, Journal of Trauma, 37(3): 459-468; Flakoll et al. (1995), Protein and glucose metabolism during isolated closed-head injury, American Journal of Physiology, 269(4Pt1): E636-E641). There are also no treatments currently available to prevent the cell death that occurs in the brain as a consequence of head injury. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Simethicone as weight gain enhancer Inventor(s): Gowan, Walter G. JR.; (Woodstock, GA), Gulian, Cynthia; (Lansdale, PA), Szymczak, Christopher; (Marlton, NJ) Correspondence: Audley A. Ciamporcero JR.; Johnson & Johnson; One Johnson & Johnson Plaza; New Brunswick; NJ; 08933-7003; US Patent Application Number: 20030072729 Date filed: April 15, 2002 Abstract: A film forming composition comprised of a film former and a weight gain enhancer selected from simethicone, polysorbate 80 and mixtures thereof, wherein the weight gain enhancer is used in an amount sufficient to increase the weight gain of the film forming composition on a substrate when dried. Excerpt(s): This Application is a continuation in part of United States application Ser. No. ______ (Attorney Docket No. MCP 303) filed Apr. 12, 2002, which claimed the benefit of U.S. application Ser. No. 60/291,127 filed on May 15, 2001 and U.S. application
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Ser. No. 60/325,726 filed Sep. 28, 2001, which are all incorporated by reference in their entireties herein. This invention relates to novel, water soluble, gelatin-free compositions for dip coating substrates, such as tablets and capsules, and methods for producing such dosage forms. This invention further relates to a method for increasing the weight gain of a water soluble, gelatin-free, film forming coating on a dip-coated tablet or caplet. During most of this century, hard gelatin capsules were a popular dosage form for prescription and over-the-counter (OTC) drugs. The ability to combine capsule halves having different colors provided manufacturers with a unique means of distinguishing various pharmaceutical products. Many patients preferred capsules over tablets, perceiving them as being easier to swallow. This consumer preference prompted pharmaceutical manufacturers to market certain products in capsule form even when they were also available in tablet form. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
SUBSTANCE TO PREVENT OR REVERSE WEIGHT GAIN INDUCED BY PSYCHOACTIVE AGENTS Inventor(s): MILLER, JON M.; (LOUISVILLE, KY) Correspondence: Donald L. Cox; Lynch, Cox, Gilman & Mahan; Aegon Center- Suite 2200; 400 W. Market; Louisville; KY; 40202; US Patent Application Number: 20030096808 Date filed: March 29, 1999 Abstract: A substance to prevent or reverse weight gain induced by psychoactive agents (10) having an antipsychotic drug (12) or mood stabilizing drug (14) in a concentration from 0.01% to 99.99% in combination with a histamine H2-receptor antagonist (16) in a concentration from 99.99% to 0.01%. The antipsychotic drug (12) is selected from a group consisting of olanzapine (12A), clozapine (12B), risperidone (12C), and quetiapine (12D). The antipsychotic drug (12) is typically in a concentration of 10% to 90%, 30% to 60% and 50%. The mood stabilizing drug (14) is selected from a group consisting of divalproex sodium (14A), valproic acid (14B), and mirtazapine (14C). The mood stabilizing drug (14) is typically in a concentration of 10% to 90%, 30% to 60% and 50%. The histamine H2-receptor antagonist (16) is selected from a group consisting of nizatidine (16A), famotidine (16B), cimetidine (16C) and ranitidine (16D). The histamine H2-receptor antagonist (16) is in a concentration of 90% to 10%. The histamine H2receptor antagonist (16) is typically in a concentration of 60% to 30% and 50%. Excerpt(s): The present invention relates to medications used for weight control. More particularly, the present invention relates to the use of a histamine H.sub.2-receptor antagonist with antipsychotic and mood stabilizing drugs to control weight. Numerous innovations for substances to prevent or reverse weight gain have been provided in the past. Even though these innovations may be suitable for the specific individual purposes to which they address, they differ from the present invention because they fail to describe or claim at least one combination of the features depicted in the present invention. Even though these innovations may be suitable for the specific individual purposes to which they address, they would not be suitable for the purposes of the present invention as heretofore described. The present invention prevents and reverses weight gain associated with the use of olanzapine and other antipsychotic drugs. The combination of psychoactive drugs and histamine H.sub.2-receptor antagonists may represent a combined single dose delivery system or multiple drug regimen taken at preselected times. The psychoactive drugs are dosed as recommended by the
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manufacturer and the histamine H.sub.2-receptor antagonists are dosed as for use in maintenance treatment of duodenal ulcer. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Tellurium containing nutrient formulation and process for enhancing the cumulative weight gain or feed efficacy in poultry Inventor(s): Albeck, Michael; (Ramat Gan, IL), Shmulewitz, Ascher; (Tel Aviv, IL), Sredni, Benjamin; (Kfar Saba, IL), Strassmann, Gideon; (Washington, DC) Correspondence: James V. Costigan, ESQ.; Hedman & Costigan, P.C.; Suite 2003; 1185 Avenue OF The Americas; New York; NY; 10036-2646; US Patent Application Number: 20030113409 Date filed: July 31, 2001 Abstract: A novel nutrient formulation containing tellurium for use in poultry, and a method of feeding it which improves subsequent livability, cumulative feed efficacy or weight gain is disclosed. Excerpt(s): This invention relates to a tellurium containing nutritional formulation that enhances the cumulative weight gain and feed efficacy in poultry. There is compelling evidence from the investigation of chick models that tellurium compounds act to influence the growth performance of chicks. The additive effects in increasing body weight are dose related and most significant at tellurium compound feed concentrations of 12.5 g/metric ton. The present invention is based on the discovery that the addition of a tellurium species to the diet of poultry a few days after hatching increases the growth rate of the young chicks. Prior research has shown that improvement of the quality of the nutrition of broilers have provided the possibility of increasing their growth rate in modem broiler strains. The increased growth is reflected in either an increased weight of the adult chicken, or a reduction in the period of time required for obtaining an adult chicken. The most dramatic growth rate increase is manifested primarily in the first four weeks after hatching. An increased growth rate in these first four weeks has been found to involve an increased weight of grown up broilers at the age of 42 days, an age that they are typically ready for consumption.(Zubair A. K., 52 WORLD POULTRY SCIENCE J. 189-201 (1996)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Topical administration of pharmacological compositions for non-systemic treatment of pruritus Inventor(s): Klein, Gerald L.; (Glendale, CA) Correspondence: Robert D Fish; Rutan & Tucker; 14th Floor; 611 Anton Boulevard; Costa Mesa; CA; 92626; US Patent Application Number: 20030212078 Date filed: March 26, 2003 Abstract: A pharmacological composition includes an anti-histaminic in spray formulation that reduces symptomatic skin itching of skin without substantially eliciting weight gain or sedation in the patient when the composition is sprayed onto the area of
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skin at a dosage of at least 10 mg/ml over a period of at least 10 applications. Particularly contemplated anti-histaminic include hydroxyzine and ketotifen. Excerpt(s): The field of the invention is topical treatment of pruritus. Pruritus is a relatively common symptom of various allergic and non-allergic conditions, and there are numerous drugs and pharmacological compositions known in the art to treat such conditions (and thereby concomitantly to reduce the pruritus). For example, hydroxyzine hydrochloride (1-(p-chlorobenzhydryl) 4-[2-(2-hydroxyethoxy)-ethyl] piperazine dihydrochloride) exhibits significant efficacy in systemic management of pruritus due to allergic conditions such as chronic urticaria, atopic and contact dermatoses, and in systemic histamine-mediated pruritus. Administration of Hydroxyzine for systemic treatment of pruritus typically employs oral delivery in tablets containing 10 mg, 25 mg, 50 mg, and 100 mg. Alternatively, Hydroxyzine can be ingested in liquid form as syrup at a hydroxyzine concentration of 10 mg/ml, or where oral administration is undesirable, hydroxyzine can be injected intramuscularly. In still another route of administration, Kanios et al. describe in U.S. Pat. No. 5,719,197 topical administration of Hydroxyzine in a substantially water insoluble formulation as a bioadhesive anti-histaminicum. Although Kanios' application of Hydroxyzine advantageously circumvents systemic administration, application of Hydroxyzine in a bioadhesive formulation is often undesirable, especially when applied over a relatively large area, or an area not covered by clothes (e.g., the face). Moreover, prolonged application of Hydroxyzine using Kanios' bioadhesive will at least to some extent result in systemic delivery of Hydroxyzine, which may lead to undesirable side effects, including drowsiness and tachycardia. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Transgenic expression of glycogen synthase kinase 3 in muscle Inventor(s): Garofalo, Robert S.; (Niantic, CT), Orena, Stephen J.; (Gales Ferry, CT), Schachter, Joel B.; (East Lyme, CT) Correspondence: Pfizer INC.; Patent Department, Ms8260-1611; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20030163836 Date filed: December 18, 2002 Abstract: The invention features a transgenic non-human mammal expressing or capable of expressing a GSK-3 transgene comprising a GSK-3 coding sequence, wherein expression of said coding sequence in the mammal is driven by an operably linked regulatory sequence that directs inducible expression in muscle. Following the induction of transgene expression, the transgenic non-human mammal exhibits hyperinsulinemia, increased weight gain on a high fat diet, and/or decreased muscle glycogen content on a high fat, as compared to a control animal not expressing the GSK-3 transgene. The invention also features methods of identifying in vivo modulators of GSK-3 activity. Excerpt(s): This application claims priority, under 35 U.S.C.sctn.119(e), from U.S. Provisional Application Ser. No. 60/343,479, filed Dec. 21, 2001. The invention features transgenic non-human mammals comprising a glycogen synthase kinase-3 (GSK-3) coding sequence that is operably linked to a regulatory sequence that directs inducible expression in muscle. These mammals exhibit hyperinsulinemia, increased weight gain on a high fat diet, and decreased muscle glycogen content on a high fat diet. The invention also features methods of identifying agents that modify in vivo GSK-3
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activity. GSK-3 was initially described as a key enzyme involved in glycogen metabolism, but is now known to regulate diverse cellular functions, including protein synthesis as well as glycogen metabolism (Cohen and Frame, Nature Reviews 2: 769-76, 2001). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Transgenic mice containing alpha-endosulfine gene disruptions Inventor(s): Baribault, Helene; (Redwood City, CA), Wiles, Michael V.; (Menlo Park, CA), Zhang, Qin; (Pleasanton, CA) Correspondence: Deltagen, INC.; 740 Bay Road; Redwood City; CA; 94063; US Patent Application Number: 20020137203 Date filed: December 13, 2001 Abstract: The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising mutations in a alpha-endosulfine gene. Such transgenic mice are useful as models for disease and for identifying agents that modulate gene expression and gene function, and as potential treatments for various disease states and disease conditions. The present invention also relates to diabetes and diabetic condition, as it demonstrates the role of the alpha-endosulfine in diabetes and diabetic conditions. The present invention further relates to weight gain and weight related conditions, such as obesity, and demonstrates the role of the alpha-endosulfine in weight gain and weight related conditions, such as obesity. In accordance with these aspects, the present invention provides methods and compositions useful in identifying, testing, and providing treatments for diabetes and diabetic conditions, weight gain and weight related conditions such as obesity. Excerpt(s): This application claims priority to U.S. Provisional Application No. 60/256,195 filed Dec. 13, 2000, the entire contents of which is incorporated herein by reference. The present invention relates to transgenic animals, compositions and methods relating to the characterization of gene function. Diabetes is defined as a state in which carbohydrate and lipid metabolism are improperly regulated by the hormone insulin (For review, see, e.g., Saltiel, Cell 104:517-529(2000)). Two major forms of diabetes have been identified, type I and II. Type I diabetes represents the minor form of the disease, affecting 5-10% of diabetic patients. It is thought to result from the autoimmune destruction of the insulin-producing beta cells of the pancreatic Islet of Langerhans. Exogenous administration of insulin typically alleviates the pathophysiology. Type II diabetes is the most common form of the disease and is possibly caused by a combination of defects in the mechanisms of insulin secretion and action. Both forms, type I and type II, have similar complications, but distinct pathophysiology. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with weight gain, you can access the U.S. Patent Office archive via the Internet at the following Web address:
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http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “weight gain” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on weight gain. You can also use this procedure to view pending patent applications concerning weight gain. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON WEIGHT GAIN Overview This chapter provides bibliographic book references relating to weight gain. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on weight gain include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “weight gain” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on weight gain: •
Do Carbohydrates Make You Fat? Source: Health. p.44,46,48. October 1998. Summary: Mason examines the weight loss hypothesis of Leighton Steward in his book `Sugar Busters.' According to Steward, eating too many carbohydrates stimulates the body to produce insulin, which in turn stimulates the liver to produce blood fats. Steward says this is what causes individuals to gain weight. The answer, Steward claims, is to consume few carbohydrates. Mason spoke with several nutrition experts, all of whom explain the fallacies behind Steward's thinking. The healthy body produces very small amounts of insulin, according to Gerald Reaven of Stanford University. Even if there is a relationship between insulin production and weight gain (which is controversial in nutritional circles), says Reaven, the tiny amount of insulin the body produces could not cause large changes. In addition, switching kinds of carbohydrates, as Steward suggests, does not change insulin levels, according to Reaven. Mason says that the Sugar Busters diet is not healthy because it relies on meat and dairy products,
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which are high in saturated fats, and because it reduces the amount of fruits and vegetables, and therefore the amounts of vitamins and minerals. •
Carbohydrates and Weight Management Source: Washington, DC: International Life Sciences Institute, Technical Committee on Carbohydrates, 61p., 1998. Contact: ILSI Press, International Life Sciences Institute, 1126 Sixteenth St., NW, Washington, DC 20036-4810. (202) 659-0074. Fax (202) 659- 3859. Summary: Rolls and Hill discuss the role of carbohydrates in weight gain and obesity. They review the areas of carbohydrate effects on hunger, satiety and food intake; diet composition and body weight regulation; and carbohydrate effect on nutrient metabolism. They suggest that total fat consumption has not declined since 1971, but Americans have become less physically active and many have quit smoking. Smoking cessation, according to Rolls and Hill, is associated with weight gain. They suggest that weight gain is best prevented, and weight loss is best promoted, by consuming a diet high in carbohydrates and fiber. Low-fat, high-carbohydrate diets are most effective at maintaining weight loss and preventing obesity. They recommend a diet high in carbohydrates for weight control.
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Practical Insulin: A Handbook for Prescribers Source: Alexandria, VA: American Diabetes Association. 2002. 59 p. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $7.95 plus shipping and handling. ISBN: 1580401538. Summary: The medical practice of many physicians now includes handling everincreasing numbers of patients with diabetes. Insulin therapy is a medical necessity for all patients with type 1 diabetes and the many patients with type 2 diabetes who cannot reach their glycemic (levels of blood glucose) without insulin therapy. This handbook offers solutions to the many common challenges involved in prescribing insulin, from choosing insulin regimens, to dealing with patient reluctance to start insulin therapy, to minimize the weight gain that often accompanies improved glycemic control. Specific topics include patient selection, insulin choices, the different types of insulin and their character, mixing insulins, insulin regimens (for type 1 and for type 2 patients), troubleshooting, patient SMBG (self monitoring of blood glucose) records, and patient education. The handbook also includes numerous appendices: endogenous insulin action, insulin storage, insulin potency, additives, insulin delivery, insulin pump, and determining insulin-to-CHO (carbohydrates) ratio. The author notes that there are no standards for how to best use insulin therapy; individual patient strategies must be implemented. 11 figures. 11 tables.
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101 Medication Tips for People with Diabetes Source: Alexandria, VA: American Diabetes Association. 1999. 122 p. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $14.95 plus shipping and handling. ISBN: 1580400329. Order number 483301.
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Summary: This book answers 101 of the most commonly asked questions about diabetes and medications to help readers become active members of their health care team, maximize their diabetes management, and stay well. Questions in chapter one provide general information on medications used to treat diabetes. Chapter two focuses on how to get the most out of oral medications. The third chapter deals with common side effects of oral medications, including gastrointestinal and liver problems, weight gain, lactic acidosis, and hypoglycemia. Questions in chapter four provide general information on the use of insulin in type 2 diabetes. This is followed by a chapter that explains how to get the most out of insulin therapy. Chapter six identifies the common side effects of insulin, including weight gain. Questions in the next chapter deal with the meditations used to treat complications, including nonprescription analgesics, tricyclic antidepressants, capsaicin cream, angiotensin converting enzyme inhibitors, laxatives, and calcium channel blockers. This is followed by chapters that answer questions about the effect of medications on diabetes; the use of nonprescription medications such as aspirin, cold and allergy medications, herbal supplements, weight loss products, and vitamin and mineral supplements; and common drug interactions that occur with diabetes medications. The final chapter answers miscellaneous questions. The book also includes a glossary and an index. •
Nutrition and the pregnant adolescent: A practical reference guide Source: Minneapolis, MN: Center for Leadership, Education, and Training in Maternal and Child Nutrition, University of Minnesota. 2000. 247 pp. Contact: Available from Kathy Kosiak, University of Minnesota School of Public Health, Division of Epidemiology, 1300 South Second Street, Suite 300, Minneapolis, MN 554541015. Telephone: (612) 626-7933 / fax: (612) 624-0315 / e-mail:
[email protected]. Available at no charge. Summary: This book focuses on clinical application of current knowledge on adolescent pregnancy emphasizing assessment, management, counseling approaches, and strategies to promote dietary change and adequate weight gain. It is written for health professionals and educators involved in the care of pregnant adolescents. Topics covered include adolescent development, nutritional needs and eating behavior, nutrition assessment, interviewing, counseling, prenatal education, and postpartum care.
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Tell Me What to Eat If I Have Diabetes Source: Franklin Lakes, NJ: Career Press, Inc. 1999. 157 p. Contact: Available from Career Press, Inc. 3 Tice Road, P.O. Box 687, Franklin Lakes, NJ 07417. (800) 227-3371. Website: www.careerpress.com or www.newpagebooks.com. PRICE: $10.99 plus shipping and handling. Summary: This book offers eating and nutrition guidelines for people who have been diagnosed with diabetes mellitus. The author focuses on type 2 diabetes, noting that diabetes can manifest differently in different patients and sometimes even changing throughout its course within one person. The author encourages readers to learn as much as they can about their disease and to utilize nutrition as an adjunct therapy and a vital component of their diabetes care. The author emphasizes the importance of following a personalized eating plan that helps keep blood glucose (sugar) levels normal, and helps protect against heart disease and weight gain without making the patient feel deprived. The book offers seven chapters that cover an overview of diabetes, the top 7 profiles of type 2 diabetes, working with a dietitian to manage diabetes, ten
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food steps to freedom, 20 recommended recipes, food shopping guidelines, and eating out at restaurants. Two of the ten recommended 'food' steps actually do not involve food: one involves monitoring the blood glucose (sugar) levels; the other the need for regular exercise. The eight remaining recommended food steps are: make dietary fiber a part of almost every meal; count carbohydrates; emphasize heart-protective fats; keep saturated fat and cholesterol low; count caloric intake; eat more fruits and vegetables; avoid eating large meals; and improve the diet with supplements as necessary. Recipes are provided for a light Denver omelet, egg muffin sandwich lite, sun dried tomato pesto spread, the Loxness monster spread, apple lover's oatmeal, honey wheat bread with flaxseed, flaxseed jam muffins, flaxseed focaccia, flaxseed maple scones, high legume fried rice, 3 minute burrito, pintos and cheese, quick fix chili and fries, lemon dijon salmon, simple salmon pasta salad, easy omega 3 fatty acid tuna sandwich, oat bran meat loaf, light club sandwich, monosaturated side salad, easy 3 bean salad, quick ranch dip with vegetables, spicy hummus with crudites and crackers, iced caf mocha, and oatmeal raisin bites. A brief subject index concludes the book. •
Medical Management of Pregnancy Complicated by Diabetes. 3rd ed Source: Alexandria, VA: American Diabetes Association. 2000. 176 p. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $39.95 plus shipping and handling. ISBN: 1580400132. Summary: This book, which is part of the American Diabetes Association's Clinical Education Series, provides health professionals with protocols that have resulted in healthy infants in pregnancies complicated by type 1, type 2, or gestational diabetes. The first section focuses on prepregnancy counseling and management of women with preexisting diabetes or previous gestational diabetes. The next section discusses contraceptive methods, including oral contraceptives, the norplant system, barrier methods, intrauterine devices, the rhythm method, and permanent sterilization. This is followed by a section that examines the psychological impact of diabetes and pregnancy. Topics include the response to pregnancy in women with preexisting diabetes, the response to a diagnosis of gestational diabetes, long term adaptation, personality types and individualizing treatment, pregnancy crises, and the importance of a team approach and a support system. The fourth section focuses on blood glucose monitoring. Topics include glycosylated hemoglobin measurements in pregnancy for women with preexisting or gestational diabetes, self monitoring of blood glucose and urine ketones, and medical tests to evaluate maternal status in women with preexisting or gestational diabetes. The next section offers guidelines for managing morning sickness with dietary remedies, insulin adjustments, and medical management. The sixth section discusses nutritional management during pregnancy in women with preexisting diabetes. Topics include patient responsibility; the nutrient needs of pregnancy; diet and eating habits; vitamin and mineral supplementation; calorie level; weight gain; meal planning; recordkeeping; use of sodium, caffeine, and artificial sweeteners; the management of hypoglycemia; and postpartum nutritional management. Section seven focuses on the use of insulin during pregnancy in women with preexisting diabetes. Topics include metabolic alterations during normal gestation, therapeutic insulin use, dosage adjustment, insulin during labor and delivery, postpartum insulin requirements, and oral hypoglycemic agents. The next section describes diagnostic tests and methods of fetal surveillance, including ultrasonography, alpha fetoprotein testing, genetic testing, fetal monitoring, and amniocentesis. The ninth
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section discusses gestational diabetes, focusing on epidemiology, screening, diagnosis, nutritional management, insulin therapy, exercise, and obstetric management. Section ten addresses the issue of neonatal care of infants of women with diabetes. Topics include perinatal mortality and morbidity, resuscitation, nursery care, and long term followup. The final section discusses postpartum followup of women with gestational diabetes. The book includes an index and resources for health care professionals. 3 figures. 39 tables. Numerous references. •
Pregnancy After a Loss: A Guide to Pregnancy After a Miscarriage, Stillbirth, or Infant Death Source: New York, NY: Berkley Books/Penguin Putnam, Inc. 1999. 391 p. Contact: Available from Berkley Books/Penguin Putnam, Inc., 375 Hudson Street, New York, NY 10014. (800) 788-6262 (orders), (800) 631-8571 (customer service hotline), (800) 227-9604 (Fax),
[email protected] (E-mail), http://www.penguinputnam.com (Web Site). $14.95. ISBN 0-425-17047-0. Summary: This book, written by a woman who lost her son, Patrick, to an umbilical cord problem on her due date, is designed to give hope and practical information to other women who have suffered a pregnancy loss. The author interviewed nearly 100 women while writing this book, all of whom made it through pregnancy after a loss and now have one or more healthy babies. The book focuses on the feelings that are unique to women who have suffered a pregnancy loss, and provides advice on reducing anxiety. Medical aspects of pregnancy loss are described in simple, straightforward language. Chapter 1 takes readers down the road that a bereaved mother would travel to find out why her baby died. This chapter covers the followup visit with the obstetrician, which is when the parents discuss the autopsy and any genetic testing that was done on the baby. If these do not provide an answer, the doctor may suggest that the mother be tested for autoimmune disorders, uterine abnormalities, genetic disorders, viral and bacterial infections, and hormone imbalances. Other common reasons for pregnancy loss are described (i.e., neural tube defects, placental problems, umbilical cord problems, incompetent cervix, and maternal illness) as are common reasons for early infant death: congenital problems, streptococcus infection, and sudden infant death syndrome. Chapter 2 discusses the subject of getting ready to get pregnant again, both physically and emotionally. This chapter covers the advantages and disadvantages of getting pregnant right away, factors that will affect one's decision to get pregnant, when partners disagree on the timing of another pregnancy, and where to find support and guidance during the decision-making process. Even if a woman has waited 6 months or a year to get pregnant again, there are certain things she should do to prepare for the pregnancy. Mothers to be should get a thorough physical exam; get into shape; take folic acid; keep track of her periods; and avoid drugs, alcohol, and cigarettes. This chapter also covers the pros and cons of choosing a new doctor or staying with the old one, questions one should ask each doctor under consideration, the stress of not getting pregnant right away, infertility problems and treatment, and when the pregnancy is a surprise. Chapter 4 focuses on the first trimester of a new pregnancy, including concerns over telling others about the pregnancy, suggestions for alleviating the anxiety, what to expect during the prenatal visits, tests one can have done at this time, and the signs of an impending miscarriage. Chapter 5 focuses on the second trimester, including concerns about answering awkward questions, the gender of the baby, delivering too early, exercising, and sexual intercourse. Feelings that may be common during this trimester are panic over the baby's movements, reluctance to bond with the baby, anxiety about surpassing the anniversary of the previous baby's death, superstitions
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about the pregnancy, and fear. Prenatal tests that can be offered at this time and symptoms that are not normal during the second trimester also are covered. Chapter 6 examines the concerns mothers are likely to have during the third trimester regarding early delivery, setting up the nursery, baby shower offers, choosing a name, and excessive weight gain. Feelings that may be common during this time include obsession over the baby's movements, constant worry, and being annoyed by unsolicited advice. Tips for alleviating the anxiety include taking a prepared childbirth class, writing a birth plan, getting a doula, calling the doctor frequently, insisting on frequent prenatal visits, eliminating unnecessary stress, and practicing relaxation techniques. The nature of prenatal visits during the third trimester, tests that are usually done at this time, monitoring the baby's kicks, and danger signals in late pregnancy also are discussed. Chapter 7 deals with the truly high-risk pregnancy. Common reasons for high-risk status are a history of preterm labor or delivery, incompetent cervix, impending multiple birth, history of placental problems, history of two or more miscarriages, genetic problems, chronic medical conditions, and pregnancy after age 35. Bed rest is a commonly prescribed treatment in high-risk pregnancies. This chapter provides suggestions for surviving extended bed rest as well as a chart of activities to help mothers and their OB/GYNs mutually define what she can and can't do. Other topics that are discussed include hospitalization, the impact of that and bed rest on family and career, selective reduction in cases of multiples, feelings that are common among mothers during bed rest, and tips for relieving the anxiety. The signs and treatment of preterm labor also are discussed. Chapter 8 deals with labor and delivery, including fetal monitoring during labor, bonding with the baby, feelings commonly reported after birth, what to expect if your baby goes to the NICU, and tips for relieving anxiety. Chapter 9 talks about the consequences of pregnancy loss on parenting the subsequent child. It is common for parents to feel anxious and overprotective, but their loss also may make them exceptional parents. There is often continued sadness and introspection and a totally changed outlook on life. This chapter also reviews some of the private and public ways in which parents have chosen to remember their infants who died. Chapter 10 looks at pregnancy after a loss from a father's perspective, including feelings that are common to fathers who are expecting again and ways in which the mother can ease her spouse's anxiety. A list of resources includes support organizations for pregnancy and infant loss, high-risk pregnancy, subsequent pregnancy, infertility, and pregnancy/childbirth; publishers of relevant books; and internet resources. •
Eating Hints for Cancer Patients: Before, During and After Treatment Source: Bethesda, MD: National Cancer Institute (NCI), National Institutes of Health (NIH). 1999. 60 p. Contact: Available from National Cancer Institute (NCI). Publications Ordering Service, P.O. Box 24128, Baltimore, MD 21227. Voice (800) 422-6237. TTY (800) 332-8615. Fax (301) 330-7968. PRICE: Single copy free; bulk rates available. NIH Publication Number 99-2079. Summary: This booklet contains a variety of ideas about food needs and eating problems that patients undergoing cancer therapy may encounter. The authors emphasize the need for eating well during cancer treatment and outline the nutrition problems that may arise with different cancer treatments. Strategies for coping with side effects are provided for loss of appetite, sore mouth or throat, changed sense of taste or smell, dry mouth, nausea, vomiting, diarrhea, constipation, weight gain, tooth decay, and lactose intolerance. The next section provides suggestions for increasing protein and calorie intake, including the use of healthy snacks. Another section discusses diets for
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patients with special needs, including the clear liquid diet, full liquid diet, soft diet, fiber restricted diet, low lactose diet, and commercial products to improve nutrition. The booklet includes a glossary of related terms and the contact information for two resource organizations: the Cancer Information Service (800-422-6237) and the American Cancer Society (800-227-2345). The booklet then provides 40 pages of recipes designed to help patients achieve better nutrition during cancer treatment. A recipe index is provided. Colorful drawings illustrate the booklet. 8 tables. •
Healthy Eating for a Healthy Life Source: Washington, DC: American Association of Retired Persons (AARP). 1994. 26 p. Contact: Available from AARP Fulfillment. 601 E Street, NW, Washington, DC 20049. PRICE: Single copy free. Stock number D15565 (mention when ordering). Summary: This booklet encourages older readers to adopt healthy eating patterns for a healthy quality of life. The authors address weight problems from both ends of the spectrum: too much and too little. Seven sections cover: the measurement of nutritional health; how good nutrition and exercise can improve quality of life; the USDA Food Guide Pyramid and how to use it; food labels and nutrition facts; special dietary concerns, including weight loss, weight gain, and dietary supplements; eating at restaurants; and taking control of one's health. A final section provides resource lists of national organizations, community resources, and other AARP publications that may be of interest. The booklet is written in non-technical language.
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Understanding Gestational Diabetes: A Practical Guide to a Healthy Pregnancy. Revised ed Source: Bethesda, MD: National Institute of Child Health and Human Development. 1993. 46 p. Contact: Available from National Diabetes Information Clearinghouse (NDIC). 1 Information Way, Bethesda, MD 20892-3560. (800) 860-8747 or (301) 654-3327. E-mail:
[email protected]. PRICE: Single copy free. Bulk copies available from National Institute of Child Health and Human Development. 31 Center Drive, MSC 2425, Building 31, Room 2A32, Bethesda, MD 20892. (301) 496-5133. Summary: This booklet for pregnant women and their families explains gestational diabetes and its impact on the health of mother and baby. It addresses many questions about diet, exercise, measurement of blood glucose levels, and general medical and obstetric care of women with gestational diabetes. Screening methods for gestational diabetes are discussed. The primary focus of this health guide is on diet and weight gain. Several tables are included to assist the pregnant woman in following a nutritionally sound diet that fosters an appropriate weight gain and that keeps blood glucose levels as normal as possible. Footnotes cite 4 bibliographic citations and a brief glossary is included. Blank Self Blood Glucose Monitoring Diary and Food and Exercise Record Sheet charts are appended.
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Nutrition in pregnancy and lactation. (5th ed.) Source: St. Louis, MO: C.V. Mosby Company. 1993. 537 pp. Contact: Available from C.V. Mosby Company, 11830 Westline Industrial Drive, Saint Louis, MO 63146. Telephone: (800) 325-4177 or (314) 872-8370 / fax: (314) 432-1380. $27.95 plus $3.50 shipping and handling,10 percent discount for orders of 10 books or more. (ISBN 0-8016-6569-8).
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Summary: This comprehensive textbook on maternal nutrition and lactation provides information on nutrient deficiencies and excesses during pregnancy, kilocalorie requirements of pregnancy, weight gain guidelines for various subgroups of pregnant women, hyperemesis gravidarum, maternal diabetes mellitus, PKU, human milk composition, and adolescent pregnancy. •
Health diary: Myself, my baby. (2nd ed.) Source: Rockville, MD: Health Resources and Services Administration, U.S. Department of Health and Human Services. 1994. 90 pp. Contact: Available from Superintendent of Documents, U.S. Government Printing Office, P.O. Box 371954, Pittsburgh, PA 15250-7954. Telephone: (202) 512-1991 for public information (D.C. office) or (202) 512-1800 for ordering and publication information (D.C. office) / fax: (202) 512-1293 (public information); (202) 512-2250 (ordering) / Web site: http://www.access.gpo.gov. $9.00; also available from the Web site www.nmchc.org at no charge. Summary: This diary is designed to help the pregnant woman keep a record of prenatal care and health care of the baby up to the age of two years. Beginning pages contain space for the mother's health history and notes on her symptoms of pregnancy. Subsequent pages explain how to get prenatal care, what to expect at prenatal care visits, and key components of a healthy pregnancy. There is space to make dietary notes, track weight gain, and keep a schedule of prenatal visits. Section one ends with advice on postpartum care and family planning. In section two of this book the mother develops a record of the baby's birth, health care, and early development.
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Practical Carbohydrate Counting: A How-to-Teach Guide for Health Professionals Source: Alexandria, VA: American Diabetes Association. 2001. 59 p. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $12.95 plus shipping and handling. ISBN: 1580401236. Summary: This handbook helps health care providers teach patients with diabetes how to use carbohydrate counting as one part of their diabetes management plan. In basic carbohydrate counting, goals are to draw attention to the foods that contain carbohydrate, and to encourage people to eat consistent amounts of carbohydrate at meals and snacks (if necessary or desired) at similar times each day. Advanced carbohydrate counting is appropriate for people who use multiple daily injections (MDI) of insulin or continuous subcutaneous insulin infusion (CSII) via an insulin pump. Their goal is to learn to match the amount of rapid (lispro or aspart) or short acting (regular) insulin they take with or before eating to the amount of carbohydrate they choose to eat. This handbook includes five chapters: the case for carbohydrate counting, including educator skills and time, and helpful carbohydrate counting teaching tools; basic carbohydrate counting, including case studies; advanced carbohydrate counting, including case studies; and special considerations and situations, including high protein and high fat meals, adjusting insulin for fiber content, glycemic index, weight gain, restaurant meals, special food situations, alcohol, activity and exercise, and sick day management and stress. The handbook also lists resource organizations through which readers can gain access to diabetes educators and registered dietitians. Appendices include a chart of glycemic control target goals for people with diabetes; a meal planning form, a list of carbohydrate counting resources, a recordkeeping form for
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carbohydrate counting, a teaching checklist, a chart of recommended amounts of carbohydrates for different weight loss programs and different patients by age and gender. The handbook concludes with a brief subject index and basic information about the American Diabetes Association. 23 references. •
Annual Review of Diabetes 2003 Source: Alexandria, VA: American Diabetes Association. 2003. 168 p. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. E-mail:
[email protected]. Fax: (770) 4429742. Website: www.diabetes.org. PRICE: $49.95 plus shipping and handling. Summary: This issue of the Annual Review of Diabetes includes twenty research articles in three categories: epidemiology and pathogenesis, treatment, and complications. Specific topics include the rise of childhood type 1 diabetes in the 20th century; immunological markers in the diagnosis and prediction of autoimmune type 1a diabetes; adults with prediabetes; the energy homeostasis system and weight gain; the metabolic syndrome and incidence of type 2 diabetes; the peroxisome proliferator; the use of oral glucose tolerance tests in clinical practice; the economic costs of diabetes in the United States; diet and exercise among adults with type 2 diabetes; trends for achieving weight loss and increased physical activity; postprandial (after a meal) glucose control; strategies for the treatment of dyslipidemia; self-management education of adults with type 2 diabetes and its impact on glycemic control; common drug pathways and interactions; the interactions of prescribed medications and over-thecounter medications; obstructive sleep apnea in patients with diabetes; gestational diabetes and the incidence of type 2 diabetes; glucose monitoring in gestational diabetes; genetic studies of late diabetes complications; and eating disorders in adolescent girls and young adult women with type 1 diabetes. Each article concludes with a list of references.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “weight gain” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “weight gain” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “weight gain” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Conquering the Fatique, Depression, and Weight Gain by Valerie Saxion (2003); ISBN: 0972456392; http://www.amazon.com/exec/obidos/ASIN/0972456392/icongroupinterna
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Dr. David Reuben's Quick Weight-Gain Program (tm) : Safe, Easy Weight Gain for Every Age and Situation by M.D. David Reuben (Author); ISBN: 0517702053; http://www.amazon.com/exec/obidos/ASIN/0517702053/icongroupinterna
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Eat Up!: The Healthy Weight Gain Cookbook by Lee Gold; ISBN: 073440395X; http://www.amazon.com/exec/obidos/ASIN/073440395X/icongroupinterna
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Elizabeth Takes Off: On Weight Gain, Weight Loss, Self Image, and Self-Esteem by Elizabeth Taylor; ISBN: 0399132694; http://www.amazon.com/exec/obidos/ASIN/0399132694/icongroupinterna
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Food Combining 2-Day Detox: Beat Weight Gain & Protect Your Health the All Natural Way by Kathryn Marsden; ISBN: 1891696041; http://www.amazon.com/exec/obidos/ASIN/1891696041/icongroupinterna
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From Conception to Healthy Childbirth With Minimal Weight Gain, and Through the Terrible 2's and 3's: ¹Teaching Your Child How to Think Smart, and Not to Cry and Act Like a Baby by Diane Patton; ISBN: 1891950150; http://www.amazon.com/exec/obidos/ASIN/1891950150/icongroupinterna
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Is Your House Making You Overweight, Sick, or Tired?: Household Causes Including Improper Electricity of Weight Gain, Stress, Insomnia and Ill Health, by Margaret Rouse Shontz (2003); ISBN: 0972324372; http://www.amazon.com/exec/obidos/ASIN/0972324372/icongroupinterna
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Marriage Made Me Fat!: Understand Your Weight Gain-And Lose Pounds Permanently by Edward, Ph.D. Abramson, Edward Abramson; ISBN: 1575665565; http://www.amazon.com/exec/obidos/ASIN/1575665565/icongroupinterna
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Nature's Medicines : From Asthma to Weight Gain, from Colds to High Cholesterol -The Most Powerful All-Natural Cures by Gale Maleskey, et al (1999); ISBN: 1579540287; http://www.amazon.com/exec/obidos/ASIN/1579540287/icongroupinterna
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Nutrition and weight gain during pregnancy : a staff development program in perinatal nursing care by Grace G. Johnson; ISBN: 0865250057; http://www.amazon.com/exec/obidos/ASIN/0865250057/icongroupinterna
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Nutrition During Pregnancy : Part 1 : Weight Gain, Part 2 : Nutrient Supplements by Institute of Medicine; ISBN: 0309041384; http://www.amazon.com/exec/obidos/ASIN/0309041384/icongroupinterna
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Potatoes Not Prozac: A Natural Seven-step Dietary Plan to Control Depression, Food Cravings and Weight Gain by Kathleen DesMaisons; ISBN: 0684851490; http://www.amazon.com/exec/obidos/ASIN/0684851490/icongroupinterna
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Potatoes Not Prozac: How to Control Depression, Food Cravings and Weight Gain by Kathleen Demaisons; ISBN: 0671773771; http://www.amazon.com/exec/obidos/ASIN/0671773771/icongroupinterna
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Reversing the Weight Gain Spiral : Self Care for Life Long Weight Loss by Merlene Miller (Author); ISBN: 034536984X; http://www.amazon.com/exec/obidos/ASIN/034536984X/icongroupinterna
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Stress Relief: Enjoy Eating Without the Weight Gain, over 200 Anti-Stress Foods and Meal Pains by Margaret Carter Dean; ISBN: 0874919932; http://www.amazon.com/exec/obidos/ASIN/0874919932/icongroupinterna
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The ferret : some observations on photoperiod and gonadal activity, and their role in seasonal pelt and bodyweight changes : the synergistic effect of oestrogen and progesterone on weight gain : and a comparative study of the corpus luteum of the ferret and the rabbit by John Hammond; ISBN: 0950340006; http://www.amazon.com/exec/obidos/ASIN/0950340006/icongroupinterna
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The Premenstrual Syndrome: Depression, Pmt, Weight Gain, Aggression by Caroline Shreeve; ISBN: 0722508298; http://www.amazon.com/exec/obidos/ASIN/0722508298/icongroupinterna
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Weight Gain: Unabridged Version by Barrie Konicov; ISBN: 1856729508; http://www.amazon.com/exec/obidos/ASIN/1856729508/icongroupinterna
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Why Can't I Lose Weight?: Is Your Weight Gain a Symptom of a Hidden Health Problem? by Martin L. Budd (2002); ISBN: 0007120656; http://www.amazon.com/exec/obidos/ASIN/0007120656/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “weight gain” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
Effects of cigarette smoking and maternal weight gain on the outcome of pregnancy Author: Naeye, R. L.; Year: 1986; M.S. Hershey Medical center, Hershey, Pennsylvania, 1978
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Inadequate weight gain in breastfeeding infants: assessments and resolutions Author: Desmarais, Linda.; Year: 1980; Schaumburg, IL: La Leche League International, c1990; ISBN: 0912500670
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The weight gain of last-born children under 5 years in Bali, 1985 Author: Suryadhi, N. T.; Year: 1987; Canberra, Australia, Australian National University, Department of Demography, International Population Dynamics Program, 1986
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Weight gain and the outcome of pregnancy Author: Naeye, R. L.; Year: 1978; M.S. Hershey Medical Center, Hershey, Pennsylvania, 1978
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Weight gain during adolescent pregnancy: associated maternal characteristics and effects on outcome Author: Scholl, T. O.; Year: 1984; [1987]
Chapters on Weight Gain In order to find chapters that specifically relate to weight gain, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and weight gain using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates 11
In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
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and language you prefer, and the format option “Book Chapter.” Type “weight gain” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on weight gain: •
Acarbose: 'The European Experience' Source: in Cooper, J.W. Diabetes Mellitus in the Elderly. Binghamton, NY: Pharmaceutical Products Press. 1999. p. 47-59. Contact: Available from Pharmaceutical Products Press. 10 Alice Stret, Binghamton, NY 13904-1580. (800)429-6784. E-mail:
[email protected]. Website: www.haworthpressinc.com. PRICE: $49.95 plus shipping and handling. ISBN: 0789006820. Summary: Acarbose, an alpha glucosidase inhibitor, delays carbohydrate digestion, and thereby decreases postprandial (after a meal) blood glucose (sugar) levels. Acarbose is a useful drug, especially for the treatment of obese subjects with type 2 diabetes mellitus who fail first line therapy with diet and exercise. This article on the use of acarbose is from a volume that is devoted to the diagnosis and treatment of diabetes mellitus in the elderly. The authors present 'The European Experience' with acarbose, noting its use as first line therapy in individuals with diabetes in whom postprandial hyperglycemia (high levels of blood glucose) is significantly greater than fasting hyperglycemia, and in elderly patients with mild diabetes who are at high risk for hypoglycemia (low levels of blood glucose). No weight gain has been described with acarbose and it is effective with high carbohydrate intake. The drug is also useful in combinations with other oral hypoglycemic agents and with insulin. In type 1 subjects, acarbose may reduce glycemic fluctuations and reduce insulin dosage. Acarbose may reduce episodes of midevening and nocturnal hypoglycemia. The disadvantage of acarbose is its gastrointestinal side effects of flatulence (gas) and diarrhea; these side effects can be minimized by slowly adjusting the doses according to the patient's symptoms. 59 references.
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Sprue Syndromes Source: in Brandt, L., et al., eds. Clinical Practice of Gastroenterology. Volume One. Philadelphia, PA: Current Medicine. 1999. p. 484-493. Contact: Available from W.B. Saunders Company. Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 545-2522. Fax (800) 874-6418 or (407) 352-3445. Website: www.wbsaunders.com. PRICE: $235.00 plus shipping and handling. ISBN: 0443065209 (two volume set); 0443065217 (volume 1); 0443065225 (volume 2). Summary: Celiac sprue is a disease of the small intestine resulting from a sensitivity to gluten, the water insoluble protein of wheat, and characterized by various degrees of villous atrophy (wasting of the villi of the small intestine) and malabsorption. Tropical sprue is an idiopathic disease of the small intestine that is acquired in tropical regions. Although the clinical and histologic findings superficially may resemble those of celiac sprue, treatment is different. This chapter on sprue syndromes is from a lengthy textbook that brings practitioners up to date on the complexities of gastroenterology practice, focusing on the essentials of patient care. Most patients with celiac sprue improve after withdrawal of gluten from their diets, but a few have a more complex course or develop one or more associated extraintestinal diseases. Celiac disease is characterized by poor food absorption and intolerance to gluten. The clinical features at presentation depend on the severity of disease and the age of the person affected. The small bowel biopsy remains the standard for diagnosis. Treatment requires lifelong abstinence from dietary gluten (removing from the diet all foods that contain wheat,
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barley, and rye). Within weeks of starting the gluten free diet, most patients respond to a gluten free diet with weight gain and decreased diarrhea. Tropical sprue is an idiopathic disease of chronic malabsorption that causes subtotal villous atrophy of the entire small intestine and ultimately leads to malabsorption and nutritional deficiencies. A careful history is crucial in making the diagnosis. Tropical sprue should be suspected in patients who have been in an endemic area for more than 2 weeks and who present with intestinal symptoms of diarrhea or steatorrhea and weight loss associated with macrocytic anemia; endoscopy is helpful in confirming diagnosis. Tropical sprue patients typically respond rapidly, although temporarily, to folic acid administration and more slowly and permanently to antibiotics. 9 figures. 5 tables. 30 references. •
Prevention Strategies for Non-Insulin-Dependent Diabetes Mellitus: An Economic Perspective Source: in LeRoith, D.; Taylor, S.I.; Olefsky, J.M., eds. Diabetes Mellitus: A Fundamental and Clinical Text. Philadelphia, PA: Lippincott-Raven Publishers. 1996. p. 621-630. Contact: Available from Lippincott-Raven Publishers. 12107 Insurance Way, Hagerstown, MD 21740-5184. (800) 777-2295. Fax (301) 824-7390. PRICE: $199.00. ISBN: 0397514565. Summary: Cost effectiveness analysis is one way of comparing diverse treatments of disease. The analysis is usually done after clinical trials have established the efficacy of an intervention, when the costs and effects are known. It can also be used to examine the economic feasibility of an intervention that is as yet unproved. This chapter, from a medical textbook on diabetes, analyzes the potential cost effectiveness of various interventions on the natural history of noninsulin-dependent diabetes mellitus (NIDDM, or Type 2) from a health and economic point of view. The authors explore the potential role that primary prevention of diabetes may play in the future. Topics include the principles of cost effectiveness analysis, the modeling of disease outcomes, cost analysis, cost effectiveness analysis, sensitivity analysis, and the prospects for the primary prevention of NIDDM. The authors conclude that interventions leading to weight loss or prevention of weight gain, reduction in dietary fat, increase in complex carbohydrates, and increased exercise are lifestyle changes that reduce insulin resistance and have potential for preventing NIDDM. 5 figures. 6 tables. 48 references.
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Cessation of Tobacco Use Source: in Ciancio, S.G., ed. ADA Guide to Dental Therapeutics. 2nd ed. Chicago, IL: American Dental Association (ADA). 2000. p. 569-581. Contact: Available from American Dental Association (ADA). Catalog Sales, P.O. Box 776, St. Charles, IL 60174-0776. (800) 947-4746. Fax (888) 476-1880 or (630) 443-9970. Website: www.ada.org. PRICE: $44.95 for members; $64.95 for nonmembers, plus shipping and handling. Summary: Dentists are prescribing more medications than ever before and patients seeking dental care are using a wide range of medications for medical problems. And both dentists and patients have choices to make about the variety of nonprescription products available for treating various disorders of the mouth. This chapter on cessation of tobacco use is from a detailed guide to dental therapeutics. The author offers an overview of the rationale for clinical participation in tobacco use cessation programs and an outline for using intervention procedures. A few moments of assistance from a clinician can be significantly more effective than purely self help methods. Minimum assistance includes identifying whether patients use tobacco, advising users to stop,
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strengthening their interest in quitting, and for those who make a commitment to quit, equipping them with coping skills needed during the quitting process and providing follow up support. The author describes each of these steps in detail, then addresses special considerations, including patients who are resistant to quitting, fear of weight gain, pregnant patients, psychiatric comorbidity, and special dental considerations. Lengthy tables summarize intervention programs, dosage information for transdermal nicotine patches, and adverse effects of tobacco use cessation drugs. 3 tables. 9 references. •
Complications of Dialysis in Diabetic Patients Source: in Lameire, N. and Mehta, R.L., eds. Complications of Dialysis. New York, NY: Marcel Dekker, Inc. 2000. p. 697-704. Contact: Available from Marcel Dekker, Inc. Cimarron Road, P.O. Box 5005, Monticello, NY 12701. (800) 228-1160 or (845) 796-1919. Fax (845) 796-1772. E-mail:
[email protected]. International E-mail:
[email protected]. Website: www.dekker.com. PRICE: $250.00 plus shipping and handling. ISBN: 0824788710. Summary: Dialysis patients with diabetes mellitus comprise the largest subgroup of patients in end stage renal disease (ESRD) treatment programs in developed countries. This patient population is unfortunately also subject to greater morbidity and mortality when compared to nondiabetic dialysis patients. This chapter on the complications of dialysis in patients with diabetes is from a book that offers a comprehensive, multidisciplinary resource for the nephrologist and caregiver providing dialysis, covering all aspects of dialysis therapies and their complications. The authors of this chapter note that older age at the time of dialysis initiation and the presence of often advanced microvascular and macrovascular disease account for this excess rate of complications and death on dialysis. The management of dialysis patients with diabetes requires an aggressive, preemptive, multidisciplinary, and patient education oriented approach, which must often be led by the nephrologist (kidney specialist) who has the most frequent contact with the patient. Peripheral vascular, cardiovascular, and cerebrovascular disease, retinopathy (eye disease), gastropathy, and dialysis associated complications are the major contributors to co-morbidity in diabetic dialysis patients. Hemodialysis related complications include hypotension (low blood pressure), hypertension (high blood pressure), high interdialytic weight gain, vascular access problems, access thrombosis (clotting), ischemic monomelic neuropathy, and venous hypertension. Other problems discussed include bone disease, diabetic retinopathy, undernutrition, and hyperglycemia (high blood sugar levels). The complications of peritoneal dialysis in patients with diabetes including peritonitis, underdialysis, undernutrition, and hyperglycemia. The authors conclude by noting that the increasing prevalence of type 2 diabetes will require that nephrologists target the problems prevalent in this population in order to reduce morbidity (illness) and mortality (death). 2 tables. 46 references.
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Intensive Insulin Therapy for Patients with Type II Diabetes Source: in LeRoith, D.; Taylor, S.I.; Olefsky, J.M., eds. Diabetes Mellitus: A Fundamental and Clinical Text. Philadelphia, PA: Lippincott-Raven Publishers. 1996. p. 647-660. Contact: Available from Lippincott-Raven Publishers. 12107 Insurance Way, Hagerstown, MD 21740-5184. (800) 777-2295. Fax (301) 824-7390. PRICE: $199.00. ISBN: 0397514565.
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Summary: The benefits of normalizing glycosylated hemoglobin in patients with Type I diabetes mellitus (insulin-dependent, or IDDM) have been clearly demonstrated by the results of the Diabetes Control and Complications Trial (DCCT). This chapter, from a medical textbook on diabetes, explores the use of intensive insulin therapy for patients with Type II (noninsulin-dependent, or NIDDM) diabetes. The authors cover the different insulin therapeutic regimens available to normalize glycemia and glycosylated hemoglobin in patients with Type II diabetes mellitus; for each therapy, the authors review their application, possible benefits, and adverse effects. They note that the area of major concern when insulin therapy is used to achieve tight glucose control in Type II diabetes is the association of hyperinsulinemia with weight gain and accelerated atherosclerosis. In addition, when a meal plan, exercise, and oral antidiabetic agents fail to control glycemia, then the lowest possible dose of insulin should be used. Topics include intensive management goals, tools used to monitor glycemic control, intensive insulin strategies, the application of intensive insulin therapy, combination therapy, multiple-injection regimens, external subcutaneous insulin infusion pumps, implantable intraperitoneal insulin infusion pumps, insulin analogs, human insulin-like growth factor, the benefits of normoglycemia, insulin therapy and weight gain, and hypoglycemia. 8 figures. 5 tables. 89 references. •
Nutrition in the Kidney Transplant Recipient Source: in Danovitch, G.M., ed. Handbook of Kidney Transplantation. 3rd ed. Philadelphia, PA: Lippincott Williams and Wilkins. 2000. p. 394-410. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-3030 or (301) 223-2300. Fax (301) 223-2365. PRICE: $42.00 plus shipping and handling. ISBN: 0781720664. Summary: The nutritional management of the renal transplant recipient is an important determinant of outcome in terms of both morbidity and mortality. This chapter on nutrition in the kidney transplant recipient is from a handbook of kidney transplantation that provides practical information on therapy, patient monitoring, and patient care management. In this chapter, the author stresses that diet can be used to prevent and reduce many transplant related complications, although the precise nutrient requirements of kidney transplant recipients continue to be incompletely defined. The author offers recommendations, based on available studies in the transplantation population and on extrapolated data in comparable settings, which provide a guide to nutrition care management in the pretransplantation, acute posttransplantation, and long term posttransplantation periods. In each time period, the author discusses major concerns and assessment of nutritional status. Concerns covered include malnutrition, obesity, dyslipidemia and cardiovascular disease in the pretransplantation period; protein catabolism, fluid and electrolyte balance, and drug nutrient interactions in the immediate posttransplant period; and hyperlipidemia, homocysteine, obesity and weight gain, bone disease, hypertension (high blood pressure), posttransplant diabetes mellitus, progression of renal disease, hypoalbuminemia (low levels of protein in the blood), foodborne infectious complications, and the use of herbal supplements in the long term posttransplant period. Practical recommendations are provided for each time period of patient care. 3 tables. 23 references.
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Detection and Quanitification of Urine Loss: The Pad-Weighing Test Source: in Corcos, J.; Schick, E., eds. Urinary Sphincter. New York, NY: Marcel Dekker, Inc. 2001. p. 275-283.
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Contact: Available from Marcel Dekker, Inc. Cimarron Road, P.O. Box 5005, Monticello, NY 12701. (800) 228-1160 or (845) 796-1919. Fax (845) 796-1772. E-mail:
[email protected]. International E-mail:
[email protected]. Website: www.dekker.com. PRICE: $225.00 plus shipping and handling. ISBN: 0824704770. Summary: The urinary sphincter is the key to understanding both normal and abnormal function of the lower urinary tract. Its relationships with the bladder, the pelvic floor, and the bony structures of the pelvis are complex and incompletely understood. This chapter on the use of pad weighing tests to detect and quantify urine loss is from a textbook that presents a detailed and systematic account of the current knowledge on the anatomy, physiology, functional relationships, and range of dysfunctions that affect the urinary sphincter. The authors stress that the pad weighing test is the best available instrument to document the amount of urine lost in urinary incontinence. However, pad weighing tests cannot evaluate the effect that a given degree of incontinence has on the patient's quality of life. The authors caution that before interpreting pad test results, it is important to know the upper limit of weight gain by the pad in normal continent persons. Perineal pads can absorb perspiration, vaginal discharge, and such, even in a perfectly continent person. The authors then describe qualitative and quantitative types of pad tests. The qualitative test uses a dye to color urine and the resulting amount of staining on the pads is a rough estimate of the severity of incontinence. Quantitative tests quantify urine loss by weighing perineal pads after various lengths of time. The authors conclude that for scientific and research purposes, the 24 hour pad test should be used because it has good reproducibility, it is easy to perform, it is done in the patient's own environment, and it has a better potential to detect and quantify urine loss in urge incontinence than the 1 hour test. The pad test should also be incorporated, together with other outcome measures, in the followup of different treatment modalities. 2 tables. 53 references. •
Helpful Hints for Common Patient Problems Source: in American Dietetic Association. Clinical Guide to Nutrition Care in End-Stage Renal Disease. Chicago, IL: American Dietetic Association. 1994. p. 191-194. Contact: Available from American Dietetic Association. 216 West Jackson Boulevard Chicago, IL 60606-6995. (312) 899-0040. PRICE: $24 for members; $28 for non-members; plus shipping and handling. ISBN: 0880911247. Summary: This appendix is from a manual that provides guidelines for the clinical nutrition care of patients with end-stage renal disease (ESRD); the author lists helpful hints for common patient problems. Problems discussed include loss of appetite or changes in taste; nausea and vomiting; constipation; excessive interdialytic fluid weight gain; and reducing the potassium content of foods. 1 reference.
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Nutrition Therapy for Type 1 Diabetes Source: in Franz, M.J. and Bantle, J.P., eds. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association. 1999. p. 26-45. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $39.95 for members; $49.95 for nonmembers; plus shipping and handling. ISBN: 158040006X. Order number 561601.
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Summary: This chapter discusses the use of medical nutrition therapy (MNT) for type 1 diabetes. Topics include insulin regimens, nutrition related strategies for conventional and intensive insulin therapies, carbohydrate counting and other meal planning approaches, prevention of weight gain associated with improved metabolic control, treatment of hypoglycemia, nutrition or insulin adjustments for acute illnesses and exercise, and nutrition practice guidelines. MNT is one of the main methods of improving metabolic control in people who have type 1 diabetes. Either a conventional or an intensive insulin regimen can be implemented after a meal plan has been agreed on by the person and the dietitian. Rapid acting insulin before meals has proved helpful to many who have type 1 diabetes. The meal planning approach selected should be one the person who has diabetes can understand and use. Although carbohydrate counting is a well received system, meats and fats cannot be completely ignored because of their calories and fat content. Other meal planning approaches include exchange lists and total available glucose. People who have diabetes should receive appropriate nutrition counseling to prevent weight gain, and they should be taught how to prevent and treat hypoglycemia and hyperglycemia. Other concerns focus on nutrition strategies for acute illnesses and changes in usual exercise patterns that require insulin or carbohydrate adjustments. Nutrition practice guidelines for type 1 diabetes, which define state of the art nutrition care based on available evidence, can ensure consistent quality of care. 57 references. •
Nutrition Therapy for Children and Adolescents with Diabetes Source: in Franz, M.J. and Bantle, J.P., eds. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association. 1999. p. 211-228. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $39.95 for members; $49.95 for nonmembers; plus shipping and handling. ISBN: 158040006X. Order number 561601. Summary: This chapter examines medical nutrition therapy (MNT) for children and adolescents who have diabetes, focusing on goals, intervention and treatment strategies, and nutrition education. Children and adolescents with diabetes often present management challenges not seen in the adult population. MNT goals for this population include maintaining near normal blood glucose levels by balancing food intake with insulin and activity level; achieving optimal lipid levels; providing enough calories for normal growth and development; preventing, delaying, or treating nutrition related risk factors and complications; and improving overall health through optimal nutrition. Meal planning approaches that can be successfully implemented with children and adolescents include carbohydrate counting, the exchange system, and simplified meal planning guidelines. Physical activity is important because it generally reduces insulin requirements in children and adolescents who have diabetes. A variety of insulin regimens are available for children and adolescents with diabetes, including using lispro insulin or the insulin pump. MNT for children and adolescents who have diabetes consists of various education topics that can be discussed at the time of diagnosis or as part of the continuing education process. Initial education on meal planning for diabetes should occur within the first 1 to 2 weeks after diagnosis. Nutrition education topics that can be addressed as part of the indepth education process include monitoring, growth, and weight gain. Continuing education is needed because of the continual lifestyle changes that children and adolescents experience. 3 tables. 43 references.
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Benefits and Risks of Exercise in Type 2 Diabetes Source: in Burr, B. and Nagi, D., eds. Exercise and Sport in Diabetes. Somerset, NJ: John Wiley and Sons. 1999. p. 69-82. Contact: Available from John Wiley and Sons. One Wiley Drive, Somerset, NJ 08875. (800) 225-5945 or (732) 469-4400. Fax (732) 302-2300. E-mail:
[email protected]. Website: www.wiley.com. PRICE: $74.95 plus shipping and handling. ISBN: 0471984965. Summary: This chapter examines the benefits and risks of exercise in type 2 diabetes. The benefits of regular physical activity in type 2 diabetes include improving plasma glucose concentration in the short and long term as a result of beneficial effects on hepatic and peripheral insulin sensitivity, limiting the undesirable weight gain usually associated with initiation of sulfonylurea or insulin treatment, lowering blood pressure, improving the lipid profile, and reducing the need for insulin or oral agents. Studies have also shown that physical activity appears to be safe over a long period and may have benefits in terms of lowering mortality rates. Risks associated with physical activity include being more prone to musculoskeletal injuries and experiencing hypoglycemic episodes. Macrovascular complications or physical disabilities may prevent a large proportion of people who have type 2 diabetes from engaging in physical activity. People who have microvascular complications should restrict their physical activity to low or moderate intensity exercises or nonweight-bearing exercises. Although there are some potentially harmful effects of exercise on microvascular and macrovascular complications, the benefits of exercise outweigh the risks associated with it. Therefore, physical activity has the potential to improve the quality of life for people who have type 2 diabetes. 5 tables. 42 references.
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Nutrition Therapy for Pregnancy and Lactation Source: in Franz, M.J. and Bantle, J.P., eds. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association. 1999. p. 229-248. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $39.95 for members; $49.95 for nonmembers; plus shipping and handling. ISBN: 158040006X. Order number 561601. Summary: This chapter focuses on nutrition issues associated with pregnancy and breastfeeding. Nutrition related concerns during pregnancy include weight gain and caloric requirements, adequate nutrients, and possible need for vitamin and mineral supplements such as iron and folic acid. The problems associated with pregnancy in women with diabetes include an increased risk for fetal birth defects and increased spontaneous abortion rates. Nutrition therapy for women who have prior onset type 1 or type 2 diabetes begins with a prenatal meal plan before attempting conception so that they can attempt to achieve glycemic control and optimal body weight. The goal of medical nutrition therapy (MNT) in a pregnancy with diabetes is to maintain normal blood glucose levels while meeting the nutritional needs of pregnancy. Regular meals and snacks are very important to avoid hypoglycemia during pregnancy. Breastfeeding is recommended for women who have diabetes, and a postpartum meal plan must account for the energy demands of breastfeeding as well as its lowering effects on blood glucose. For women who develop gestational diabetes mellitus (GDM), MNT is used to achieve optimal blood glucose control with adequate nutrition for both mother and fetus. Intensive nutrition therapy, along with daily blood glucose monitoring and an exercise program, may be an alternative to insulin therapy in women who develop
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GDM. Breastfeeding is also encouraged in women who have GDM. Women should not follow a hypocaloric diet until lactation is terminated. 1 figure. 6 tables. 63 references. •
Common Side Effects of Insulin Source: in Carlisle, B.A.; Kroon, L.A.; Koda-Kimble, M.A. 101 Medication Tips for People with Diabetes. Alexandria, VA: American Diabetes Association. 1999. p. 62-65. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $14.95 plus shipping and handling. ISBN: 1580400329. Order number 483301. Summary: This chapter identifies the common side effects of insulin, including weight gain, hypoglycemia, and lumps at the injection site. Although most people who use insulin will gain weight, it can be minimized by properly adjusting the dose to just the right amount a person needs to keep blood glucose levels within the target range without causing too many lows. People who experience night sweats and morning headaches may be injecting too much insulin in relation to their evening meal or too much of the wrong type of insulin. Testing blood glucose at 3:00 a.m. and again first thing in the morning for several days may help determine whether a change needs to be made to the insulin regimen. Lumps and fat pads, which are not dangerous, occur when insulin is repeatedly injected into the same place. If injection sites are carefully rotated, a person should not have to use the same site more than once every 2 weeks.
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Nutritional Management of Water, Sodium, Potassium, Chloride and Magnesium in Renal Disease and Renal Failure Source: in Kopple, J.D. and Massry, S.G. Nutritional Management of Renal Disease. Baltimore, MD: Williams and Wilkins. 1997. p. 371-394. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-0672 or (410) 528-4223. Fax (800) 447-8438 or (410) 528-8550. PRICE: $99.00. ISBN: 068304740X. Summary: This chapter is from a medical textbook on nutrition and metabolism of individuals with renal disease or renal failure. The authors discuss the nutritional management of water, sodium, potassium, chloride, and magnesium in renal disease and renal failure. The authors first discuss normal water, sodium, chloride, potassium, and magnesium homeostasis, and then show how the normal condition is changed by renal insufficiency. Chloride is considered together with sodium because nearly all dietary chloride intake is the result of sodium chloride (salt) intake. Specific topics include sodium and the control of extracellular fluid volume, the regulation of sodium balance in health and in kidney disease, the effect of calcium channel blocker therapy on dietary sodium management, water metabolism in health and in renal insufficiency, excessive fluid weight gain in ESRD patients maintained on dialysis, normal potassium metabolism, extrarenal and renal potassium handling in health and in kidney disease, dietary management of potassium, and magnesium. 3 figures. 15 tables. 84 references. (AA-M).
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Crohn's Disease in Children and Adolescents Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 415-419.
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Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on Crohn's disease (CD) in children and adolescents is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with CD and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). Children and adolescents with CD have unique presentations, extraintestinal manifestations, and therapeutic considerations. Whereas the focus of therapy is reduction of disease activity and symptoms, management of the special nutritional, extraintestinal, and emotional features of IBD in children requires attention as well. Thus, gastroenterologists managing children with CD may be faced with patients with more refractory (resistant to treatment) disease than in their adult patients. inflammatory bowel disease (IBD) in children requires attention as well. Goals in managing pediatric patients include reducing gastrointestinal symptoms, optimizing nutritional status (linear growth, weight gain, and dietary intake), alleviating extraintestinal symptoms (arthralgia and arthritis, malaise, dermatologic lesions, etc.), and paying attention to the impact of the disease on social activities and school attendance. The indications for surgery in children with CD include medical intractability, suspected perforation or abscess, intestinal obstruction, and hemorrhage. A special circumstance in children is the potential of surgery for reversing growth failure especially when there is a localized area of resectable disease. This is optimally performed before the onset of puberty. 1 table. 13 references. •
Special Considerations and Situations Source: in Warshaw, H.S. and Bolderman, K.M. Practical Carbohydrate Counting: A How-to-Teach Guide for Health Professionals. Alexandria, VA: American Diabetes Association. 2001. p. 42-47. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $12.95 plus shipping and handling. ISBN: 1580401236. Summary: This chapter on special considerations and situations is from a handbook that helps health care providers teach patients with diabetes how to use carbohydrate counting as one part of their diabetes management plan. The author reviews the rationale for this management strategy. In basic carbohydrate counting, goals are to draw attention to the foods that contain carbohydrate, and to encourage people to eat consistent amounts of carbohydrate at meals and snacks (if necessary or desired) at similar times each day. Advanced carbohydrate counting is appropriate for people who use multiple daily injections (MDI) of insulin or continuous subcutaneous insulin infusion (CSII) via an insulin pump. Their goal is to learn to match the amount of rapid (lispro or aspart) or short acting (regular) insulin they take with or before eating to the amount of carbohydrate they choose to eat. Topics include coping with high protein or high fat meals, adjusting insulin for fiber content, the use of the glycemic index (which ranks foods based on the impact of the food on blood glucose levels compared to either glucose or white bread), weight gain, restaurant meals, special food situations (vacations and holidays, traveling), alcohol, activity and exercise, and coping with sick day management and stress.
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Surgery for Crohn's Disease: Strictureplasty Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 457-463. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on strictureplasty for Crohn's disease is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as inflammatory bowel disease (IBD). Crohn's disease is a chronic inflammatory condition of unknown etiology affecting the entire intestinal tract. No medical regimen has yet been developed that uniformly and reliably effects a cure, and operative therapy is by no means a cure for this disease. Surgery usually is reserved for patients who have developed one or more disease complications or persons whose quality of life is significantly impaired despite appropriate medical therapy. Strictureplasty (surgical repair of abnormally narrowed sections) features incision and suturing of diseased segments of the intestines. Aside from meticulous conduct of the procedure, prevention of complications from the operation lies with patient selection. The operation has proven to be safe, with a morbidity (complications or illness) rate of about 15 percent and no mortality (death) reported. Six months postoperatively, nearly all patients note relief of their obstructive symptoms and average 5 pounds of weight gain. Furthermore, about 80 percent of patients are able to discontinue steroid therapy after strictureplasty. The author reviews the specific types of surgical techniques used and concludes that strictureplasty remains relatively unchanged from its initial description almost two decades ago. 1 figure. 3 tables. 13 references.
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Miscellaneous Information For the Colostomate Source: in Gill-Thompson, N.N.; Thompson, S.J. You and Your Colostomy: Simple Explanations of Psychological and Physical Problems. Akron, OH: Worldwide Home Health Center, Inc. 1990. p. 111-113. Contact: Available from Worldwide Home Health Center, Inc. 926 East Tallmadge Avenue, Akron, OH 44310. (216) 633-0366 or (800) 621-5938 (Ohio) or (800) 223-5938 (National). PRICE: $12 plus $3 postage. Summary: This chapter, from a book about the psychological and physical issues facing people who have colostomies, focuses on ongoing care. Sections discuss when to visit the doctor and enterostomal nurse and everyday changes of life that may also affect one's colostomy (weight gain, illness, aging, emotional changes). A list of helpful hints concludes the chapter.
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Smoking Cessation in Diabetes Source: in Anderson, B.J. and Rubin, R.R., eds. Practical Psychology for Diabetes Clinicians: How to Deal with the Key Behavioral Issues Faced by Patients and Health Care Teams. Alexandria, VA: American Diabetes Association. 1996. p. 121-132. Contact: Available from American Diabetes Association. Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (404) 442-9742. PRICE: $19.95 (members); $24.95 (nonmembers). ISBN: 0945448732.
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Summary: This chapter, from a guidebook on behavioral issues for diabetes clinicians, provides a framework for helping clients with diabetes to quit smoking. Readers are encouraged to communicate the importance of smoking cessation in diabetes care; communicate an understanding of the difficulty of quitting smoking; emphasize the clinician's role as key authority and catalyst; counsel all patients to quit smoking; consider nicotine replacement; address weight gain; refer patients for available care; encourage maintenance of cessation; address relapse paradox; address emotional factors related to diabetes; arrange varied and ongoing support; organize the office staff and environment to reflect the importance of smoking cessation; and contribute to the overall campaign to promote nonsmoking. The authors discuss why each of these activities can help clients with diabetes quit smoking. 5 tables. 7 references. •
Who, What, Where, Why, and How of Type II Diabetes Source: in Magee, E. Tell Me What to Eat If I Have Diabetes. Franklin Lakes, NJ: Career Press, Inc. 1999. p. 7-13. Contact: Available from Career Press, Inc. 3 Tice Road, P.O. Box 687, Franklin Lakes, NJ 07417. (800) 227-3371. Website: www.careerpress.com or www.newpagebooks.com. PRICE: $10.99 plus shipping and handling. Summary: This introductory chapter is from a book that offers eating and nutrition guidelines for people who have been diagnosed with diabetes mellitus. The author focuses on type 2 diabetes, noting that diabetes can manifest differently in different patients and sometimes even changing throughout its course within one person. The author encourages readers to learn as much as they can about their disease and to utilize nutrition as an adjunct therapy and a vital component of their diabetes care. Type 2 diabetes is a metabolic disorder resulting from the body's inability to make or properly use insulin. Most people (90 to 95 percent) with diabetes have type 2. The warning signs of type 2 diabetes include frequent infections, blurred vision, cuts and bruises that are slow to heal, tingling or numbness in the hands or feet, unusual thirst, frequent urination, extreme hunger, unusual weight loss, extreme fatigue, and irritability. The author outlines the three keys to diabetes management success: monitoring blood glucose levels, exercising regularly, and following a personalized eating plan. The author emphasizes the importance of following a personalized eating plan that helps keep blood glucose (sugar) levels normal, and helps protect against heart disease and weight gain without making the patient feel deprived. The chapter concludes with a brief section of sources for additional information, including the American Association of Certified Diabetes Educators (800-832-6874), the American Dietetic Association's National Center for Nutrition and Dietetics (800-366-1655), and the American Diabetes Association (800-342-2383).
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Solid Organ Transplantation Source: in Lysen, L.K. Quick Reference to Clinical Dietetics. Gaithersburg, MD. Aspen Publishers, Inc. 1997. p. 156-162. Contact: Available from Aspen Publishers, Inc. Fulfillment, 7201 McKinney Circle, Frederick, MD 21704. (800) 234-1660 or (800) 638-8437. Summary: This section on solid organ transplantation is from a chapter on nutrition management for specific medical conditions; the chapter comes from a reference book on clinical dietetics. Topics include the types of organ transplantation, objective nutritional assessment parameters, subjective assessment parameters, posttransplant problems with nutrition, short-term nutrition management, and long-term nutrition
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management. Common nutritional problems arising up to 2 months after transplant include depressed appetite, early satiety, and taste changes. Longer term problems include increased appetite, excessive weight gain, hyperlipidemia, hypertension, diabetes, and osteoporosis. Transplant recipients must take immunosuppressive medications to prevent rejection of their new organs; these drugs have multiple nutrient side effects. Most of the material in the chapter is presented in table or outline form, for ease of use. Specific patient care strategies are emphasized. 52 references. (AA-M). •
Intradialytic Parenteral Nutrition Source: in American Dietetic Association. Manual of Clinical Dietetics. Chicago, IL: American Dietetic Association. 1996. p. 573-576. Contact: Available from American Dietetic Association. 216 West Jackson Boulevard, Chicago, IL 60606. (800) 877-1600 or (312) 899-0040. Fax (312) 899-4899. PRICE: $59.95 for members, $70.00 for nonmembers. ISBN: 0880911530. Summary: This section providing guidelines for intradialytic parenteral nutrition (IDPN) is from a manual that serves as a nutrition care guide for dietetics professionals, physicians, nurses, and other health professionals. The manual integrates current knowledge of nutrition, medical science, and food to set forth recommendations for healthy individuals and those for whom medical nutrition therapy (MNT) is indicated. IDPN is a method of providing intravenous nutrition support to a hemodialysis patient during the dialysis treatment. The text notes the purpose, use, modifications, and adequacy of the diet. Advantages of IDPN include the ability to remove infused fluids during the treatment, possibly increased serum albumin, nonfluid weight gain, decreased hospitalizations, and decreased mortality. Disadvantages of IDPN include cost, possible reactive hypoglycemia, liver function abnormalities, and the lack of conclusive evidence of efficacy. The IDPN solution may contain amino acids, glucose, lipids, vitamins, and minerals. It is administered using an infusion pump and connected to the venous side of the dialysis circuit. The section also outlines the related physiology. 2 tables. 5 references. (AA-M).
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Exercise and Weight Control Source: in Devlin, J.T. and Schneider, S.H., eds. Handbook of Exercise in Diabetes. Alexandria, VA: American Diabetes Association. 2002. p.344-364. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $69.95 plus shipping and handling. ISBN: 1580400191. Summary: Weight loss is important in the treatment and prevention of type 2 diabetes. Exercise may also help prevent weight gain in type 1 diabetes individuals on intensive diabetes therapy. This chapter on exercise and weight control is from a book that provides a practical, comprehensive guide to diabetes and exercise for health care professionals involved in patient care. The combination of diet, exercise, and behavior modification is the most effective approach to weight control. Current dietary interventions focus on reducing calories and dietary fat; periods of very-low-caloric (VLC) intake or portion-controlled meals may also be helpful. Low-intensity, longduration exercise is recommended for weight loss. A combination of lifestyle exercise and programmed exercise is recommended. To increase activity level, it is helpful to divide exercise into multiple short sessions. Approaches that teach patients to rearrange
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their environment to support healthy eating and exercise behaviors are important for long term maintenance of behavior change. 21 references.
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CHAPTER 8. MULTIMEDIA ON WEIGHT GAIN Overview In this chapter, we show you how to keep current on multimedia sources of information on weight gain. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on weight gain is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “weight gain” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “weight gain” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on weight gain: •
Physical Activity, Metabolism, and Weight Control Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: Dr. Stern's lecture begins with the statement that obesity is a very complex disorder. Eating too much or being inactive are oversimplified reasons for obesity, which has very firm biological bases. Scientists, says Dr. Stern, fundamentally do not understand why some individuals become obese and others do not. The vast majority of people who lose weight regain it within 5 years. This finding suggests that there are strong biological foundations for obesity. Dr. Stern discusses several animal and human studies showing how diet, exercise, and genes affect obesity and perhaps explain why maintaining weight loss is so difficult. Dr. Stern believes increasing physical activity is a key to maintaining weight loss, but it is unclear whether the effect is metabolic or psychological. Obese people are not necessarily less active, she notes, but most are. In
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her own studies of Zucker (genetically obese) rats, she found that obese rats remained obese even when they consumed fewer calories than normal-weight rats and were as physically active as normal-weight rats. She cites studies showing that sudden changes (whether increases or decreases) in physical activity affect metabolic rates in both humans and rats. When physical activity stops suddenly, one's metabolic rate drops, which would lead to weight gain if food intake remained constant. Dr. Stern discusses studies showing evidence of a strong genetic component to obesity in both humans and rats. In order to translate these findings from the laboratory to a clinical setting, Dr. Stern suggests that any weight loss program should include a low-fat diet, an individualized weight loss program, regular exercise, problem-solving skills, and a social support network. A question- and-answer period follows the lecture. •
The Biologic Basis of Obesity Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: In this lecture, Dr. Leibel describes the two types of studies he and his colleagues are conducting on defining the biologic basis of obesity: long-term studies of obesity in humans, and studies of the molecular genetics of rodent obesity. Results of long-term studies of obesity in humans have shown that body composition remains remarkably constant. This suggests, according to Dr. Leibel, that energy intake and output are regulated to maintain stored energy close to a "set point." However, the nature and origin of the regulatory "signal" are as yet unknown. The regulatory process is a fine one, since small imbalances in intake and output can have a significant impact on body weight. For example, a 3 to 4 percent excess of caloric intake over expenditure will result in weight gain of 6 to 8 pounds over 1 year. The hypothesis of a strong genetic component in obesity is supported by studies of monozygotic (identical) and dizygotic (fraternal) twins. Monozygotic twins demonstrate much lower inter-twin difference in body weight than do dizygotic pairs. Dr. Leibel goes on to describe a series of experiments involving mice and rats that become obese following removal of a section of the hypothalamus. The lesions cause alterations in both food intake and energy efficiency, which suggests that these regions of the brain affect the set point function. Several single gene mutations in mice result in an obese/diabetic phenotype. Efforts are underway to clone several of these genes and to examine their possible role in human obesity and diabetes.
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Menopause and Nutrition Source: Los Angeles, CA: National Health Video, 15 min., n.d. Contact: National Health Video. 12021 Wilshire Blvd., Suite 550, Los Angeles, CA 90025. 1-800-543-6803. Summary: This video provides information on the role of nutrition during menopause. Topics include the role of supplements such as magnesium and calcium, iron needs, weight gain, heart disease risks, and the importance of a healthy diet. The video is accompanied by an instruction resource package that includes learning objectives and activities, a before-after knowledge quiz, and handout masters.
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Taking Control : Adherence and HIV/AIDS Medication : Provider Version Contact: Northwest AIDS Education and Training Center Program, University of Washington, 1001 Broadway Ste 217, Seattle, WA, 98122-4304. Summary: This videocassette, designed for health professionals, discusses treatment adherence by patients with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS). The video defines patient adherence and examines how patients can fit adherence practices into their lives. The consequences of non-adherence, particularly the development of multidrug-resistant HIV/AIDS and its emotional impact, are discussed. Some of the barriers to patient adherence and treatment are identified. These barriers include fear of a doctor's judgement by patients who fail to remain adherent, unsupportive doctors, the rigorous dosage schedules demanded by many contemporary drugs, fear or weariness of side effects, weight gain or loss, access to food to take with medications, mental health issues, substance abuse, and homelessness. Adherence can be improved through clinic support for patients; the development of more flexible, individualized regimens; effective case management; and peer support. The video includes clips of HIV-positive individuals describing the benefits of treatment adherence.
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Obesity and Type II Diabetes Source: Los Angeles, CA: National Health Video, Inc. 2000. (videocassette). Contact: Available from National Health Video, Inc. 12021 Wilshire Boulevard, Suite 550, Los Angeles, CA 90025. (800) 543-6803. Fax (310) 477-8198. E-mail:
[email protected]. PRICE: $89.00 plus shipping and handling. Summary: This videotape discusses the relationship between type 2 diabetes and obesity. Obesity presents special problems for people who have diabetes because excess body fat decreases the body's ability to use insulin, strains the pancreas, and makes the body less able to use the insulin it produces. Although the causes of obesity are not well understood, factors such as age, heredity, and gender have been associated with weight gain. A weight loss of just 10 to 20 pounds can improve blood glucose levels, blood pressure, and cholesterol. Methods of losing weight include eating a variety of foods in moderation, incorporating moderate activity into a daily schedule, undergoing stomach restrictive and intestinal bypass procedures (recommended only for people who are severely obese), using diet medications, and enrolling in a weight loss program. Other topics include the role of obesity in diseases other than diabetes and the growing problem of childhood obesity. The videotape is accompanied by a teaching resource guide and a transcript of the tape.
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Digestive System: Your Personal Power Plant Source: Charleston, WV: Cambridge Educational. 199x. (videocassette). Contact: Available from Films for the Humanities and Sciences. P.O. Box 2053, Princeton, NJ 08543-2053. (800) 257-5126 or (609) 275-1400. Fax (609) 275-3767. E-mail:
[email protected]. Website: www.films.com. PRICE: $89.00; plus shipping and handling. Order number BYA8164. Summary: This videotape on the digestive system is one of a series of educational programs on the human body. The program focuses on four areas: the necessity of food as the fuel for living; the way the digestive system turns food into fuel; the role of the brain in controlling the food intake system; and the way each part of the digestive system works. The program uses a resource recovery (recycling) plant to explain how
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the digestive system creates energy. After a brief discussion of how food affects weight gain, nutrition, and disease, the program reviews the anatomy and physiology of each part of the digestive system: the mouth, salivary glands, esophagus, stomach, small intestine, and large intestine, as well as the accessory organs (the teeth, tongue, salivary glands, liver, gallbladder, and pancreas). Five aspects of the process of creating fuel from food are covered: ingestion, digestion, peristalsis, absorption, and defecation. The program also reviews the role of the hypothalamus in eating (as an appetite stimulator and a measure of satiety). Other topics include the role of gastric emptying, the way the intestine transfers nutrients to the bloodstream (through the villi), the food guide pyramid and the importance of a varied diet, weight control, the role of exercise and physical activity, eating disorders, ulcers, peritonitis, and cancer of the gastrointestinal tract (notably the importance of early detection and prevention). The program provides a summary after each section and teaches the related vocabulary with repetition. •
Smoking and Diabetes Source: Los Angeles, CA: National Health Video, Inc. 1998. (videocassette). Contact: Available from National Health Video, Inc. 12021 Wilshire Blvd., Suite 550, Los Angeles, CA 90025. (800) 543-6803. Fax (310) 477-8198. E-mail:
[email protected]. PRICE: $89.00 plus shipping and handling. Order number 272. Summary: This videotape provides people who have diabetes with information on the effect of smoking on the disease. Smoking has a greater adverse effect on people who have diabetes than on otherwise healthy smokers. For example, the risk of heart disease is 14 times higher in a person has diabetes and smokes. In addition, vasoconstriction can lead to blindness and severe peripheral neuropathy. Other adverse effects of smoking in a person with diabetes include increasing the risk of high blood pressure, stroke, respiratory disease, various cancers, and periodontal disease; impeding the control of infection; limiting joint mobility; and contributing to impotence. The video offers tips on quitting, including learning about smoking habits and using a substitute for smoking when a pattern is identified, setting a quitting date, and using nicotine replacement therapy. In addition, the video presents suggestions on avoiding postcessation weight gain.
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CHAPTER 9. PERIODICALS AND NEWS ON WEIGHT GAIN Overview In this chapter, we suggest a number of news sources and present various periodicals that cover weight gain.
News Services and Press Releases One of the simplest ways of tracking press releases on weight gain is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “weight gain” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to weight gain. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “weight gain” (or synonyms). The following was recently listed in this archive for weight gain: •
Nicotine gum cuts weight gain in the short-term Source: Reuters Health eLine Date: November 21, 2003
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Nicotine gum cuts weight gain in ex-smokers - at least initially Source: Reuters Industry Breifing Date: November 21, 2003
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Dieting may promote weight gain in children Source: Reuters Medical News Date: October 07, 2003
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Study says kids' diets may promote weight gain Source: Reuters Health eLine Date: October 06, 2003
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Weight gain from antipsychotic drugs is reversible Source: Reuters Health eLine Date: September 10, 2003
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Exposure to antidepressants in breast milk does not affect infant weight gain Source: Reuters Medical News Date: May 05, 2003
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Early neonatal weight gain associated with insulin resistance in adolescence Source: Reuters Medical News Date: March 27, 2003
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More kids mean more weight gain for mom, dad: study Source: Reuters Health eLine Date: February 17, 2003
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Some boys' fast weight gain may up blood pressure Source: Reuters Health eLine Date: February 10, 2003
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Boys with rapid childhood weight gain have higher blood pressures Source: Reuters Medical News Date: February 10, 2003
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More steps, less bites stop weight gain: experts Source: Reuters Health eLine Date: February 06, 2003
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Weight gain in US continues upward trend: CDC Source: Reuters Health eLine Date: October 08, 2002
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Study unravels mystery of diabetes drug weight gain Source: Reuters Health eLine Date: September 23, 2002
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"Surprising" mechanism behind thiazolidinedione-related weight gain uncovered Source: Reuters Medical News Date: September 23, 2002
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Nocturnal nasogastric refeeding enhances weight gain in anorexia nervosa Source: Reuters Medical News Date: September 02, 2002 The NIH
Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date
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at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “weight gain” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “weight gain” (or synonyms). If you know the name of a company that is relevant to weight gain, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “weight gain” (or synonyms).
Newsletters on Weight Gain Find newsletters on weight gain using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “weight gain.” Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter.” Type “weight gain” (or synonyms) into the “For these words:” box. The following list was generated using the options described above:
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Use of Low-Dose Prednisone in the Management of Rheumatoid Arthritis, The Source: Bulletin on the Rheumatic Diseases. 50(12): 1-4. 2001. Contact: Available from Arthritis Foundation. 1330 West Peachtree Street, Atlanta, GA 30309. (800) 268-6942 or (404) 872-7100. Fax (404) 872-9559. Website: www.arthritis.org. Summary: This newsletter provides health professionals with information on the use of low dose prednisone, a glucocorticoid, in the management of rheumatoid arthritis (RA). RA, a chronic, symmetric polyarthritis that can lead to joint deformity and destruction, is associated with a significant increase in economic loss, morbidity, and mortality. Glucocorticoids have been used in the treatment of RA since 1948. These 21 carbon steroid molecules activate a cytoplasmic glucocorticoid receptor that ultimately results in the prevention of gene expression of various proinflammatory proteins and the inhibition of class I and II major histocompatibility complexes, adhesion molecules, inducible nitric oxide, and cyclooxygenase 2 enzyme. The side effects of glucocorticoids are well known. However, side effects can be minimized by using low doses. Potential side effects of low dose prednisone are osteopenia, bruising, weight gain, and formation of either cataracts or glaucoma. The article reviews evidence demonstrating the effectiveness of low dose corticosteroids in managing RA and suggests appropriate dosing. The article recommends that prednisone, at a dose not to exceed 10 milligrams per day be initiated as early as possible in the treatment of RA, usually with another disease modifying antirheumatic drug. 1 table and 22 references.
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “weight gain” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on weight gain: •
Holiday Weight Gain Source: AICR Science News. Issue 17, p.2. September 2000. Contact: American Institute for Cancer Research. 1759 R St. NW, Washington, DC 20009. (202)328-7744. www.aicr.org. Summary: A study at the National Institutes of Health followed 165 adults for 1 year, and recorded their weight changes. Racially diverse subjects were recruited from a variety of occupations. They ranged in age from 19 to 82 years and were unaware they were being screened for weight data. The vast majority of subjects experienced little change in weight during the holiday period between Thanksgiving and New Year's Day. Only 10 percent of subjects gained 5 or more pounds during this time, and these individuals tended to be overweight or obese at the outset of the study. However, the average subject maintained whatever weight gain he or she experienced during September to November and from November to January into the following year. The cumulative effect of yearly weight gain during the fall and winter likely contributes to the substantial increase in body weight that frequently occurs during adulthood.
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Holiday Weight Gain May Contribute to Overweight and Obesity Source: WIN Notes. p. 1, 4. Fall 2000. Contact: Weight-control Information Network. 1-877-WIN-4627. Summary: According to a study from the National Institutes of Health (NIH), the weight Americans gain over the winter holidays may be a major contributor to the increase in body weight that often occurs during adulthood. Researchers from the National Institute of Child Health and Human Development (NICHD) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) measured actual seasonal weight changes in 195 adults from September through March with followup measurements of 165 subjects in June and September/October. Participants' average net weight gain between September and March was 1.06 pounds, with 75 percent of that gain occurring during the holiday period from mid-November to mid-January. For the 165 participants who returned in June and either September or October, the average weight gain for the full year was 1.36 pounds, leading researchers to conclude that weight gained during the winter holidays is not lost during the warmer months. The research team concluded that promotion of weight stability during the fall and winter months may be a useful strategy for preventing the weight gain that occurs during adulthood. The finding that participants who reported more physical activity had less weight gain points to the need for more research into increased physical activity as a means for preventing holiday weight gain among persons at risk. This study appears in the March 23, 2000, issue of The New England Journal of Medicine.
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Menopausal Weight Gain Source: Mayo Clinic Women's HealthSource. December 1998. Contact: Mayo Clinic Women's HealthSource, P.O. Box 56931, Boulder, CO 80322-6931. Summary: This article discusses the changes a woman can expect to go through during perimenopause and menopause. The author points out the changes of puberty and pregnancy as models for the change of menopause. According to the author, lowered estrogen production contributes to the mood swings, sleep disturbances, and hot flashes of menopause. For most women, their metabolism also slows down, and their lean muscle mass diminishes. This can lead to weight gain. A starvation diet is not the answer, according to the author, who says that exercise is a better choice. Exercise boosts the metabolism, burns fat, and can strengthen bones. All forms of exercise are potentially beneficial, including aerobic exercise to burn fat, stretching to increase flexibility, and strength training to improve muscle mass and strengthen bones. Other topics discussed include hormone replacement therapy and a healthy diet.
•
Weight Gain in Menopausal Years Source: Healthy Weight Journal. 8(4):69-70; July/August 1994. Contact: Healthy Living Institute, 402 S. 14th St., Hettinger, ND 58639. (701) 567-2645. Summary: This article looks at weight gain during the menopausal years. This is considered a major concern for women and the health care professionals who care for them. The results of a study of weight increase among menopausal women at the University of Pittsburgh is summarized. The study showed a weight gain was highly related to increase and heart disease risk factors. Large weight increases for most women in this study occurred between the ages of 42 and 53. Hormone therapy added
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slightly to the change of weight gain in this population. Those with the lowest exercise levels gained the most weight.
Academic Periodicals covering Weight Gain Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to weight gain. In addition to these sources, you can search for articles covering weight gain that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for weight gain. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with weight gain. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to weight gain: Minoxidil •
Systemic - U.S. Brands: Loniten http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202373.html
Progestins for Noncontraceptive Use •
Systemic - U.S. Brands: Amen; Aygestin; Crinone; Curretab; Cycrin; DepoProvera; Gesterol 50; Gesterol LA 250; Hy/Gestrone; Hylutin; Megace; Prodrox; Prometrium; Pro-Span; Provera http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202758.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
12
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
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Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
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MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
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Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database
A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “weight gain” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “weight gain” (or synonyms) into the “For these words:” box. The following is a sample result: •
Maternal weight gain: A report of an expert work group Source: Arlington, VA: National Center for Education in Maternal and Child Health. 1997. 14 pp. Contact: Available from National Maternal and Child Health Clearinghouse, 2070 Chain Bridge Road, Suite 450, Vienna, VA 22182-2536. Telephone: (703) 356-1964 or (888) 4344MCH / fax: (703) 821-2098 / e-mail:
[email protected] / Web site: http://www.nmchc.org. Summary: This report discusses the relationship between maternal weight gain and pregnancy outcome, including infant weight at term. The focus was on research related to maternal weight gain published since 1990, whether the current recommendations for weight gain during pregnancy are still valid, and needs for future research. Topics include social, cultural, and physical determinants of maternal weight gain; maternal outcomes; infant outcomes; and weight gain by pregnant adolescents, by racial and ethnic minorities, and by women pregnant with twins or triplets. The report gives recommendations for practice and research. [Funded by the Maternal and Child Health Bureau].
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “weight gain” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. 15 16
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH).
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Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 25118 368 912 245 14 26657
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “weight gain” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
17
Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html.
18
The HSTAT URL is http://hstat.nlm.nih.gov/.
19
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 20 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 21
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on weight gain can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to weight gain. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to weight gain. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “weight gain”:
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Other guides Eating Disorders http://www.nlm.nih.gov/medlineplus/eatingdisorders.html Prenatal Care http://www.nlm.nih.gov/medlineplus/prenatalcare.html
You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on weight gain. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
Fatty Liver Source: Cedar Grove, NJ: American Liver Foundation. 1997. [2 p.]. Contact: Available from American Liver Foundation. Information and Distribution Center, 1425 Pompton Avenue, Suite 3, Cedar Grove, NJ 07009-1000. (800) GO-LIVER, ext. 234 or (888) 4HEP-ABC. Fax (973) 256-3214. E-mail:
[email protected]. Website: www.liverfoundation.org. PRICE: $0.50 for single copy; bulk orders available; plus shipping and handling. Summary: Fatty liver is the accumulation of fat in liver cells (fatty infiltration of the liver). Fat accumulates in the liver usually in connection with heavy use of alcohol, extreme weight gain, or diabetes mellitus. Fatty liver can also occur with poor diet and certain illnesses, such as tuberculosis, intestinal bypass surgery for obesity, and certain drugs such as corticosteroids. This fact sheet reviews fatty liver. Written in a question and answer format, the fact sheet covers the causes of fatty liver, symptoms, diagnostic tests that may be used to confirm the condition, how fatty liver occurs, and treatment options. The author concludes that simple fatty liver does not require treatment, since it does not result in damage to liver cells or clinical disease. The treatment of other types of fatty liver is related to the cause. The fact sheet concludes with the contact information for the American Liver Foundation, a nonprofit, national voluntary health organization (www.liverfoundation.org).
•
Be good to your baby before it is born: Your guide to a healthy pregnancy Source: White Plains, NY: March of Dimes Birth Defects Foundation. 1994. 13 pp.
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Contact: Available from Supply Division, March of Dimes Birth Defects Foundation, 1275 Mamaroneck Avenue, White Plains, NY 10605. Telephone: (914) 428-7100 or (888) MODIMES or (914) 997-4764 TTY / e-mail:
[email protected] / Web site: http://www.modimes.org. $5.00 package of 50; may be available from local chapter offices. Summary: Guiding the pregnant woman from her first prenatal visit through delivery, this pamphlet covers topics of importance during pregnancy. Prenatal care checkups, diet and weight gain, exercise, sex, and common pregnancy problems are reviewed. There is a Spanish version as well as an English one. •
Tyrosinemia Source: Cedar Grove, NJ: American Liver Foundation. 1997. 1 p. Contact: Available from American Liver Foundation. Information and Distribution Center, 1425 Pompton Avenue, Suite 3, Cedar Grove, NJ 07009-1000. (800) GO-LIVER, ext. 234 or (888) HEP-ABC. Fax (973) 256-3214. E-mail:
[email protected]. Website: www.liverfoundation.org. PRICE: $0.50 for single copy; bulk orders available; plus shipping and handling. Summary: Hereditary tyrosinemia is a genetic inborn error of metabolism associated with severe liver disease in infancy. This fact sheet from the American Liver Foundation (ALF) offers a brief overview of tyrosinemia. The disease is inherited in an autosomal recessive fashion which means that both parents must be carriers of the gene for the disease. There are two clinical appearances of tyrosinemia: the acute form, which features babies with poor weight gain, enlarged liver and spleen, distended abdomen, swelling of the legs, and increased tendency to bleeding, particularly nose bleeds. Despite vigorous therapy, death from liver failure frequently occurs between 3 and 9 months of age in these children. The more chronic form of tyrosinemia features a gradual onset and less severe clinical features; enlargement of the liver and spleen are prominent, the abdomen is distended with fluid, weight gain may be poor, and vomiting and diarrhea occur frequently. Affected patients usually develop cirrhosis (scarring of the liver) and its complications. Children with either type of tyrosinemia will require liver transplantation. Strict attention to excellent nutrition, adequate vitamin and mineral intake, prevents nutritional deterioration and helps keep the patient as well as possible for transplantation. Prenatal diagnosis is possible, which allows for genetic counseling and consideration of termination of pregnancy in affected infants. The fact sheet concludes with the contact information for ALF (800-GO-LIVER, www.liverfoundation.org ).
•
Neonatal Hepatitis Source: Cedar Grove, NJ: American Liver Foundation. 1997. 2 p. Contact: Available from American Liver Foundation. Information and Distribution Center, 1425 Pompton Avenue, Suite 3, Cedar Grove, NJ 07009-1000. (800) GO-LIVER, ext. 234 or (888) HEP-ABC. Fax (973) 256-3214. E-mail:
[email protected]. Website: www.liverfoundation.org. PRICE: $0.50 for single copy; bulk orders available; plus shipping and handling. Summary: Neonatal hepatitis is inflammation of the liver that occurs only in early infancy, usually between one and two months after birth. This fact sheet from the American Liver Foundation (ALF) offers a brief overview of neonatal hepatitis. About 20 percent of infants with neonatal hepatitis were infected by their mother with a virus
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that caused the inflammation before birth or shortly after birth. These viruses include cytomegalovirus, rubella (measles), and hepatitis A, B, or C viruses. In the remaining 80 percent of the cases, no specific virus can be identified as the cause. Neonatal hepatitis presents with jaundice (yellow eyes and skin) that appears at one to two months of age, lack of weight gain and development, and enlarged liver and spleen. The infant cannot absorb vitamins for proper growth. Liver biopsy is often used for diagnosis, in part to differentiate neonatal hepatitis from biliary atresia. Patients with neonatal hepatitis caused by rubella or cytomegalovirus are at risk of developing an infection of the brain that could lead to mental retardation or cerebral palsy. Many of these infants will also have permanent liver disease from the destruction of liver cells and the resulting scarring (cirrhosis). Infants who develop cirrhosis ultimately will need a liver transplant. Chronic neonatal hepatitis will lead to the inability of the liver to eliminate toxins in the bile. This can cause itching, skin eruptions, and irritability. There is no specific treatment for neonatal hepatitis. Vitamin supplements are usually prescribed and many infants are given phenobarbital, a drug used to control seizures, but which also stimulates the liver to excrete additional bile. The fact sheet concludes with the contact information for ALF (800-GO-LIVER, www.liverfoundation.org). •
Your Child and Prednisone: Answers to Parents' Questions About Prednisone Source: Valencia, CA: Children's Liver Association for Support Services (C.L.A.S.S.). 1996. 18 p. Contact: Available from Children's Liver Association for Support Services (C.L.A.S.S.). 26444 Emerald Dove Drive, Valencia, CA 91355. (877) 679-8256 or (661) 255-0353. E-mail:
[email protected]. Website: www.classkids.org. PRICE: Single copy free; available on the Internet at http://www.classkids.org/library/pred.htm. Summary: Prednisone is one of the most universally prescribe immunosuppressant drugs. It is used to prevent rejection after organ transplantation, and also to treat autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus (SLE), polymyositis, and others. This brochure educates parents about the use of prednisone in children. Written in question and answer format, the brochure covers the uses of prednisone, how the drug works, the use of newer immunosuppressant drugs such as cyclosporine and tacrolimus, administration and dosage of prednisone, the side effects, and weaning the patient off of it. Prednisone works by doing many things to the immune cells that fight infection and cause rejection; the result is that all inflammatory processes are slowed and weakened. By turning down the body's ability to produce inflammation, an organ transplant can survive longer. Prednisone is used to supplement the use of other anti-rejection drugs. Pretension is given orally, or by intravenous (IV) route. Side effects can include ulcers and abdominal pain, high blood pressure, weight gain, acne, cataracts, difficulty sleeping, brittle (easily broken) bones, high blood sugar and a tendency to develop diabetes, muscular weakness, excess hair growth, mood swings and personality changes, and slowed growth in children. The booklet concludes with a glossary of related terms. The brochure also offers a brief description of Children's Liver Association for Support Services (CLASS), a nonprofit organization dedicated to addressing the emotional, educational, and financial needs of families coping with childhood liver disease and transplantation.
•
Managing Your Child's Eating Problems During Cancer Treatment Source: Bethesda, MD: National Cancer Institute (NCI), National Institutes of Health (NIH). March 1994. 33 p.
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Contact: Available from National Cancer Institute (NCI). Publications Ordering Service, P.O. Box 24128, Baltimore, MD 21227. (800) 422-6237. TTY (800) 332-8615. Fax (301) 3307968. Website: rex.nci.nih.gov. PRICE: Single copy free. NIH Publication Number 942038. Summary: This booklet contains a variety of ideas that have helped parents cope with their children's eating problems related to cancer treatment. The author describes the nutrition problems that may be associated with different cancer treatments and lists simple steps for the home care management of these problems. The booklet offers strategies for coping with the side effects of cancer therapy, including loss of appetite, sore mouth or throat, changed sense of taste, dry mouth, nausea, vomiting, diarrhea, constipation, weight gain, tooth decay, and lactose intolerance. A final section offers suggestions for increasing the child's intake of protein and calories. The booklet concludes with a glossary of terms and definitions related to diet, nutrition, and cancer treatment. The booklet also provides a brief description of the Cancer Information Service (800-4-CANCER) and the American Cancer Society (800-227-2345). 4 tables. •
Post Transplant Diet Source: Birmingham, AL: University of Alabama at Birmingham Hospital. 1998. 30 p. Contact: Available from University of Alabama at Birmingham Hospital. University Hospital. Department of Food and Nutrition Services, 619 South 19th Street, Birmingham, AL 35233. (205) 934-8055. Fax (205) 934-2987. PRICE: $3.25 for single copy; $2.75 each for five or more copies, plus shipping and handling. Summary: This booklet describes a dietary program that is designed to help people with transplants avoid some of the problems associated with their post-transplant drug therapy. The most common side effects of immunosupressive drugs include weight gain, increased blood sugar, increased blood pressure, increased fats in the blood (cholesterol and triglycerides), fluid and sodium gain, and weakened bones (osteoporosis). The booklet first reminds readers of the important role of diet therapy, and then outlines strategies to cut down on fats, sodium (salt), and starches and sweets. The booklet then reviews guidelines for fruits and vegetables, meat and meat substitutes, milk and milk products, and beverages. Other topics covered include reading labels, dining out, food preparation and recommended substitutions, bag lunches, herbs and spices to flavor foods, tips for weight control. The booklet then offers a chart of food groups, which summarizes the recommended foods, foods that are allowed in small amounts, and foods that are not recommended in each of the following groups: fats and oils; meat, poultry, and fish; dairy products; starches; fruits and vegetables; snacks and desserts; soups; and seasonings. A form for a sample meal pattern is provided; the dietitian can work with the patient to establish guidelines for each food group at each meal. The booklet concludes with nine pages of recipes, each of which has the nutrient analysis per serving noted. 3 tables.
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CHO Counting and CSII for Health Professionals Source: Salt Lake City, UT: Diabetes Health Center. 1994. 16 p. Contact: Available from Disetronic Medical Systems. 5201 E. River Road, Suite 312, Minneapolis, MN 55421-1014. (800) 688-4578 or (800) 280-7801 or (612) 551-1941. PRICE: Single copy free. Summary: This booklet familiarizes health professionals with the use of carbohydrate counting in people with diabetes who are adopting the intensive therapy approach to
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their diabetes management. The authors stress that it is helpful for the person with diabetes to be introduced to carbohydrate counting in conjunction with the move to intensive therapy in preparation for insulin pump therapy. Topics include the basics of carbohydrate counting, including nutrition assessment, calculating the meal plan, and weighing and measuring food for carbohydrate counting; other factors in foods that may impact blood glucose levels, including fat, fiber, protein, gastroparesis, and individualization; nutrition labels and carbohydrate counting; record keeping; insulin/carbohydrate ratios; and special considerations, including weight gain, shift work, and hypoglycemia awareness. The booklet concludes with a chart of the estimated time required to teach carbohydrate counting to patients. 10 references. •
Feeding an Infant with a Cleft Source: Chapel Hill, NC: Cleft Palate Foundation (CPF). 1997. 22 p. Contact: Available from Cleft Palate Foundation, Inc. 104 South Estes Drive, Suite 204, Chapel Hill, NC 27514. (800) 242-5338 or (919) 933-9044. Fax (919) 933-9604. Website: www.cleft.com. PRICE: Single copy free. Summary: This booklet offers strategies to help the parents of a baby born with a facial cleft (cleft lip or cleft palate) cope with feeding and nourishing their infant. The authors present some commonly accepted principles concerning the feeding of infants in general and then apply those principles to the feeding of an infant with a cleft. The authors emphasize that, following an initial period of consultation, decision making, and adjustment, feeding experiences between parent and infant should be easy and enjoyable. It should result in consistent and appropriate weight gain for the infant. Topics include the functions of feeding (beyond nourishment), quantity of nourishment needed, time required for feeding, frequency of feedings, breast feeding, feeding breast milk by bottle, formula feeding, positions for holding the infant during feeding, management of nasal regurgitation, use of palatal obturators, and introducing solid foods. The booklet concludes with a suggested food guide for babies and a list of the answers to questions parents commonly have. Line drawings illustrate the different types of clefts, and the different feeding positions discussed. 11 figures. 1 table.
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Steps to Gain Weight for Adults Source: Minneapolis, MD: Health Partner, Center for Health Promotion, 8p., 1991. Contact: Center for Health Promotion, Health Partners, Box 1309, 8100 34th Avenue, South, Minneapolis, MN 55440-1309. (612) 883-6713. Summary: This booklet provides suggestions for adults on how to eat well and increase calorie intake to promote weight gain. The steps involved in building a proper diet and weight increase include eating nutritious foods, adding extra calories, eating more often, avoiding filling but low-calorie foods, frying commercial supplements, and getting adequate rest and exercise. Recipes are included.
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Getting the Most from Your Treatment: What You Need to Know about Hemodialysis Source: New York, NY: National Kidney Foundation. 1998. 31 p. Contact: Available from National Kidney Foundation. 30 East 33rd Street, New York, NY 10016. (800) 622-9010. Website: www.kidney.org. PRICE: Single copy free. Summary: This booklet summarizes the use of hemodialysis to treat kidney diseases. The booklet tells readers why it is important to get the right amount of hemodialysis,
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how to care for the hemodialysis access, the complication of anemia and how it is treated, why diet restrictions must be followed carefully, how to help prevent bone disease and heart problems, how to cope with kidney disease and its treatment, how to get involved in one's own treatment plan and additional resources that are available. The brochure outlines the roles of each of the various health care team members who may be involved in the care of a person on hemodialysis. One section encourages readers to educate themselves about their disease and its treatment and to be very involved in their own health care. The brochure concludes with a section that summarizes the 13 laboratory tests commonly used to monitor patients with kidney disease: Kt per V and URR, nPNA, albumin (BCG test), hematocrit, hemoglobin, TSAT and serum ferritin, parathyroid hormone (PTH), calcium, phosphorus, potassium, target weight, average daily weight gain, and blood pressure. The brochure is written in nontechnical language and illustrated with simple line drawings. The brochure is one in a series of materials from an educational program of the National Kidney Foundation Dialysis Outcomes Quality Initiative. •
Carbohydrate Counting: Moving On (Level 2) Source: Alexandria, VA, and Chicago, IL: American Diabetes Association and The American Dietetic Association. 1995. 32 p. Contact: Available from American Diabetes Association. Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (404) 442-9742. PRICE: $15 (members) or $18 (nonmembers) for package of 10 booklets plus accompanying professional information (2 pages). Order Number CCCL2. Also available from The American Dietetic Association. 216 W. Jackson Boulevard, Chicago, IL 60606-6995. (800) 877-1600, ext. 5000. Summary: This booklet, the second in a series of three, builds on the basic concepts of carbohydrate counting as introduced in the first booklet. Readers develop their record keeping skills and learn to identify patterns in their blood glucose levels that are related to the food they eat, diabetes medications, and their physical activity levels. This technique, called pattern management, is presented in detail. Topics include food labels and carbohydrate counting; eating at restaurants; considerations about fat and protein; weight gain and hypoglycemia; and dietary fiber. The booklet includes examples and practice exercises for readers to practice their skills at pattern management. The series is designed for people with IDDM, NIDDM, and gestational diabetes mellitus (GDM). 9 references.
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Acute Rejection Episode Source: Lenexa, KS: North American Transplant Coordinators Organization. 199x. 2 p. Contact: Available from North American Transplant Coordinators Organization. P.O. Box 15384, Lenexa, KS 66285-5384. (913) 492-3600. PRICE: 0.25. Summary: This brief brochure answers questions about acute rejection commonly asked by patients undergoing kidney transplantation. Topics include a definition of acute rejection; when it usually occurs; symptoms of a rejection episode, including decreased urine output, fever, tenderness or swelling over the kidney, a rise in blood pressure, swelling of the hands and feet, weight gain, and flu-like feeling; how acute rejection episodes are diagnosed; the role of biopsy; and treatment options. The brochure emphasizes that early detection of rejection is the key to successful treatment. The brochure includes the address and telephone number of the North American Transplant Coordinators Organization.
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You Can Control Your Weight as You Quit Smoking Source: Bethesda, MD: NIDDK, NIH, 10p., 1998. Contact: Weight-control Information Network, 1 WIN Way, Bethesda, MD 20892-3665. (800) 946-8098. FAX: (301) 984-7196. Email
[email protected]. Web address: http://www.niddk.nih.gov/health/nutrit/win.htm. Summary: This brochure discusses how to quit smoking without gaining weight. The causes of possible weight gain after quitting smoking are discussed, as are the risks of smoking and the benefits of quitting. Tips to maintain weight and minimize weight gain are offered, such as becoming more physically active and improving eating habits. The brochure also gives suggestions on the smoking cessation process. A list of resources closes the pamphlet.
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Information About Kidney Care for Kids Source: Cincinnati, OH: Kidney Foundation of Greater Cincinnati. 1996. [1 p.]. Contact: Available from Kidney Foundation of Greater Cincinnati. 220 Victory Parkway, Suite 510, Cincinnati, OH 45206. (513) 961-8105. Fax (513) 961-8120. PRICE: Single copy free. Summary: This brochure discusses kidneys and kidney disorders in children. The brochure is from the African American Health Education Program of the Kidney Foundation of Greater Cincinnati. This program was specially designed for adults and children in the African American community at risk for kidney disease, particularly those who have, or who are at risk of having, high blood pressure or diabetes. The mission of the program is to prevent or slow down the onset of kidney disease within the African American community through ministry, education, and counseling. The brochure answers common questions about the role of the kidneys as a filtering and regulating system that helps to maintain blood pressure, the internal chemistry and hormones in the body, bone metabolism, and red blood cell production; and the most common kidney disorders in children, including urinary tract infections (UTI), nephrotic syndrome, glomerulonephritis, and hypertension (high blood pressure). The brochure includes a check list of the warning signs of kidney disease in children, including persistent changes in the frequency or appearance of urine, poor appetite, slow growth or weight gain, persistent abdominal pain, difficulties with urination, loss of energy, lower back pain, bedwetting in children over 4 or 5 years of age (especially if the child was previously dry all night), or unexplained low grade fever.
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Quit Smoking Without Gaining Weight: Ten Ways to Stay Fit While You Quit! Source: Santa Cruz, CA: Journeyworks Publishing, 9p., 1995. Contact: Journeyworks Publishing, PO Box 8466, Santa Cruz, CA 95061, (408) 423-1400. Summary: This brochure encourages smokers to quit and offers 10 suggestions for avoiding weight gain during the smoking cessation process. These suggestions include increasing physical activity, reducing stress, planning ahead for cessation, joining a support group, and planning menus.
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Gestational Diabetes: Diabetes When You're Pregnant Source: Santa Cruz, CA: ETR Associates. 2000. 6 p.
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Contact: Available from ETR Associates. 4 Carbonero Way, Scotts Valley, CA 950664200. (800) 321-4407. Fax (800) 435-8433. Website: www.etr.org. PRICE: Single copy free; $16.00 for 50 copies, discounts for larger orders. Summary: This brochure focuses on gestational diabetes. This form of diabetes occurs during pregnancy if a woman has too much sugar in her blood. A one hour glucose test and a glucose tolerance test are used to diagnose gestational diabetes. The brochure provides a checklist of health risks for gestational diabetes and suggests ways women can manage gestational diabetes. Tips include eating healthy foods every day, eating small meals and snacks, drinking eight glasses of water per day, drinking caffeine free drinks, taking vitamin supplements, avoiding foods that increase blood sugar, avoiding alcoholic beverages, checking blood sugar levels, quitting smoking, being physically active, and keeping track of weight gain. Other topics include labor, delivery, and follow up. •
Are You Ready to Quit Smoking? Source: Alexandria, VA: American Diabetes Association. 2001. [4 p.]. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. E-mail:
[email protected]. Website: www.diabetes.org. PRICE: $4.90 for package of 50; plus shipping and handling. Order number: 5983-17. Summary: This brochure helps readers with diabetes understand the negative impact of smoking. Topics include the risk factors associated with smoking, the difficulties of stopping smoking, weight gain associated with smoking, practical strategies to approaching any smoking cessation program, the top 10 benefits of giving up smoking, and the importance of getting assistance in any smoking cessation attempt. One sidebar reports a mock interview between a certified diabetes educator and a patient discussing these issues. The brochure includes space for readers to record their goals and plans for quitting smoking and their health care provider's contact information. The brochure is copiously illustrated with brightly colored graphics.
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New Beginnings: Post-Transplant Booklet Source: Nutley, NJ: Kidney Transplant Patient Partnering Program, Roche Laboratories. 1996. 8 p. Contact: Available from Kidney Transplant Patient Partnering Program. P.O. Box 16514, Kansas City, MO 64133. (800) 893-1995. Price: Single copy free. Summary: This brochure is part of the Kidney Transplant Partnering Program, an educational service of Roche Laboratories. The brochure focuses on life after the kidney transplant. The author emphasizes the patient's role in decision making and in all aspects of patient care management. Topics include concerns about rejection; returning to a normal lifestyle; taking antirejection medications; living with side effects, including swelling, increased appetite, unwanted hair growth, weight gain, tremors, and mood swings; finding and using support groups and other resources; and dealing with financial considerations. The brochure emphasizes the attitude of a kidney transplant as the beginning of a positive new phase in the patient's life. The brochure concludes with a glossary of related terms. The Kidney Transplant Patient Partnering Program was developed to help patients and their families understand and cope with the many physical and psychological issues that arise because of the kidney transplant process. (AA-M).
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Quit Smoking Without Gaining Weight. Good News for Smokers. Ten Ways to Stay Fit While You Quit! Source: Santa Cruz, CA: Journeyworks Publishing, 6p, 1995. Contact: Journeyworks Publishing, P.O. Box 8466, Santa Cruz, CA 95061. (408) 423-1400. Summary: This brochure offers suggestions to smokers who wish to quit smoking but are afraid of the accompanying weight gain. It is possible for people to stop smoking and maintain weight if they plan to increase physical activity, reduce stress, seek support, and change health habits.
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What You Should Know About Sugars Source: Washington DC: International Food Information Council Foundation. 1994. 4 p. Contact: Available from What You Should Know About Sugars. P.O. Box 1144, Rockville, MD 20850. (202) 296-6540. PRICE: Single copy free; send self-addressed stamped envelope. Summary: This brochure provides an overview of sugars and their role in a healthful diet. Written in a question-and-answer format, the brochure defines various types of sugar and discusses why sugars are added to foods, the safety of sugars, how the body uses sugars, how sugars fit into a healthful diet, how sugars are noted on the food label, the use of the terms sugar-free and reduced sugar on the labels of food packages, the relationship between sugars and hyperactivity, the role of sugar in the etiology of diabetes, the role of sugar in weight gain, hypoglycemia, and the role of sugars in tooth decay. One sidebar summarizes the different types of sugars used in foods, including fructose, glucose, high fructose corn syrup, and sucrose. 2 figures. 3 references.
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Gestational Diabetes: Caring for Yourself and Your Baby Source: Minneapolis, MN: International Diabetes Center, Park Nicollet Medical Foundation. 1995. 29 p. Contact: Available from HealthSource. 3800 Park Nicollet Boulevard, Minneapolis, MN 55416-9963. (800) 372-7776. PRICE: $2.95. ISBN: 1885115210. Summary: This brochure provides basic information about gestational diabetes. It covers caring for mother and baby with blood glucose control and monitoring; emotional balance; nutrition needs during pregnancy, including carbohydrate, protein, fat, making food choices, caloric intake, and weight gain; food and blood glucose control; physical activity and blood glucose control; taking insulin; testing guidelines and goals, including those for blood glucose and ketones; record-keeping; and postpregnancy considerations. The booklet features lists of practical suggestions for implementing each recommendation. The booklet also includes blank forms for readers to use for keeping blood glucose records. Simple charts and line drawings illustrate the booklet.
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Feeling Good About Not Using Tobacco Source: Midland, MI: Health Enhancement Systems. 1998. 6 p. Contact: Available from Health Enhancement Systems. P.O. Box 1035, Midland, MI 48641-1035. (800) 326-2317. Fax (517) 839-0025. PRICE: $0.98 each for a pack of 10 to 50 brochures; bulk quantities available; plus shipping and handling. Item number HESTF4.
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Summary: This brochure provides readers with information on feeling good about smoking cessation. The brochure begins by presenting ideas to help readers overcome some of the potential barriers to long term success such as feeling a nicotine craving, being in an environment where they are likely to smoke, and being frustrated with weight gain. This is followed by information on establishing goals that are specific, measurable, achievable, relevant, and trackable. Other topics include ways to reward oneself for striving to permanently quit using tobacco and ways friends or family members can be supportive. The brochure includes a personal wellness contract and a list of helpful organizations. •
Nutrition during pregnancy Source: Washington, DC: American College of Obstetricians and Gynecologists. 1992. 12 panels. Contact: Available from American College of Obstetricians and Gynecologists, 409 12th Street, S.W., Washington, DC 20024-2188. Telephone: (202) 638-5577 or (202) 863-2518 reference desk / Web site: http://www.acog.org/. $15.00 per pack of 50; discounts available for bulk orders. Summary: This brochure, developed for consumers, provides current information on nutrition during pregnancy. The components of a healthy diet, based on the four food groups, and basic nutrients such as protein, carbohydrates, fats, vitamins and minerals, and water are discussed. Information on meal planning, proper weight gain during pregnancy, and easing discomforts such as morning sickness, heartburn, and constipation is included. Special concerns are addressed regarding adolescents; vegetarians; breastfeeding women; women who use alcohol, tobacco, and other drugs; and women with lactose intolerance.
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Know the Facts About HIV and AIDS Contact: American Academy of Pediatrics, Committee on School Health, PO Box 927, Elk Grove Village, IL, 60009, (847) 228-5005, http://www.aap.org. Summary: This brochure, written for parents, provides general information about the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) and discusses how to teach children and adolescents about HIV/AIDS. HIV is spread from person to person by vaginal, anal, and oral intercourse; through contact with blood by sharing syringes or needles for drug use or other activities such as tattooing or body piercing; from mother to child during pregnancy, childbirth, or breastfeeding; and through blood transfusions or blood products. HIV is not transmitted through shaking hands, hugging, sitting next to someone, sharing bathrooms, eating food prepared by an HIV-positive person, breathing air, getting bit by an insect, giving blood, or swimming in pools. Parents are advised to teach young children that they should not touch anyone else's open sores, that they should never touch a syringe or a needle, that they should tell an adult when a syringe or needle is found, and that they cannot contract HIV from other infected children. The brochure recommends that parents educate preteens and teenagers about the advantages of sexual abstinence over safer sex in HIV prevention, safer sex, and the relationship between drug use, particularly injection drug use, and HIV/AIDS. The brochure identifies the symptoms of HIV/AIDS. These may include persistent fevers, loss of appetite, frequent diarrhea, poor weight gain or rapid weight loss, chronic lymph node swelling, persistent tiredness of lethargy, white spots in the mouth, and reoccurring or unusual infections. Individuals involved in risk behaviors should be tested for HIV.
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Dialysis Report Card: Understanding Your Lab Values Source: New York, NY: National Kidney Foundation. 1998. (chart). Contact: Available from National Kidney Foundation. 30 East 33rd Street, New York, NY 10016. (800) 622-9010. Website: www.kidney.org. PRICE: Single copy free. Summary: This chart helps patients on dialysis track important laboratory data and visualize where they stand in relation to established goals. The report card format offers room to record lab values for a 1-year period and is intended to help discussion among patients and the renal health care team about adequacy of treatment. The report card offers space to record 16 values: Kt per V, URR, nPNA, albumin (BCG test), hematocrit, hemoglobin, TSAT, serum ferritin, parathyroid hormone, calcium, phosphorus, potassium, target weight, average daily weight gain, predialysis blood pressure, and postdialysis blood pressure. The card also includes a space for the patient's individual goal numbers in each of these tests. The reverse side of the chart offers a few sentences of explanation for each of the 16 tests. These explanations focus primarily on the daily steps that patients can take to help their own health care be more successful. This report card is one of a series of materials from an educational program of the National Kidney Foundation Dialysis Outcomes Quality Initiative.
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OI Issues: Nutrition Source: Osteogenesis Imperfecta Foundation. 1999. 5 p. Contact: Available online from Osteogenesis Imperfecta Foundation. Website: www.oif.org. Summary: This fact sheet discusses the role of good nutrition in the diets of patients with osteogenesis imperfecta (OI). Children and adults with OI should eat a balanced diet; follow the Food Guide Pyramid; avoid excessive weight gain; and adjust portion size, meal frequency, and total calories depending upon the severity of OI, activity level, body size, and dental health. Although calcium intake does not affect the collagen defects that cause OI, adequate calcium promotes bone mass and prevents bone loss. Because patients with OI often have limited mobility, it is especially important to control weight that would put extra pressure on already weak bones. This can be done by limiting portion size. Another method for maintaining a healthy weight is by getting most calories from low fat, high nutrient foods. A high-fiber diet along with physical activity can help relieve constipation, a problem for some patients with OI. Healthy eating tips for parents and adults and a list of useful nutrition websites are included.
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Smoking and Your Digestive System Source: Bethesda, MD: National Digestive Diseases Information Clearinghouse. 1991. 4 p. Contact: Available from National Digestive Diseases Information Clearinghouse (NDDIC). 2 Information Way, Bethesda, MD 20892-3570. (800) 891-5389 or (301) 6543810. Fax (301) 634-0716. E-mail:
[email protected]. Website: www.niddk.nih.gov. PRICE: Full-text available online at no charge; single copy free; bulk copies available. Order Number: DD-52. Summary: This fact sheet explains that smoking is known to have harmful effects on all parts of the digestive system. Topics include how smoking contributes to heartburn, the relationship between smoking and peptic ulcers, how smoking affects the liver, the relationship between smoking and weight gain or loss, and reversing the damage that
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smoking causes to the digestive system. A brief final section describes the activities of the National Digestive Diseases Information Clearinghouse. •
Williams Syndrome Source: Bethesda, MD: National Institute of Neurological Disorders and Stroke. 1997. [1 p.]. Contact: Available from National Institute of Neurological Disorders and Stroke. Office of Scientific and Health Reports, P.O. Box 5801, Bethesda, MD 20824. (800) 352-9424 or (301) 496-5751. PRICE: Single copy free. Summary: This fact sheet from the National Institute of Neurological Disorders and Stroke describes Williams syndrome, a rare, congenital (present at birth) disorder characterized by physical and developmental problems. Common features include elfin facial features, heart and blood vessel problems, hypercalcemia, low birth weight, slow weight gain, feeding problems, irritability during infancy, dental and kidney abnormalities, hyperacusis (sensitive hearing), musculoskeletal problems, an impulsive and outgoing personality, limited spatial skills and motor control, and intellectual disability (i.e., developmental delay, learning disabilities, mental retardation, or attention deficit disorder). The fact sheet describes the syndrome, treatment options, prognosis, and present research efforts on the disorder. The fact sheet concludes with the telephone numbers and addresses for four organizations through which readers can obtain more information. 6 references.
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Immunosuppressants Source: New York, NY: National Kidney Foundation. 1993. [3 p.]. Contact: Available from National Kidney Foundation of Southern California. 5777 West Century Boulevard, Suite 1450, Los Angeles, CA 90045-7404. (310) 641-8152. Fax (310) 641-5246. Website: www.kidneysocal.org. PRICE: Single copy free; bulk copies available. Summary: This fact sheet offers kidney disease patients an overview of immunosuppressants, a group of drugs or medicines that suppress or lower the body's ability to reject a transplanted organ. These drugs are also called antirejection drugs. Examples of immunosuppressants used for kidney transplants are cyclosporine, azathioprine, prednisone, and FK506. The fact sheet, written in question and answer format, explains the use of immunosuppressants, what to do if a scheduled dose is missed, different drugs and dosages used for different patients, signs or symptoms of rejection (even while on immunosuppressants), the problem of increased risk of infection while on these drugs, specific recommendations for different drugs, the possible side effects of these drugs, and how to get additional information. Prednisone should be taken with meals or food because it can be irritating to the stomach. Side effects can include weight gain, muscle weakness, acne, trouble sleeping, stomach ulcers, diabetes, and cataracts. Azathioprine should be taken once a day. Side effects can include low white blood cell count, liver problems, anemia, and nightmares. Cyclosporine comes in liquid and capsule form; it is usually taken twice a day, but the dose can be adjusted based on the amount in the patient's blood. Side effects can include kidney damage (nephrotoxicity), overgrowth of gums (gingival hyperplasia), hair growth, hair darkening, high blood pressure, tremors of the hands, and liver problems. FK506 is a drug whose actions and side effects are similar to cyclosporine. The fact sheet concludes with a brief description of the National Kidney Foundation (NKF) and its activities.
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Lupus Guide Patient Information Handouts: Nutrition and Lupus Source: Bethesda, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1998. 2 p. Contact: Available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse. 1 AMS Circle, Bethesda, MD 20892-3675. (877) 226-4267 or (301) 495-4484. Fax (301) 718-6366. TTY (301) 565-2966. E-mail:
[email protected]. Website: www.niams.nih.gov. PRICE: Available only as part of a package of patient information sheets; single copy of package free. Order Number: AR-205. Summary: This fact sheet provides people who have systemic lupus erythematosus and the patient care team with information about the role of good nutrition in treating lupus. Good nutrition has an important role in the overall treatment plan. Although there are no specific dietary guidelines for people with lupus, they should be aware of such issues as weight loss or poor appetite, weight gain, and gastrointestinal problems associated with medications. In addition to discussing these issues, the fact sheet explains the role of diet in various conditions, including osteoporosis, steroid-induced diabetes, kidney disease, and cardiovascular disease. The fact sheet also includes space for making additional notes.
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Diabetes and Pregnancy Source: Alexandria, VA: American Diabetes Association. 199x. 4 p. Contact: Available from American Diabetes Association, Inc. Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. PRICE: $9.95 (members), $11.95 (nonmembers) for 50 copies; single copy free. Order number CDBD22. Summary: This fact sheet, which is one in a series of 42 fact sheets about daily living and coping with diabetes, provides information about diabetes and pregnancy. Topics include good prenatal care; insulin and diabetes pills; blood glucose testing; food and weight gain during pregnancy; pregnancy and exercise; delivery; postdelivery; and breastfeeding. The fact sheet notes that the key to a healthy pregnancy is tight blood glucose control both before and during pregnancy. They recommend a patient care team consisting of an obstetrician who handles high-risk pregnancies and has cared for other women with diabetes, a pediatrician, a registered dietitian, and a diabetes nurse educator. (AA-M).
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Facts about prenatal nutrition Source: San Diego, CA: San Diego Regional Center for the Developmentally Disabled. n.d. 1 p. Contact: Available from James O. Cleveland, Ed, D., San Diego- Imperial Counties Developmental Services, 4355 Ruffin Road, Suite 205, San Diego, CA 92123. Telephone: (619) 576-2813 / fax: 619-576-2873. Summary: This pamphlet answers some common questions about nutrition and weight gain for pregnant women. A complete chart of daily food needs shows food groups, examples from each group, and number of servings needed in the first trimester of pregnancy and in the last two trimesters of pregnancy.
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Eating for two: Nutrition during pregnancy Source: White Plains, NY: March of Dimes Birth Defects Foundation. 1994. 2 pp. (folded). Contact: Available from Supply Division, March of Dimes Birth Defects Foundation, 1275 Mamaroneck Avenue, White Plains, NY 10605. Telephone: (914) 428-7100 or (888) MODIMES or (914) 997-4764 TTY / e-mail:
[email protected] / Web site: http://www.modimes.org. $5.00 per pack of 50. Summary: This pamphlet for pregnant and breastfeeding women provides information on their nutritional needs and developing a healthy diet during pregnancy. It folds open to produce a poster explaining role of the food pyramid in making nutrition decisions. The pamphlet includes information on folic acid and weight gain, and it provides hints that will promote the health of the mother and baby.
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Kidney Disease and Lupus Source: Rockville, MD: Lupus Foundation of America. 1999. 6 p. Contact: Available from Lupus Foundation of America. 1300 Piccard Drive, Suite 200, Rockville, MD 20850-4303. (800) 558-0121 or (301) 670-9292. Fax (301) 670-9486. Website: www.lupus.org/lupus. PRICE: Available as part of a package of 21 different lupus related brochures for $3.95 plus shipping and handling. Summary: This pamphlet provides people who have systemic lupus erythematosus (SLE) with information on the kidney disease that accompanies it. This type of kidney disease, which is known as lupus nephritis or lupus glomerulonephritis, may affect about one third of those who have SLE. Symptoms that indicate the possibility of lupus nephritis include foamy, frothy urine; nocturnal urination; and fluid retention with weight gain and swelling. The clinical path of lupus nephritis is highly variable, with some people experiencing mild abnormalities and others experiencing more persistent, severe ones. Studies that can be performed to test for lupus nephritis are urinalysis, blood studies, 24 hour urine collection, imaging, and kidney biopsy. Corticosteroids and cytotoxic or immunosuppressive drugs are the major forms of drug therapy used to treat lupus nephritis. Despite treatment, some people may experience progressive loss of kidney function. These people will need hemodialysis or peritoneal dialysis and eventually kidney transplantation. The pamphlet also provides information on the Lupus Foundation of America. 1 table.
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Your Kidney Transplant: Good Nutrition, Better Health Source: Hamilton, Ontario: St. Joseph's Hospital, Nephrology Program. 1996. 9 p. Contact: Available from Veena Juneja, Renal Dietitian. St. Joseph's Hospital, 50 Charlton Avenue East, Hamilton, Ontario, L8N 4A6, Canada. PRICE: $2.00 per copy plus $2.00 shipping and handling. Summary: This patient education booklet provides a basic overview of posttransplant self care. Topics include the role of good nutrition in better health; the effects of antirejection medications; symptoms of complications; weight gain issues, including determining a healthy weight, why weight gain is typical after a transplant, and tips for weight watching; nutritional concerns, including the four food groups, getting enough fluids, the types of dietary fats, how to lower fat and cholesterol levels in the diet, and determining how much transfatty acid is in a product; physical activity; and working with a health care provider or team. The booklet is illustrated with simple line drawings.
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Dietary Guidelines For Post-Gastrectomy Dumping Syndrome Source: Rochester, MN: Mayo Clinic, Patient and Health Education Center. 1990. 2 p. Contact: Available from Mayo Clinic, Patient and Health Education Center. 200 First Street, SW, Rochester MN 55905. (507) 284-2511. PRICE: $0.80 plus shipping and handling (for health care professionals only). Order Number MC 833. Summary: This patient education brochure offers dietary suggestions for managing post-gastrectomy dumping syndrome. Symptoms of this syndrome may include diarrhea, nausea, vomiting, abdominal fullness, and gas. Topics include the importance of eating well-balanced, regularly scheduled meals; the role of sugars, protein-rich foods, dairy products, and fat-containing foods; fluid intake; and monitoring weight gain or loss. A sample menu for a suggested daily intake is provided. The brochure concludes with blank spaces for the listing of health care providers and phone numbers.
•
Nutrition for children with special health care needs Source: Birmingham, AL: Sparks Center for Developmental and Learning Disorders, University of Alabama at Birmingham. n.d. 10 brochures. Contact: Available from Janet Isaacs, University of Alabama at Birmingham, Sparks Center for Developmental and Learning Disorders, 1720 Seventh Avenue South, Birmingham, AL 35294. Telephone: (205) 934-5471 / fax: (205) 975-2380 / e-mail:
[email protected]. $2.50 (plus $3.00 if not prepaid). Summary: This set of brochures is designed to help parents of children with special health care needs promote their child's nutrition and good eating habits. A general brochure on nutritional goals, discussing growth, good feeding skills, disease resistance, energy, and normal elimination contains 9 subject specific brochures on: chewing, positioning for eating, weight gain, self-feeding, swallowing, relieving constipation, fluid needs, drinking from a cup, and preventing iron deficiency anemia.
•
Taking Care of Everyone: The Story of My Husband's Kidney Transplant, A Caregiver's Guide Source: Nutley, NJ: Kidney Transplant Patient Partnering Program, Roche Laboratories. 1997. 25 p. Contact: Available from Kidney Transplant Patient Partnering Program. P.O. Box 16514, Kansas City, MO 64133. (800) 893-1995. Price: Single copy free. Summary: This spiral-bound booklet offers the journal of a woman as she provides care for her husband before, during, and after he received a kidney transplant. The author notes that she and her husband were excited and hopeful about getting a kidney transplant, but they were also nervous and overwhelmed. She decided to keep a journal. Sections document waiting for a kidney, the ups and downs, financial issues, incorporating dialysis time into normal life, the role of the children and how to help them feel more involved, the importance of a positive outlook, the extra responsibilities placed on the caregiver, the need for the caregiver to take care of her-or himself, living in the present (even while waiting for a donated kidney), the need for counseling and talking about what is happening, support groups, handling the call from the hospital about a possible kidney, immediate postoperative issues, spending time at the hospital with one's spouse (and how to pack a necessaries bag), managing the hospital routine, asking friends to help (or accepting the help that is offered), recording medical information and questions to ask the physician, recuperating at home, handling the
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medications (antirejection drugs), handling weight gain, the importance of exercising, and rejection episodes. The journal is illustrated with colorful line drawings and it features uplifting quotations. •
Weight Management for Athletes: Sample Menus Source: Wisconsin: Dairy Council of Wisconsin, 1p., 1992. Contact: Dairy Council of Wisconsin, (800) 325-9121. Summary: This two-sided factsheet focuses on the importance of healthy eating for athletes. The factsheet offers tips for eating a well-balanced diet and suggestions for healthy weight loss, weight gain, and weight management strategies. The reverse side offers sample menus for 1,500, 2,000, and 3,000 calorie diets. The reader is advised to match food intake with his/her current activity level.
•
Update for Nutrition During Pregnancy and Lactation: An Implementation Guide Source: [Arlington, VA]: National Center for Education in Maternal and Child Health. 1998. 2 pp. Contact: Available from Librarian, National Center for Education in Maternal and Child Health, 2000 15th Street, North, Suite 701, Arlington, VA 22201-2617. Telephone: (703) 524-7802 / fax: (703) 524- 9335 / e-mail:
[email protected] / Web site: http://www.ncemch.org. Photocopy available at no charge. Summary: This update provides information to supplement the report Nutrition During Pregnancy and Lactation: An Implementation Guide. Topics covered are special recommendations for women before pregnancy; folate intake during pregnancy; calcium; the Maternal Weight Gain Expert Work Group; and HIV, AIDS, and other medical contraindications to breast feeding. A list of publications providing information about maternal nutrition research and projects available form the National Maternal and Child Health Clearinghouse is included. [Funded by the Maternal and Child Health Bureau]. Healthfinder™
Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •
You Can Control Your Weight as You Quit Smoking Summary: Advice for smokers who wish to quit but are afraid that they will experience post-cessation weight gain. Source: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4667
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The NIH Search Utility The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to weight gain. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to weight gain. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with weight gain. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about weight gain. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at
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http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “weight gain” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “weight gain”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “weight gain” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “weight gain” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.23
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
23
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)24: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
24
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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•
South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on weight gain: •
Basic Guidelines for Weight Gain Weight gain - unintentional Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003084.htm
•
Signs & Symptoms for Weight Gain Anxiety Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Appetite increased Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003134.htm Constipation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003125.htm Decreased urinary output Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003147.htm
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Depression Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003213.htm Edema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Fainting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003092.htm Fatigue Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Hair loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003246.htm Hunger Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003134.htm Insomnia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003210.htm Muscle weakness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003174.htm Overweight Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003101.htm Palpitations Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003081.htm Sensitivity to cold Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003095.htm Shortness of breath Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Sweating Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003218.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm •
Background Topics for Weight Gain Alcohol consumption Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001944.htm Endocrine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002351.htm
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Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Metabolism Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002257.htm Physical activity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Physical examination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002274.htm Smoking Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002032.htm
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
•
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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WEIGHT GAIN DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 5-alpha: Enzyme converting testosterone to dihydrotestosterone. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal fat: Fat (adipose tissue) that is centrally distributed between the thorax and pelvis and that induces greater health risk. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Abscess: Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection. [NIH] Absenteeism: Chronic absence from work or other duty. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acne Vulgaris: A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors. [NIH] Acoustic: Having to do with sound or hearing. [NIH] Actin: Essential component of the cell skeleton. [NIH] Actinin: A protein factor that regulates the length of R-actin. It is chemically similar, but immunochemically distinguishable from actin. [NIH] Activities of Daily Living: The performance of the basic activities of self care, such as dressing, ambulation, eating, etc., in rehabilitation. [NIH] Acuity: Clarity or clearness, especially of the vision. [EU] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing
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of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adolescent Nutrition: Nutrition of children aged 13-18 years. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adrenergic Agents: Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters. [NIH]
Adult-Onset Diabetes: Former term for noninsulin-dependent or type II diabetes. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerobic Exercise: A type of physical activity that includes walking, jogging, running, and dancing. Aerobic training improves the efficiency of the aerobic energy-producing systems that can improve cardiorespiratory endurance. [NIH] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the
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complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Aggressiveness: The quality of being aggressive (= characterized by aggression; militant; enterprising; spreading with vigour; chemically active; variable and adaptable). [EU] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Agoraphobia: Obsessive, persistent, intense fear of open places. [NIH] A-HA: First enzyme in the biosynthetic pathway of branched-chain amino acids. [NIH] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Akathisia: 1. A condition of motor restlessness in which there is a feeling of muscular quivering, an urge to move about constantly, and an inability to sit still, a common extrapyramidal side effect of neuroleptic drugs. 2. An inability to sit down because of intense anxiety at the thought of doing so. [EU] Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity
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(allergy). [EU] Allograft: An organ or tissue transplant between two humans. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-fetoprotein: AFP. A protein normally produced by a developing fetus. AFP levels are usually undetectable in the blood of healthy nonpregnant adults. An elevated level of AFP suggests the presence of either a primary liver cancer or germ cell tumor. [NIH] Alpha-Linolenic Acid: A fatty acid that is found in plants and involved in the formation of prostaglandins. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alum: A type of immune adjuvant (a substance used to help boost the immune response to a vaccine). Also called aluminum sulfate. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amenorrhea: Absence of menstruation. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Motifs: Commonly observed structural components of proteins formed by simple combinations of adjacent secondary structures. A commonly observed structure may be composed of a conserved sequence which can be represented by a consensus sequence. [NIH]
Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acid Substitution: The naturally occurring or experimentally induced replacement of one or more amino acids in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH]
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Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Ammonium Sulfate: Sulfuric acid diammonium salt. It is used in fractionation of proteins. [NIH]
Amniocentesis: Percutaneous transabdominal puncture of the uterus during pregnancy to obtain amniotic fluid. It is commonly used for fetal karyotype determination in order to diagnose abnormal fetal conditions. [NIH] Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Amphetamines: Analogs or derivatives of amphetamine. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopression, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation. [NIH] Amygdala: Almond-shaped group of basal nuclei anterior to the inferior horn of the lateral ventricle of the brain, within the temporal lobe. The amygdala is part of the limbic system. [NIH]
Amylase: An enzyme that helps the body digest starches. [NIH] Anabasine: A botanical insecticide. [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anaemia: A reduction below normal in the number of erythrocytes per cu. mm., in the quantity of haemoglobin, or in the volume of packed red cells per 100 ml. of blood which occurs when the equilibrium between blood loss (through bleeding or destruction) and blood production is disturbed. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable. [NIH] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered antigen. The reaction may include rapidly progressing urticaria, respiratory distress, vascular collapse, systemic shock, and death. [NIH] Anastomosis: A procedure to connect healthy sections of tubular structures in the body after the diseased portion has been surgically removed. [NIH]
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Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgenic: Producing masculine characteristics. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angina Pectoris: The symptom of paroxysmal pain consequent to myocardial ischemia usually of distinctive character, location and radiation, and provoked by a transient stressful situation during which the oxygen requirements of the myocardium exceed the capacity of the coronary circulation to supply it. [NIH] Angiotensin converting enzyme inhibitor: A drug used to decrease pressure inside blood vessels. [NIH] Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] Animal Husbandry: The science of breeding, feeding, and care of domestic animals; includes housing and nutrition. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Anorexia Nervosa: The chief symptoms are inability to eat, weight loss, and amenorrhea. [NIH]
Anorexiant: A drug, process, or event that leads to anorexia. [NIH] Anovulation: Suspension or cessation of ovulation in animals and humans. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anthropometry: The technique that deals with the measurement of the size, weight, and proportions of the human or other primate body. [NIH]
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Antiallergic: Counteracting allergy or allergic conditions. [EU] Antiangiogenic: Having to do with reducing the growth of new blood vessels. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticholinergic: An agent that blocks the parasympathetic nerves. Called also parasympatholytic. [EU] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antidepressant: A drug used to treat depression. [NIH] Antidiabetic: An agent that prevents or alleviates diabetes. [EU] Antidiabetic Agent: A substance that helps a person with diabetes control the level of glucose (sugar) in the blood so that the body works as it should. [NIH] Antidote: A remedy for counteracting a poison. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]
Anti-Obesity Agents: Agents that increase energy expenditure and weight loss by neural and chemical regulation. Beta-adrenergic agents and serotoninergic drugs have been
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experimentally used in patients with non-insulin dependent diabetes mellitus (NIDDM) to treat obesity. [NIH] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipruritic: Relieving or preventing itching. [EU] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antipsychotic Agents: Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in schizophrenia, senile dementia, transient psychosis following surgery or myocardial infarction, etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Anxiety Disorders: Disorders in which anxiety (persistent feelings of apprehension, tension, or uneasiness) is the predominant disturbance. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Apathy: Lack of feeling or emotion; indifference. [EU] Apnea: A transient absence of spontaneous respiration. [NIH] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Appetitive Behavior: Animal searching behavior. The variable introductory phase of an
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instinctive behavior pattern or sequence, e.g., looking for food, or sequential courtship patterns prior to mating. [NIH] Aqueous: Having to do with water. [NIH] Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in platelets. EC 1.13.11.31. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arcuate Nucleus: A nucleus located in the middle hypothalamus in the most ventral part of the third ventricle near the entrance of the infundibular recess. Its small cells are in close contact with the ependyma. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arthralgia: Pain in the joint. [NIH] Articular: Of or pertaining to a joint. [EU] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-amino-acids is obtained by the hydrolysis of proteins. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Aspirate: Fluid withdrawn from a lump, often a cyst, or a nipple. [NIH] Aspiration: The act of inhaling. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs
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to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Atherogenic: Causing the formation of plaque in the lining of the arteries. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] ATP: ATP an abbreviation for adenosine triphosphate, a compound which serves as a carrier of energy for cells. [NIH] Atrial: Pertaining to an atrium. [EU] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Auditory: Pertaining to the sense of hearing. [EU] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Autopsy: Postmortem examination of the body. [NIH] Auxin: A natural organic compound formed in actively growing parts of plants, particularly
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in the growing points of shoots, which in minute concentrations regulates cell expansion and other developmental processes. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Back Pain: Acute or chronic pain located in the posterior regions of the trunk, including the thoracic, lumbar, sacral, or adjacent regions. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriuria: The presence of bacteria in the urine with or without consequent urinary tract infection. Since bacteriuria is a clinical entity, the term does not preclude the use of urine/microbiology for technical discussions on the isolation and segregation of bacteria in the urine. [NIH] Balloon Dilatation: Nonoperative repair of occluded vessels, ducts, or valves by insertion of a balloon catheter. It is used, amoung other things, to treat varices, torn retinas, renal and biliary calculi, gastric, bronchial and rectal stenoses, and heart valves, and includes catheterization with Fogarty and Foley catheters. [NIH] Baroreflex: A negative feedback system which buffers short-term changes in blood pressure. Increased pressure stretches blood vessels which activates pressoreceptors (baroreceptors) in the vessel walls. The net response of the central nervous system is a reduction of central sympathetic outflow. This reduces blood pressure both by decreasing peripheral vascular resistance and by lowering cardiac output. Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure. [NIH]
Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] Bed Rest: Confinement of an individual to bed for therapeutic or experimental reasons. [NIH] Behavior Therapy: The application of modern theories of learning and conditioning in the treatment of behavior disorders. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Bentonite: A colloidal, hydrated aluminum silicate that swells 12 times its dry size when added to water. [NIH]
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Benzamides: Benzoic acid amides. [NIH] Benzene: Toxic, volatile, flammable liquid hydrocarbon biproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile Ducts: Tubes that carry bile from the liver to the gallbladder for storage and to the small intestine for use in digestion. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Atresia: Atresia of the biliary tract, most commonly of the extrahepatic bile ducts. [NIH]
Biliary Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioassay: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU]
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Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bipolar Disorder: A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence. [NIH] Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [NIH] Blood Cell Count: A count of the number of leukocytes and erythrocytes per unit volume in a sample of venous blood. A complete blood count (CBC) also includes measurement of the hemoglobin, hematocrit, and erythrocyte indices. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood transfusion: The administration of blood or blood products into a blood vessel. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Body Composition: The relative amounts of various components in the body, such as percent body fat. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Image: Individuals' personal concept of their bodies as objects in and bound by space, independently and apart from all other objects. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bone Density: The amount of mineral per square centimeter of bone. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by photon absorptiometry or x-ray computed tomography. [NIH]
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Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachial: All the nerves from the arm are ripped from the spinal cord. [NIH] Brachial Artery: The continuation of the axillary artery; it branches into the radial and ulnar arteries. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Breast Feeding: The nursing of an infant at the mother's breast. [NIH] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]
Bupropion: A unicyclic, aminoketone antidepressant. The mechanism of its therapeutic actions is not well understood, but it does appear to block dopamine uptake. The hydrochloride is available as an aid to smoking cessation treatment. [NIH] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic disease. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in
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the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium channel blocker: A drug used to relax the blood vessel and heart muscle, causing pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cell membranes or on the release and binding of calcium in intracellular pools. Since they are inducers of vascular and other smooth muscle relaxation, they are used in the drug therapy of hypertension and cerebrovascular spasms, as myocardial protective agents, and in the relaxation of uterine spasms. [NIH] Calcium Channels: Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue. [NIH] Calcium Chloride: A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Caloric intake: Refers to the number of calories (energy content) consumed. [NIH] Calorimeter: Measures the amounts of heat absorbed or given off by a solid, a liquid, or a gas. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the Solanaceae. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU]
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Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardioselective: Having greater activity on heart tissue than on other tissue. [EU] Cardiotoxicity: Toxicity that affects the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Castration: Surgical removal or artificial destruction of gonads. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catalytic Domain: The region of an enzyme that interacts with its substrate to cause the enzymatic reaction. [NIH] Cataracts: In medicine, an opacity of the crystalline lens of the eye obstructing partially or totally its transmission of light. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Catheters: A small, flexible tube that may be inserted into various parts of the body to inject
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or remove liquids. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cecum: The beginning of the large intestine. The cecum is connected to the lower part of the small intestine, called the ileum. [NIH] Celiac Disease: A disease characterized by intestinal malabsorption and precipitated by gluten-containing foods. The intestinal mucosa shows loss of villous structure. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell Lineage: The developmental history of cells as traced from the first division of the original cell or cells in the embryo. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Cerebellum: Part of the metencephalon that lies in the posterior cranial fossa behind the brain stem. It is concerned with the coordination of movement. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [NIH]
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Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Cetirizine: A potent second-generation histamine H1 antagonist that is effective in the treatment of allergic rhinitis, chronic urticaria, and pollen-induced asthma. Unlike many traditional antihistamines, it does not cause drowsiness or anticholinergic side effects. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemopreventive: Natural or synthetic compound used to intervene in the early precancerous stages of carcinogenesis. [NIH] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones. [NIH] Child Behavior: Any observable response or action of a child from 24 months through 12 years of age. For neonates or children younger than 24 months, infant behavior is available. [NIH]
Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking dopamine receptors. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup. [NIH] Cholecystectomy: Surgical removal of the gallbladder. [NIH] Cholecystokinin: A 33-amino acid peptide secreted by the upper intestinal mucosa and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety. [NIH] Choleretic: A choleretic agent. [EU]
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Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [NIH] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [NIH] Choroid Plexus: A villous structure of tangled masses of blood vessels contained within the third, lateral, and fourth ventricles of the brain. It regulates part of the production and composition of cerebrospinal fluid. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens. [NIH] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Cimetidine: A histamine congener, it competitively inhibits histamine binding to H2 receptors. Cimetidine has a range of pharmacological actions. It inhibits gastric acid secretion, as well as pepsin and gastrin output. It also blocks the activity of cytochrome P450. [NIH] Circadian: Repeated more or less daily, i. e. on a 23- to 25-hour cycle. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Claviceps: A genus of ascomycetous fungi, family Clavicipitaceae, order Hypocreales, parasitic on various grasses. The sclerotia contain several toxic alkaloids. Claviceps purpurea on rye causes ergotism. [NIH] Cleft Palate: Congenital fissure of the soft and/or hard palate, due to faulty fusion. [NIH]
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Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coca: Any of several South American shrubs of the Erythroxylon genus (and family) that yield cocaine; the leaves are chewed with alum for CNS stimulation. [NIH] Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [NIH] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is
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differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Colostomy: An opening into the colon from the outside of the body. A colostomy provides a new path for waste material to leave the body after part of the colon has been removed. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Comorbidity: The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the
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standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Compress: A plug used to occludate an orifice in the control of bleeding, or to mop up secretions; an absorbent pad. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Consensus Sequence: A theoretical representative nucleotide or amino acid sequence in which each nucleotide or amino acid is the one which occurs most frequently at that site in the different sequences which occur in nature. The phrase also refers to an actual sequence which approximates the theoretical consensus. A known conserved sequence set is represented by a consensus sequence. Commonly observed supersecondary protein structures (amino acid motifs) are often formed by conserved sequences. [NIH] Conserved Sequence: A sequence of amino acids in a polypeptide or of nucleotides in DNA or RNA that is similar across multiple species. A known set of conserved sequences is represented by a consensus sequence. Amino acid motifs are often composed of conserved sequences. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constriction: The act of constricting. [NIH] Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU]
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Contraception: Use of agents, devices, methods, or procedures which diminish the likelihood of or prevent conception. [NIH] Contraceptive: An agent that diminishes the likelihood of or prevents conception. [EU] Contractility: Capacity for becoming short in response to a suitable stimulus. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Controlled clinical trial: A clinical study that includes a comparison (control) group. The comparison group receives a placebo, another treatment, or no treatment at all. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]
Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Disease: Disorder of cardiac function due to an imbalance between myocardial function and the capacity of the coronary vessels to supply sufficient flow for normal function. It is a form of myocardial ischemia (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH]
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Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Coronary Vessels: The veins and arteries of the heart. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Corrosion: Irreversible destruction of skin tissue. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] Corticotropin-Releasing Hormone: A neuropeptide released by the hypothalamus that stimulates the release of corticotropin by the anterior pituitary gland. [NIH] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cotinine: 1-Methyl-5-(3-pyridyl)-2-pyrrolidinone antidepressant. Synonym: Scotine. [NIH]
fumarate.
Stimulant
proposed
as
Courtship: The mutual attraction between individuals of the opposite sex. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Creatine: An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. [NIH]
Creatine Kinase: A transferase that catalyzes formation of phosphocreatine from ATP + creatine. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic isoenzymes have been identified in human tissues: MM from skeletal muscle, MB from myocardial tissue, and BB from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins. EC 2.7.3.2. [NIH] Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Cribriform: Pierced with small holes as in a sieve. Refers to the appearance of a tumor when viewed under a microscope. The tumor appears to have open spaces or small holes inside. [NIH]
Criterion: A standard by which something may be judged. [EU]
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Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyanosis: A bluish or purplish discoloration of the skin and mucous membranes due to an increase in the amount of deoxygenated hemoglobin in the blood or a structural defect in the hemoglobin molecule. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cyproheptadine: A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc. [NIH] Cyst: A sac or capsule filled with fluid. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytokinin: One of a group of N-substituted adenines which promote the division of plant cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a
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continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeletal Proteins: Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible. [NIH]
Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Dairy Products: Raw and processed or manufactured milk and milk-derived products. These are usually from cows (bovine) but are also from goats, sheep, reindeer, and water buffalo. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Daunorubicin: Very toxic anthracycline aminoglycoside antibiotic isolated from Streptomyces peucetius and others, used in treatment of leukemias and other neoplasms. [NIH]
Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Decision Making: The process of making a selective intellectual judgment when presented with several complex alternatives consisting of several variables, and usually defining a course of action or an idea. [NIH] Defecation: The normal process of elimination of fecal material from the rectum. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or
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withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Delusions: A false belief regarding the self or persons or objects outside the self that persists despite the facts, and is not considered tenable by one's associates. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH] Dentists: Individuals licensed to practice dentistry. [NIH] Depersonalization: Alteration in the perception of the self so that the usual sense of one's own reality is lost, manifested in a sense of unreality or self-estrangement, in changes of body image, or in a feeling that one does not control his own actions and speech; seen in depersonalization disorder, schizophrenic disorders, and schizotypal personality disorder. Some do not draw a distinction between depersonalization and derealization, using depersonalization to include both. [EU] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Derealization: Is characterized by the loss of the sense of reality concerning one's surroundings. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process
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of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Dextrorotatory: Turning towards the right hand. [NIH] DHEA: Dehydroepiandrosterone. A substance that is being studied as a cancer prevention drug. It belongs to the family of drugs called steroids. [NIH] Diabetes Insipidus: A metabolic disorder due to disorders in the production or release of vasopressin. It is characterized by the chronic excretion of large amounts of low specific gravity urine and great thirst. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diabetic Retinopathy: Retinopathy associated with diabetes mellitus, which may be of the background type, progressively characterized by microaneurysms, interretinal punctuate macular edema, or of the proliferative type, characterized by neovascularization of the retina and optic disk, which may project into the vitreous, proliferation of fibrous tissue, vitreous hemorrhage, and retinal detachment. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialysate: A cleansing liquid used in the two major forms of dialysis--hemodialysis and peritoneal dialysis. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diastolic pressure: The lowest pressure to which blood pressure falls between contractions of the ventricles. [NIH] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados. [NIH]
Dietary Fiber: The remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins. [NIH] Dietetics: The study and regulation of the diet. [NIH] Dietitian: An expert in nutrition who helps people plan what and how much food to eat. [NIH]
Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH]
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Digital photography: A type of photography in which images can be viewed on a computer screen. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disaccharides: Sugars composed of two monosaccharides linked by glycoside bonds. [NIH] Disease Outbreaks: Sudden increase in the incidence of a disease. The concept includes epidemics. [NIH] Disease Reservoirs: Animate or inanimate sources which harbor disease-causing organisms and thus serve as potential sources of disease outbreaks. Reservoirs should be distinguished from vectors and carriers, which are agents of disease transmission rather than continuing sources of potential disease outbreaks. [NIH] Disease Transmission: The transmission of infectious disease or pathogens. When transmission is within the same species, the mode can be horizontal (disease transmission, horizontal) or vertical (disease transmission, vertical). [NIH] Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Disposition: A tendency either physical or mental toward certain diseases. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Diurnal: Occurring during the day. [EU] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] DNA Topoisomerase: An enzyme catalyzing ATP-independent breakage of single-stranded DNA, followed by passage and rejoining of another single-stranded DNA. This enzyme class brings about the conversion of one topological isomer of DNA into another, e.g., the relaxation of superhelical turns in DNA, the interconversion of simple and knotted rings of single-stranded DNA, and the intertwisting of single-stranded rings of complementary
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sequences. (From Enzyme Nomenclature, 1992) EC 5.99.1.2. [NIH] Dogfish: Sharks of the family Squalidae. The subfamily Squalinae are called dogfish sharks and comprise eight genera with about 44 species. Dogfish often appear in schools near shore and are destructive to fish and fishing gear. Their liver is valued for its oil and its flesh is often made into fertilizer. The Squalus acanthias or spiny dogfish figures heavily in biological research, especially with reference to its rectal gland in water-electrolyte studies. [NIH]
Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dosage Forms: Completed forms of the pharmaceutical preparation in which prescribed doses of medication are included. They are designed to resist action by gastric fluids, prevent vomiting and nausea, reduce or alleviate the undesirable taste and smells associated with oral administration, achieve a high concentration of drug at target site, or produce a delayed or long-acting drug effect. They include capsules, liniments, ointments, pharmaceutical solutions, powders, tablets, etc. [NIH] Dosage schedule: A scheme set up to determine and regulate size, frequency and number of doses. [EU] Dose-dependent: Refers to the effects of treatment with a drug. If the effects change when the dose of the drug is changed, the effects are said to be dose dependent. [NIH] Double-blinded: A clinical trial in which neither the medical staff nor the person knows which of several possible therapies the person is receiving. [NIH] Doxorubicin: Antineoplastic antibiotic obtained from Streptomyces peucetics. It is a hydroxy derivative of daunorubicin and is used in treatment of both leukemia and solid tumors. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Residues: Drugs and their metabolites which are found in the edible tissues and milk of animals after their medication with specific drugs. This term can also apply to drugs found in adipose tissue of humans after drug treatment. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Dumping Syndrome: Gastrointestinal nonfunctioning pylorus. [NIH]
symptoms
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Duodenal Ulcer: An ulcer in the lining of the first part of the small intestine (duodenum). [NIH]
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Duodenum: The first part of the small intestine. [NIH] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dyslipidemia: Disorders in the lipoprotein metabolism; classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high-density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low-density lipoprotein (LDL) cholesterol and low levels of HDL cholesterol predispose to premature atherosclerosis. [NIH] Dyspareunia: Painful sexual intercourse. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dystonia: Disordered tonicity of muscle. [EU] Dystrophin: A muscle protein localized in surface membranes which is the product of the Duchenne/Becker muscular dystrophy gene. Individuals with Duchenne muscular dystrophy usually lack dystrophin completely while those with Becker muscular dystrophy have dystrophin of an altered size. It shares features with other cytoskeletal proteins such as spectrin and alpha-actinin but the precise function of dystrophin is not clear. One possible role might be to preserve the integrity and alignment of the plasma membrane to the myofibrils during muscle contraction and relaxation. MW 400 kDa. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] Ectopic: Pertaining to or characterized by ectopia. [EU] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Ego: The conscious portion of the personality structure which serves to mediate between the demands of the primitive instinctual drives, (the id), of internalized parental and social prohibitions or the conscience, (the superego), and of reality. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Electroacupuncture: A form of acupuncture using low frequency electrically stimulated needles to produce analgesia and anesthesia and to treat disease. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid
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morphological changes and the differentiation of basic structures. [NIH] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH] Emesis: Vomiting; an act of vomiting. Also used as a word termination, as in haematemesis. [EU]
Empirical: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Enanthate: An oily injectable contraceptive given every 8 weeks. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalocele: Cerebral tissue herniation through a congenital or acquired defect in the skull. The majority of congenital encephaloceles occur in the occipital or frontal regions. Clinical features include a protuberant mass that may be pulsatile. The quantity and location of protruding neural tissue determines the type and degree of neurologic deficit. Visual defects, psychomotor developmental delay, and persistent motor deficits frequently occur. [NIH]
Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endocrinology: A subspecialty of internal medicine concerned with the metabolism, physiology, and disorders of the endocrine system. [NIH] Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]
Endometrium: The layer of tissue that lines the uterus. [NIH] Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH]
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Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Energy Intake: Total number of calories taken in daily whether ingested or by parenteral routes. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Ependyma: A thin membrane that lines the ventricles of the brain and the central canal of the spinal cord. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Ergot: Cataract due to ergot poisoning caused by eating of rye cereals contaminated by a fungus. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH]
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Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Escalation: Progressive use of more harmful drugs. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Estradiol: The most potent mammalian estrogenic hormone. It is produced in the ovary, placenta, testis, and possibly the adrenal cortex. [NIH] Estrogen: One of the two female sex hormones. [NIH] Estrogen Replacement Therapy: The use of hormonal agents with estrogen-like activity in postmenopausal or other estrogen-deficient women to alleviate effects of hormone deficiency, such as vasomotor symptoms, dyspareunia, and progressive development of osteoporosis. This may also include the use of progestational agents in combination therapy. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ethmoid: An unpaired cranial bone which helps form the medial walls of the orbits and contains the themoidal air cells which drain into the nose. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Ethnobotany: The plant lore and agricultural customs of a people. In the field of medicine, the emphasis is on traditional medicine and the existence and medicinal uses of plants and their constituents, both historically and in modern times. [NIH] Evacuation: An emptying, as of the bowels. [EU] Excipient: Any more or less inert substance added to a prescription in order to confer a suitable consistency or form to the drug; a vehicle. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Excrete: To get rid of waste from the body. [NIH] Exercise Test: Controlled physical activity, more strenuous than at rest, which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used. The intensity of exercise is often graded, using criteria such as rate of work done, oxygen consumption, and heart rate. Physiological data obtained from an exercise test may be used for diagnosis, prognosis, and evaluation of disease severity, and to evaluate therapy. Data may also be used in prescribing exercise by determining a person's exercise capacity. [NIH] Exercise Tolerance: The exercise capacity of an individual as measured by endurance (maximal exercise duration and/or maximal attained work load) during an exercise test. [NIH]
Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Expiration: The act of breathing out, or expelling air from the lungs. [EU] Extracellular: Outside a cell or cells. [EU]
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Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extrarenal: Outside of the kidney. [EU] Extravascular: Situated or occurring outside a vessel or the vessels. [EU] Extravascular Lung Water: Water present within the lungs; its volume is roughly equal to, or a little less than, the intracellular blood volume of the lungs. Accumulations of extravascular lung water result in pulmonary edema. [NIH] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Facial: Of or pertaining to the face. [EU] Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and salivary glands, and convey afferent information for taste from the anterior two-thirds of the tongue and for touch from the external ear. [NIH] Facial Nerve Diseases: Diseases of the facial nerve or nuclei. Pontine disorders may affect the facial nuclei or nerve fascicle. The nerve may be involved intracranially, along its course through the petrous portion of the temporal bone, or along its extracranial course. Clinical manifestations include facial muscle weakness, loss of taste from the anterior tongue, hyperacusis, and decreased lacrimation. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Famotidine: A competitive histamine H2-receptor antagonist. Its main pharmacodynamic effect is the inhibition of gastric secretion. [NIH] Fat: Total lipids including phospholipids. [NIH] Fathers: Male parents, human or animal. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Fatty Liver: The buildup of fat in liver cells. The most common cause is alcoholism. Other causes include obesity, diabetes, and pregnancy. Also called steatosis. [NIH] Febrile: Pertaining to or characterized by fever. [EU] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Feeding Behavior: Behavioral responses or sequences associated with eating including modes of feeding, rhythmic patterns of eating, and time intervals. [NIH]
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Femoral: Pertaining to the femur, or to the thigh. [EU] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH] Ferritin: An iron-containing protein complex that is formed by a combination of ferric iron with the protein apoferritin. [NIH] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH] Fetal Development: Morphologic and physiologic growth and development of the mammalian embryo or fetus. [NIH] Fetal Monitoring: Physiologic or biochemical monitoring of the fetus. It is usually done during labor and may be performed in conjunction with the monitoring of uterine activity. It may also be performed prenatally as when the mother is undergoing surgery. [NIH] Fetoprotein: Transabdominal aspiration of fluid from the amniotic sac with a view to detecting increases of alpha-fetoprotein in maternal blood during pregnancy, as this is an important indicator of open neural tube defects in the fetus. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fissure: Any cleft or groove, normal or otherwise; especially a deep fold in the cerebral cortex which involves the entire thickness of the brain wall. [EU] Flatulence: Production or presence of gas in the gastrointestinal tract which may be expelled through the anus. [NIH] Flatus: Gas passed through the rectum. [NIH] Fluid Therapy: Therapy whose basic objective is to restore the volume and composition of the body fluids to normal with respect to water-electrolyte balance. Fluids may be administered intravenously, orally, by intermittent gavage, or by hypodermoclysis. [NIH] Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants. [NIH] Fluphenazine: A phenothiazine used in the treatment of psychoses. Its properties and uses are generally similar to those of chlorpromazine. [NIH] Foetal: Of or pertaining to a fetus; pertaining to in utero development after the embryonic period. [EU]
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Foetoplacental: Pertaining to the fetus and placenta. [EU] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Follicles: Shafts through which hair grows. [NIH] Food Deprivation: The withholding of food in a structured experimental situation. [NIH] Food Habits: Acquired or learned food preferences. [NIH] Food Preferences: The selection of one food over another. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fossa: A cavity, depression, or pit. [NIH] Fourth Ventricle: An irregularly shaped cavity in the rhombencephalon, between the medulla oblongata, the pons, and the isthmus in front, and the cerebellum behind. It is continuous with the central canal of the cord below and with the cerebral aqueduct above, and through its lateral and median apertures it communicates with the subarachnoid space. [NIH]
Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Fructose: A type of sugar found in many fruits and vegetables and in honey. Fructose is used to sweeten some diet foods. It is considered a nutritive sweetener because it has calories. [NIH] Fundus: The larger part of a hollow organ that is farthest away from the organ's opening. The bladder, gallbladder, stomach, uterus, eye, and cavity of the middle ear all have a fundus. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Furosemide: A sulfamyl saluretic and diuretic. It has a fast onset and short duration of action and is used in edema and chronic renal insufficiency. [NIH] Galactosemia: Buildup of galactose in the blood. Caused by lack of one of the enzymes needed to break down galactose into glucose. [NIH] Galanin: A neurotransmitter. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH]
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Gallstones: The solid masses or stones made of cholesterol or bilirubin that form in the gallbladder or bile ducts. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastrectomy: An operation to remove all or part of the stomach. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastric Emptying: The evacuation of food from the stomach into the duodenum. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]
Gastric Mucosa: Surface epithelium in the stomach that invaginates into the lamina propria, forming gastric pits. Tubular glands, characteristic of each region of the stomach (cardiac, gastric, and pyloric), empty into the gastric pits. The gastric mucosa is made up of several different kinds of cells. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas). [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gastroparesis: Nerve or muscle damage in the stomach. Causes slow digestion and emptying, vomiting, nausea, or bloating. Also called delayed gastric emptying. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Counseling: Advising families of the risks involved pertaining to birth defects, in order that they may make an informed decision on current or future pregnancies. [NIH]
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Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genistein: An isoflavonoid derived from soy products. It inhibits protein-tyrosine kinase and topoisomerase-ii (dna topoisomerase (atp-hydrolysing)) activity and is used as an antineoplastic and antitumor agent. Experimentally, it has been shown to induce G2 phase arrest in human and murine cell lines. [NIH] Genital: Pertaining to the genitalia. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geographic Locations: All of the continents and every country situated within, the United States and each of the constituent states arranged by region, Canada and each of its provinces, Australia and each of its states, the major bodies of water and major islands on both hemispheres, and selected major cities. Although the geographic locations are not printed in index medicus as main headings, in indexing they are significant in epidemiologic studies and historical articles and for locating administrative units in education and the delivery of health care. [NIH] Geriatric: Pertaining to the treatment of the aged. [EU] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Gestational Age: Age of the conceptus. In humans, this may be assessed by medical history, physical examination, early immunologic pregnancy tests, radiography, ultrasonography, and amniotic fluid analysis. [NIH] Gibberellin: One of a class of plant hormones that promote elongation. Synthesis occurs mainly in leaves and roots. They function by stimulating cell division and the hydrolisis of sugars to glucose and fructose, and stimulate extensive growth, especially of internodes. [NIH]
Ginger: Deciduous plant rich in volatile oil (oils, volatile). It is used as a flavoring agent and has many other uses both internally and topically. [NIH] Gingival Hyperplasia: A pathological increase in the depth of the gingival crevice surrounding a tooth at the gum margin. [NIH] Ginseng: An araliaceous genus of plants that contains a number of pharmacologically active agents used as stimulants, sedatives, and tonics, especially in traditional medicine. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the
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result of immune glomerular injury. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucose tolerance: The power of the normal liver to absorb and store large quantities of glucose and the effectiveness of intestinal absorption of glucose. The glucose tolerance test is a metabolic test of carbohydrate tolerance that measures active insulin, a hepatic function based on the ability of the liver to absorb glucose. The test consists of ingesting 100 grams of glucose into a fasting stomach; blood sugar should return to normal in 2 to 21 hours after ingestion. [NIH] Glucose Tolerance Test: Determination of whole blood or plasma sugar in a fasting state before and at prescribed intervals (usually 1/2 hr, 1 hr, 3 hr, 4 hr) after taking a specified amount (usually 100 gm orally) of glucose. [NIH] Glucosidases: Enzymes that hydrolyze O-glucosyl-compounds. (Enzyme Nomenclature, 1992) EC 3.2.1.-. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Gluten: The protein of wheat and other grains which gives to the dough its tough elastic character. [EU] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycogen Synthase: An enzyme that catalyzes the transfer of D-glucose from UDPglucose
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into 1,4-alpha-D-glucosyl chains. EC 2.4.1.11. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Glycosidic: Formed by elimination of water between the anomeric hydroxyl of one sugar and a hydroxyl of another sugar molecule. [NIH] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonadotropin: The water-soluble follicle stimulating substance, by some believed to originate in chorionic tissue, obtained from the serum of pregnant mares. It is used to supplement the action of estrogens. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Survival: The survival of a graft in a host, the factors responsible for the survival and the changes occurring within the graft during growth in the host. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granule: A small pill made from sucrose. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and
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pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Haloperidol: Butyrophenone derivative. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Behavior: Behaviors expressed by individuals to protect, maintain or promote their health status. For example, proper diet, and appropriate exercise are activities perceived to influence health status. Life style is closely associated with health behavior and factors influencing life style are socioeconomic, educational, and cultural. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Status: The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heart Valves: Flaps of tissue that prevent regurgitation of blood from the ventricles to the atria or from the pulmonary arteries or aorta to the ventricles. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Heartburn: Substernal pain or burning sensation, usually associated with regurgitation of gastric juice into the esophagus. [NIH] Hematocrit: Measurement of the volume of packed red cells in a blood specimen by centrifugation. The procedure is performed using a tube with graduated markings or with automated blood cell counters. It is used as an indicator of erythrocyte status in disease. For example, anemia shows a low hematocrit, polycythemia, high values. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [NIH]
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Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobin M: A group of abnormal hemoglobins in which amino acid substitutions take place in either the alpha or beta chains but near the heme iron. This results in facilitated oxidation of the hemoglobin to yield excess methemoglobin which leads to cyanosis. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]
Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatitis C: A form of hepatitis, similar to type B post-transfusion hepatitis, but caused by a virus which is serologically distinct from the agents of hepatitis A, B, and E, and which may persist in the blood of chronic asymptomatic carriers. Hepatitis C is parenterally transmitted and associated with transfusions and drug abuse. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Herpes Zoster: Acute vesicular inflammation. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterotrophic: Pertaining to organisms that are consumers and dependent on other organisms for their source of energy (food). [NIH] Heterozygote: An individual having different alleles at one or more loci in homologous chromosome segments. [NIH] Hiccup: A spasm of the diaphragm that causes a sudden inhalation followed by rapid closure of the glottis which produces a sound. [NIH] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH]
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Hirsutism: Excess hair in females and children with an adult male pattern of distribution. The concept does not include hypertrichosis, which is localized or generalized excess hair. [NIH]
Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Holidays: Days commemorating events. Holidays also include vacation periods. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hormone Replacement Therapy: Therapeutic use of hormones to alleviate the effects of hormone deficiency. [NIH] Hormone therapy: Treatment of cancer by removing, blocking, or adding hormones. Also called endocrine therapy. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human growth hormone: A protein hormone, secreted by the anterior lobe of the pituitary, which promotes growth of the whole body by stimulating protein synthesis. The human gene has already been cloned and successfully expressed in bacteria. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH]
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Hydroxyzine: A histamine H1 receptor antagonist that is effective in the treatment of chronic urticaria, dermatitis, and histamine-mediated pruritus. Unlike its major metabolite cetirizine, it does cause drowsiness. It is also effective as an antiemetic, for relief of anxiety and tension, and as a sedative. [NIH] Hyperacusis: An abnormally disproportionate increase in the sensation of loudness in response to auditory stimuli of normal volume. Cochlear diseases; vestibulocochlear nerve diseases; facial nerve diseases; stapes surgery; and other disorders may be associated with this condition. [NIH] Hyperandrogenism: A state characterized or caused by an excessive secretion of androgens by the adrenal cortex, ovaries, or testes. The clinical significance in males is negligible, so the term is used most commonly with reference to the female. The common manifestations in women are hirsutism and virilism. It is often caused by ovarian disease (particularly the polycystic ovary syndrome) and by adrenal diseases (particularly adrenal gland hyperfunction). [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypercalcemia: Abnormally high level of calcium in the blood. [NIH] Hypercholesterolemia: Abnormally high levels of cholesterol in the blood. [NIH] Hyperemesis: Excessive vomiting. [EU] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthyroidism: Excessive functional activity of the thyroid gland. [NIH] Hypertrichosis: Localized or generalized excess hair. The concept does not include hirsutism, which is excess hair in females and children with an adult male pattern of distribution. [NIH] Hypertriglyceridemia: Condition of elevated triglyceride concentration in the blood; an inherited form occurs in familial hyperlipoproteinemia IIb and hyperlipoproteinemia type IV. It has been linked to higher risk of heart disease and arteriosclerosis. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]
Hypoglycemic Agents: Agents which lower the blood glucose level. [NIH] Hypophyseal: Hypophysial. [EU] Hypotension: Abnormally low blood pressure. [NIH] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypotonia: A condition of diminished tone of the skeletal muscles; diminished resistance of
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muscles to passive stretching. [EU] Hypoxemia: Deficient oxygenation of the blood; hypoxia. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Ileum: The lower end of the small intestine. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group. [NIH]
Immersion: The placing of a body or a part thereof into a liquid. [NIH] Immune adjuvant: A drug that stimulates the immune system to respond to disease. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulins: Glycoproteins present in the blood (antibodies) and in other tissue. They are classified by structure and activity into five classes (IgA, IgD, IgE, IgG, IgM). [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] Impotence: The inability to perform sexual intercourse. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH]
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Incision: A cut made in the body during surgery. [NIH] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubator: Consists of a transparent plastic cubicle, electrical heating equipment, safety and warning devices, and oxygen and air filtering and regulating apparatus; an enclosed transparent boxlike apparatus for housing prematurely born babies under optimum conditions. [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indigestion: Poor digestion. Symptoms include heartburn, nausea, bloating, and gas. Also called dyspepsia. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant Behavior: Any observable response or action of a neonate or infant up through the age of 23 months. [NIH] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Informed Consent: Voluntary authorization, given to the physician by the patient, with full comprehension of the risks involved, for diagnostic or investigative procedures and medical and surgical treatment. [NIH] Infuse: To pour (a liquid) into something. [EU] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH]
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Infusion Pumps: Fluid propulsion systems driven mechanically, electrically, or osmotically that are used to inject (or infuse) over time agents into a patient or experimental animal; used routinely in hospitals to maintain a patent intravenous line, to administer antineoplastic agents and other drugs in thromboembolism, heart disease, diabetes mellitus (insulin infusion systems is also available), and other disorders. [NIH] Infusion Pumps, Implantable: Implanted fluid propulsion systems with self-contained power source for providing long-term controlled-rate delivery of drugs such as chemotherapeutic agents or analgesics. Delivery rate may be externally controlled or osmotically or peristaltically controlled with the aid of transcutaneous monitoring. [NIH] Ingestion: Taking into the body by mouth [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inlay: In dentistry, a filling first made to correspond with the form of a dental cavity and then cemented into the cavity. [NIH] Inoculum: The spores or tissues of a pathogen that serve to initiate disease in a plant. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU] Inpatients: Persons admitted to health facilities which provide board and room, for the purpose of observation, care, diagnosis or treatment. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insomnia: Difficulty in going to sleep or getting enough sleep. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin Infusion Systems: Portable or implantable devices for infusion of insulin. Includes open-loop systems which may be patient-operated or controlled by a pre-set program and are designed for constant delivery of small quantities of insulin, increased during food ingestion, and closed-loop systems which deliver quantities of insulin automatically based on an electronic glucose sensor. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]
Interferon: A biological response modifier (a substance that can improve the body's natural
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response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-6: Factor that stimulates the growth and differentiation of human B-cells and is also a growth factor for hybridomas and plasmacytomas. It is produced by many different cells including T-cells, monocytes, and fibroblasts. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intervention Studies: Epidemiologic investigations designed to test a hypothesized causeeffect relation by modifying the supposed causal factor(s) in the study population. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestinal Obstruction: Any impairment, arrest, or reversal of the normal flow of intestinal contents toward the anus. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intraocular: Within the eye. [EU] Intraocular pressure: Pressure of the fluid inside the eye; normal IOP varies among individuals. [NIH] Intraperitoneal: IP. Within the peritoneal cavity (the area that contains the abdominal organs). [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Introspection: Examination by a person of his own feelings, thoughts, and mental state. [NIH]
Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ions: An atom or group of atoms that have a positive or negative electric charge due to a
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gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irritable Bowel Syndrome: A disorder that comes and goes. Nerves that control the muscles in the GI tract are too active. The GI tract becomes sensitive to food, stool, gas, and stress. Causes abdominal pain, bloating, and constipation or diarrhea. Also called spastic colon or mucous colitis. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Islet: Cell producing insulin in pancreas. [NIH] Isoenzyme: Different forms of an enzyme, usually occurring in different tissues. The isoenzymes of a particular enzyme catalyze the same reaction but they differ in some of their properties. [NIH] Isoflavones: 3-Phenylchromones. Isomeric form of flavones in which the benzene group is attached to the 3 position of the benzopyran ring instead of the 2 position. [NIH] Isoleucine: An essential branched-chain amino acid found in many proteins. It is an isomer of LEUCINE. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
Jejunoileal Bypass: A surgical procedure consisting of the anastomosis of the proximal part of the jejunum to the distal portion of the ileum, so as to bypass the nutrient-absorptive segment of the small intestine, to treat morbid obesity. [NIH] Jejunum: That portion of the small intestine which extends from the duodenum to the ileum; called also intestinum jejunum. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Karyotype: The characteristic chromosome complement of an individual, race, or species as defined by their number, size, shape, etc. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Ketotifen: A cycloheptathiophene that interferes with the release of inflammatory mediators and blocks histamine H1 receptors. It has been proposed as an anti-asthmatic and for the treatment of rhinitis, skin allergies, and anaphylaxis. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney stone: A stone that develops from crystals that form in urine and build up on the inner surfaces of the kidney, in the renal pelvis, or in the ureters. [NIH] Kidney Transplantation: The transference of a kidney from one human or animal to another. [NIH]
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Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactation: The period of the secretion of milk. [EU] Lactose Intolerance: The disease state resulting from the absence of lactase enzyme in the musocal cells of the gastrointestinal tract, and therefore an inability to break down the disaccharide lactose in milk for absorption from the gastrointestinal tract. It is manifested by indigestion of a mild nature to severe diarrhea. It may be due to inborn defect genetically conditioned or may be acquired. [NIH] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Levo: It is an experimental treatment for heroin addiction that was developed by German scientists around 1948 as an analgesic. Like methadone, it binds with opioid receptors, but it is longer acting. [NIH] Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Limbic: Pertaining to a limbus, or margin; forming a border around. [EU] Limbic System: A set of forebrain structures common to all mammals that is defined
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functionally and anatomically. It is implicated in the higher integration of visceral, olfactory, and somatic information as well as homeostatic responses including fundamental survival behaviors (feeding, mating, emotion). For most authors, it includes the amygdala, epithalamus, gyrus cinguli, hippocampal formation (see hippocampus), hypothalamus, parahippocampal gyrus, septal nuclei, anterior nuclear group of thalamus, and portions of the basal ganglia. (Parent, Carpenter's Human Neuroanatomy, 9th ed, p744; NeuroNames, http://rprcsgi.rprc.washington.edu/neuronames/index.html (September 2, 1998)). [NIH] Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Linoleic Acids: Eighteen-carbon essential fatty acids that contain two double bonds. [NIH] Lip: Either of the two fleshy, full-blooded margins of the mouth. [NIH] Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3. [NIH] Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipodystrophy: A collection of rare conditions resulting from defective fat metabolism and characterized by atrophy of the subcutaneous fat. They include total, congenital or acquired, partial, abdominal infantile, and localized lipodystrophy. [NIH] Lipopolysaccharides: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liposomal: A drug preparation that contains the active drug in very tiny fat particles. This fat-encapsulated drug is absorbed better, and its distribution to the tumor site is improved. [NIH]
Liposome: A spherical particle in an aqueous medium, formed by a lipid bilayer enclosing an aqueous compartment. [EU] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Litter: Appliance consisting of an oblong frame over which is stretched a canvas or other material, used for carrying an injured or disabled person. [NIH] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood
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and aids in digestion by secreting bile. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Locomotor: Of or pertaining to locomotion; pertaining to or affecting the locomotive apparatus of the body. [EU] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Long-Term Care: Care over an extended period, usually for a chronic condition or disability, requiring periodic, intermittent, or continuous care. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lumen: The cavity or channel within a tube or tubular organ. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lupus Nephritis: Glomerulonephritis associated with systemic lupus erythematosus. It is classified into four histologic types: mesangial, focal, diffuse, and membranous. [NIH] Lutein Cells: The cells of the corpus luteum which are derived from the granulosa cells and the theca cells of the Graafian follicle. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH]
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Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macronutrients: Nutrients in the diet that are the key sources of energy, namely protein, fat, and carbohydrates. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Maintenance therapy: Treatment that is given to help a primary (original) treatment keep working. Maintenance therapy is often given to help keep cancer in remission. [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malaise: A vague feeling of bodily discomfort. [EU] Malaria: A protozoan disease caused in humans by four species of the genus Plasmodium (P. falciparum (malaria, falciparum), P. vivax (malaria, vivax), P. ovale, and P. malariae) and transmitted by the bite of an infected female mosquito of the genus Anopheles. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high fever, sweating, shaking chills, and anemia. Malaria in animals is caused by other species of plasmodia. [NIH] Malaria, Falciparum: Malaria caused by Plasmodium falciparum. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations. [NIH] Malaria, Vivax: Malaria caused by Plasmodium vivax. This form of malaria is less severe than malaria, falciparum, but there is a higher probability for relapses to occur. Febrile paroxysms often occur every other day. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammary: Pertaining to the mamma, or breast. [EU] Mammography: Radiographic examination of the breast. [NIH] Mania: Excitement of psychotic proportions manifested by mental and physical
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hyperactivity, disorganization of behaviour, and elevation of mood. [EU] Manic: Affected with mania. [EU] Manic-depressive psychosis: One of a group of psychotic reactions, fundamentally marked by severe mood swings and a tendency to remission and recurrence. [NIH] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mean blood pressure: The average blood pressure, taking account of the rise and fall that occurs with each heartbeat. It is often estimated by multiplying the diastolic pressure by two, adding the systolic pressure, and then dividing this sum by three. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Meat Products: Articles of food which are derived by a process of manufacture from any portion of carcasses of any animal used for food (e.g., head cheese, sausage, scrapple). [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Median Eminence: Raised area on the infundibular hypothalamus at the floor of the third ventricle of the brain which contains the primary capillary network of the hypophyseal portal system. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medical Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency. [NIH] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medroxyprogesterone: (6 alpha)-17-Hydroxy-6-methylpregn-4-ene-3,20-dione. A synthetic progestational hormone used in veterinary practice as an estrus regulator. [NIH] Medroxyprogesterone Acetate: An injectable contraceptive, generally marketed under the name Depo-Provera. [NIH] Megaloblastic: A large abnormal red blood cell appearing in the blood in pernicious anaemia. [EU] Megestrol: 17-Hydroxy-6-methylpregna-3,6-diene-3,20-dione. A progestational hormone used most commonly as the acetate ester. As the acetate, it is more potent than progesterone both as a progestagen and as an ovulation inhibitor. It has also been used in the palliative treatment of breast cancer. [NIH] Megestrol Acetate: A drug that belongs to the group of hormones called progestins, used as hormone therapy to block estrogen and to suppress the effects of estrogen and androgens. [NIH]
Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH]
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Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Menarche: The establishment or beginning of the menstrual function. [EU] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Menopause: Permanent cessation of menstruation. [NIH] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH]
Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mesolimbic: Inner brain region governing emotion and drives. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH]
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Micronutrients: Essential dietary elements or organic compounds that are required in only small quantities for normal physiologic processes to occur. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Midaxillary line: An imaginary vertical line that passes midway between the anterior and posterior axillary (armpit) folds. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Milliliter: A measure of volume for a liquid. A milliliter is approximately 950-times smaller than a quart and 30-times smaller than a fluid ounce. A milliliter of liquid and a cubic centimeter (cc) of liquid are the same. [NIH] Millimeter: A measure of length. A millimeter is approximately 26-times smaller than an inch. [NIH] Mineralocorticoids: A group of corticosteroids primarily associated with the regulation of water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II. [NIH] Minority Groups: A subgroup having special characteristics within a larger group, often bound together by special ties which distinguish it from the larger group. [NIH] Miscarriage: Spontaneous expulsion of the products of pregnancy before the middle of the second trimester. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular Structure: The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds. [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoamine: Enzyme that breaks down dopamine in the astrocytes and microglia. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH]
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Monotherapy: A therapy which uses only one drug. [EU] Mood Disorders: Those disorders that have a disturbance in mood as their predominant feature. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Movement Disorders: Syndromes which feature dyskinesias as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucociliary: Pertaining to or affecting the mucus membrane and hairs (including eyelashes, nose hair, .): mucociliary clearing: the clearance of mucus by ciliary movement ( particularly in the respiratory system). [EU] Mucociliary Clearance: Rate of ciliary and secretory activity of the respiratory submucosal glands. It is a non-specific host defense mechanism, measurable in vivo by mucus transfer, ciliary beat frequency, and clearance of radioactive tracers. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables. [NIH] Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Mycotoxicosis: Poisoning caused by the ingestion of mycotoxins (toxins of fungal origin). [NIH]
Mycotoxins: Toxins derived from bacteria or fungi. [NIH] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myelin: The fatty substance that covers and protects nerves. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH]
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Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myofibrils: Highly organized bundles of actin, myosin, and other proteins in the cytoplasm of skeletal and cardiac muscle cells that contract by a sliding filament mechanism. [NIH] Nadir: The lowest point; point of greatest adversity or despair. [EU] Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors. [NIH] Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of naloxone. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence. [NIH] Narcolepsy: A condition of unknown cause characterized by a periodic uncontrollable tendency to fall asleep. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Nasogastric: The process of passing a small, flexible plastic tube through the nose or mouth into the stomach or small intestine. [NIH] Natriuresis: The excretion of abnormal amounts of sodium in the urine. [EU] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neonatal Hepatitis: Irritation of the liver with no known cause. Occurs in newborn babies. Symptoms include jaundice and liver cell changes. [NIH] Neonatal period: The first 4 weeks after birth. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephrologist: A doctor who treats patients with kidney problems or hypertension. [NIH]
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Nephropathy: Disease of the kidneys. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neural tube defects: These defects include problems stemming from fetal development of the spinal cord, spine, brain, and skull, and include birth defects such as spina bifida, anencephaly, and encephalocele. Neural tube defects occur early in pregnancy at about 4 to 6 weeks, usually before a woman knows she is pregnant. Many babies with neural tube defects have difficulty walking and with bladder and bowel control. [NIH] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [NIH] Neuroendocrinology: The study of the anatomical and functional relationships between the nervous system and the endocrine system. [NIH] Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of emotion and in psychotic patients cause a reduction in confusion and agitation and normalization of psychomotor activity. [EU] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH]
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Niacin: Water-soluble vitamin of the B complex occurring in various animal and plant tissues. Required by the body for the formation of coenzymes NAD and NADP. Has pellagra-curative, vasodilating, and antilipemic properties. [NIH] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] Nidation: Implantation of the conceptus in the endometrium. [EU] Nipples: The conic organs which usually give outlet to milk from the mammary glands. [NIH]
Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nizatidine: A histamine H2 receptor antagonist with low toxicity that inhibits gastric acid secretion. The drug is used for the treatment of duodenal ulcers. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Normal Distribution: Continuous frequency distribution of infinite range. Its properties are as follows: 1) continuous, symmetrical distribution with both tails extending to infinity; 2) arithmetic mean, mode, and median identical; and 3) shape completely determined by the mean and standard deviation. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nurseries: Facilities which provide care for infants. [NIH] Nursing Care: Care given to patients by nursing service personnel. [NIH] Nutrition Assessment: Evaluation and measurement of nutritional variables in order to assess the level of nutrition or the nutritional status of the individual. Nutrition surveys may be used in making the assessment. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH]
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Nutritional Support: The administration of nutrients for assimilation and utilization by a patient by means other than normal eating. It does not include fluid therapy which normalizes body fluids to restore water-electrolyte balance. [NIH] Observational study: An epidemiologic study that does not involve any intervention, experimental or otherwise. Such a study may be one in which nature is allowed to take its course, with changes in one characteristic being studied in relation to changes in other characteristics. Analytical epidemiologic methods, such as case-control and cohort study designs, are properly called observational epidemiology because the investigator is observing without intervention other than to record, classify, count, and statistically analyze results. [NIH] Obsession: A recurrent, persistent thought, image, or impulse that is unwanted and distressing (ego-dystonic) and comes involuntarily to mind despite attempts to ignore or suppress it. Common obsessions involve thoughts of violence, contamination, and selfdoubt. [EU] Oestrogen: A generic term for oestrus-producing steroid compounds; the female sex hormones. In humans, oestrogen is formed in the ovary, possibly the adrenal cortex, the testis, and the foetoplacental unit; it has various functions in both sexes. It is responsible for the development of the female secondary sex characteristics, and during the menstrual cycle it acts on the female genitalia to produce an environment suitable for the fertilization, implantation, and nutrition of the early embryo. Oestrogen is used in oral contraceptives and as a palliative in cancer of the breast after menopause and cancer of the prostate; other uses include the relief of the discomforts of menopause, inhibition of lactation, and treatment of osteoporosis, threatened abortion, and various functional ovarian disorders. [EU]
Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Olfactory Bulb: Ovoid body resting on the cribriform plate of the ethmoid bone where the olfactory nerve terminates. The olfactory bulb contains several types of nerve cells including the mitral cells, on whose dendrites the olfactory nerve synapses, forming the olfactory glomeruli. The accessory olfactory bulb, which receives the projection from the vomeronasal organ via the vomeronasal nerve, is also included here. [NIH] Oligo: Chemical and mineral elements that exist in minimal (oligo) quantities in the body, in foods, in the air, in soil; name applied to any element observed as a microconstituent of plant or animal tissue and of beneficial, harmful, or even doubtful significance. [NIH] Oligomenorrhea: Abnormally infrequent menstruation. [NIH] Oligosaccharides: Carbohydrates consisting of between two and ten monosaccharides connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form. [NIH] Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] On-line: A sexually-reproducing population derived from a common parentage. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]
Optic Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is
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formed by the meeting of all the retinal ganglion cell axons as they enter the optic nerve. [NIH]
Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Ornithine: An amino acid produced in the urea cycle by the splitting off of urea from arginine. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteogenesis: The histogenesis of bone including ossification. It occurs continuously but particularly in the embryo and child and during fracture repair. [NIH] Osteogenesis Imperfecta: A collagen disorder resulting from defective biosynthesis of type I collagen and characterized by brittle, osteoporotic, and easily fractured bones. It may also present with blue sclerae, loose joints, and imperfect dentin formation. There are four major types, I-IV. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovarian Follicle: Spheroidal cell aggregation in the ovary containing an ovum. It consists of an external fibro-vascular coat, an internal coat of nucleated cells, and a transparent, albuminous fluid in which the ovum is suspended. [NIH] Ovariectomy: The surgical removal of one or both ovaries. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overall survival: The percentage of subjects in a study who have survived for a defined period of time. Usually reported as time since diagnosis or treatment. Often called the survival rate. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH]
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Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Ovulation: The discharge of a secondary oocyte from a ruptured graafian follicle. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxandrolone: A synthetic hormone with anabolic and androgenic properties. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidative Phosphorylation: Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds. [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Oxytocin: A nonapeptide posterior pituitary hormone that causes uterine contractions and stimulates lactation. [NIH] Palatal Obturators: Appliances that close a cleft or fissure of the palate. [NIH] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Panic: A state of extreme acute, intense anxiety and unreasoning fear accompanied by disorganization of personality function. [NIH] Panic Disorder: A type of anxiety disorder characterized by unexpected panic attacks that last minutes or, rarely, hours. Panic attacks begin with intense apprehension, fear or terror and, often, a feeling of impending doom. Symptoms experienced during a panic attack include dyspnea or sensations of being smothered; dizziness, loss of balance or faintness; choking sensations; palpitations or accelerated heart rate; shakiness; sweating; nausea or other form of abdominal distress; depersonalization or derealization; paresthesias; hot flashes or chills; chest discomfort or pain; fear of dying and fear of not being in control of oneself or going crazy. Agoraphobia may also develop. Similar to other anxiety disorders, it may be inherited as an autosomal dominant trait. [NIH] Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical antiinflammatory. It is also commonly used as an embedding material in histology. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered
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parenterally as an antihypocalcaemic, hypoparathyroidism with tetany. [EU]
especially
in
the
treatment
of
acute
Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parenteral Nutrition: The administering of nutrients for assimilation and utilization by a patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously). [NIH] Paresthesias: Abnormal touch sensations, such as burning or prickling, that occur without an outside stimulus. [NIH] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parietal Lobe: Upper central part of the cerebral hemisphere. [NIH] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression. [NIH]
Particle: A tiny mass of material. [EU] Partnership Practice: A voluntary contract between two or more doctors who may or may not share responsibility for the care of patients, with proportional sharing of profits and losses. [NIH] Parturition: The act or process of given birth to a child. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Care Management: Generating, planning, organizing, and administering medical and nursing care and services for patients. [NIH] Patient Care Team: Care of patients by a multidisciplinary team usually organized under the leadership of a physician; each member of the team has specific responsibilities and the whole team contributes to the care of the patient. [NIH] Patient Compliance: Voluntary cooperation of the patient in following a prescribed
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regimen. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Patient Selection: Criteria and standards used for the determination of the appropriateness of the inclusion of patients with specific conditions in proposed treatment plans and the criteria used for the inclusion of subjects in various clinical trials and other research protocols. [NIH] Pelvic: Pertaining to the pelvis. [EU] Penicillin: An antibiotic drug used to treat infection. [NIH] Pensions: Fixed sums paid regularly to individuals. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences among presented objects, whether these be pairs of words, pairs of number series, or multiple sets of these or other symbols such as geometric figures. [NIH] Perennial: Lasting through the year of for several years. [EU] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Perineal: Pertaining to the perineum. [EU] Perineum: The area between the anus and the sex organs. [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Perioperative: Around the time of surgery; usually lasts from the time of going into the hospital or doctor's office for surgery until the time the patient goes home. [NIH] Peripheral Neuropathy: Nerve damage, usually affecting the feet and legs; causing pain, numbness, or a tingling feeling. Also called "somatic neuropathy" or "distal sensory polyneuropathy." [NIH] Peristalsis: The rippling motion of muscles in the intestine or other tubular organs characterized by the alternate contraction and relaxation of the muscles that propel the contents onward. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and
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covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] Perspiration: Sweating; the functional secretion of sweat. [EU] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Pharmaceutical Preparations: Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form. [NIH] Pharmaceutical Solutions: Homogeneous liquid preparations that contain one or more chemical substances dissolved, i.e., molecularly dispersed, in a suitable solvent or mixture of mutually miscible solvents. For reasons of their ingredients, method of preparation, or use, they do not fall into another group of products. [NIH] Pharmacodynamic: Is concerned with the response of living tissues to chemical stimuli, that is, the action of drugs on the living organism in the absence of disease. [NIH] Pharmacogenetics: A branch of genetics which deals with the genetic components of variability in individual responses to and metabolism (biotransformation) of drugs. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It promotes binding to inhibitory GABA subtype receptors, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations. [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor
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of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phenylpropanolamine: A sympathomimetic that acts mainly by causing release of norepinephrine but also has direct agonist activity at some adrenergic receptors. It is most commonly used as a nasal vasoconstrictor and an appetite depressant. [NIH] Pheromones: Chemical substances which, when secreted by an individual into the environment, cause specific reactions in other individuals, usually of the same species. The substances relate only to multicellular organisms. This includes kairomones. Allomones are repellent pheromones. [NIH] Phosphates: Inorganic salts of phosphoric acid. [NIH] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [NIH] Phosphodiesterase Inhibitors: Compounds which inhibit or antagonize the biosynthesis or actions of phosphodiesterases. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylates: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photoperiod: The time period of daily exposure that an organism receives from daylight or artificial light. It is believed that photoperiodic responses may affect the control of energy balance and thermoregulation. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plant Growth Regulators: Any of the hormones produced naturally in plants and active in controlling growth and other functions. There are three primary classes: auxins, cytokinins,
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and gibberellins. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polyarthritis: An inflammation of several joints together. [EU] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polycystic Ovary Syndrome: Clinical symptom complex characterized by oligomenorrhea or amenorrhea, anovulation, and regularly associated with bilateral polycystic ovaries. [NIH] Polydipsia: Chronic excessive thirst, as in diabetes mellitus or diabetes insipidus. [EU] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU]
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Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polyuria: Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes. [NIH] Population Control: Includes mechanisms or programs which control the numbers of individuals in a population of humans or animals. [NIH] Portal System: A system of vessels in which blood, after passing through one capillary bed, is conveyed through a second set of capillaries before it returns to the systemic circulation. It pertains especially to the hepatic portal system. [NIH] Positive pressure ventilation: Provision of oxygen under pressure by a mechanical respirator. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postmenopause: The physiological period following the menopause, the permanent cessation of the menstrual life. Since in the United States the age of the menopause ranges between 48 and 55 years, generally conceived as middle age, the postmenopause often refers to women considerably older. [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postoperative: After surgery. [NIH] Postprandial: Occurring after dinner, or after a meal; postcibal. [EU] Postprandial Blood Glucose: Blood taken 1-2 hours after eating to see the amount of glucose (sugar) in the blood. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU]
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Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] Pregnancy Tests: Tests to determine whether or not an individual is pregnant. [NIH] Premenopausal: Refers to the time before menopause. Menopause is the time of life when a women's menstrual periods stop permanently; also called "change of life." [NIH] Premenstrual: Occurring before menstruation. [EU] Premenstrual Syndrome: A syndrome occurring most often during the last week of the menstrual cycle and ending soon after the onset of menses. Some of the symptoms are emotional instability, insomnia, headache, nausea, vomiting, abdominal distension, and painful breasts. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prenatal Care: Care provided the pregnant woman in order to prevent complications, and decrease the incidence of maternal and prenatal mortality. [NIH] Pressoreceptors: Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls. [NIH] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary Biliary Cirrhosis: A chronic liver disease. Slowly destroys the bile ducts in the liver. This prevents release of bile. Long-term irritation of the liver may cause scarring and cirrhosis in later stages of the disease. [NIH] Primary endpoint: The main result that is measured at the end of a study to see if a given treatment worked (e.g., the number of deaths or the difference in survival between the treatment group and the control group). What the primary endpoint will be is decided before the study begins. [NIH] Primary Prevention: Prevention of disease or mental disorders in susceptible individuals or populations through promotion of health, including mental health, and specific protection, as in immunization, as distinguished from the prevention of complications or after-effects of existing disease. [NIH] Private Practice: Practice of a health profession by an individual, offering services on a person-to-person basis, as opposed to group or partnership practice. [NIH] Problem Solving: A learning situation involving more than one alternative from which a selection is made in order to attain a specific goal. [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an
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antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should fertilization occur. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol is used in the treatment or prevention of many disorders including acute myocardial infarction, arrhythmias, angina pectoris, hypertension, hypertensive emergencies, hyperthyroidism, migraine, pheochromocytoma, menopause, and anxiety. [NIH] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane).
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The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protective Agents: Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent. [NIH]
Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Protein-Tyrosine Kinase: An enzyme that catalyzes the phosphorylation of tyrosine residues in proteins with ATP or other nucleotides as phosphate donors. EC 2.7.1.112. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus
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of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pruritus: An intense itching sensation that produces the urge to rub or scratch the skin to obtain relief. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychomotor: Pertaining to motor effects of cerebral or psychic activity. [EU] Psychopathology: The study of significant causes and processes in the development of mental illness. [NIH] Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Psychotropic: Exerting an effect upon the mind; capable of modifying mental activity; usually applied to drugs that effect the mental state. [EU] Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Puerperium: Period from delivery of the placenta until return of the reproductive organs to their normal nonpregnant morphologic state. In humans, the puerperium generally lasts for six to eight weeks. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs,
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may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulmonary Embolism: Embolism in the pulmonary artery or one of its branches. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Pupil: The aperture in the iris through which light passes. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pustular: Pertaining to or of the nature of a pustule; consisting of pustules (= a visible collection of pus within or beneath the epidermis). [EU] Pylorus: The opening in a vertebrate from the stomach into the intestine. [EU] Pyramidal Cells: Projection neurons in the cerebral cortex and the hippocampus. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region. [NIH] Pyramidal Tracts: Fibers that arise from cells within the cerebral cortex, pass through the medullary pyramid, and descend in the spinal cord. Many authorities say the pyramidal tracts include both the corticospinal and corticobulbar tracts. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radial Artery: The direct continuation of the brachial trunk, originating at the bifurcation of the brachial artery opposite the neck of the radius. Its branches may be divided into three groups corresponding to the three regions in which the vessel is situated, the forearm, wrist, and hand. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radioactive: Giving off radiation. [NIH] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] Radius: The lateral bone of the forearm. [NIH] Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects. [NIH] Randomization: Also called random allocation. Is allocation of individuals to groups, e.g., for experimental and control regimens, by chance. Within the limits of chance variation, random allocation should make the control and experimental groups similar at the start of
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an investigation and ensure that personal judgment and prejudices of the investigator do not influence allocation. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Ranitidine: A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers. [NIH] Reality Testing: The individual's objective evaluation of the external world and the ability to differentiate adequately between it and the internal world; considered to be a primary ego function. [NIH] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectal: By or having to do with the rectum. The rectum is the last 8 to 10 inches of the large intestine and ends at the anus. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Relaxation Techniques: The use of muscular relaxation techniques in treatment. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the
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extent to which we can assume that it will yield the same result if repeated a second time. [NIH]
Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [NIH] Reproduction Techniques: Methods pertaining to the generation of new individuals. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Research Support: Financial support of research activities. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respirator: A mechanical device that helps a patient breathe; a mechanical ventilator. [NIH] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Respiratory Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Respiratory System: The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about. [NIH] Resting metabolic rate: RMR accounts for 65 to 75 percent of daily energy expenditure and represents the minimum energy needed to maintain all physiological cell functions in the resting state. The principal determinant of RMR is lean body mass (LBM). Obese subjects have a higher RMR in absolute terms than lean individuals, an equivalent RMR when corrected for LBM and per unit surface area, and a lower RMR when expressed per kilogram of body weight. Obese persons require more energy for any given activity because of a larger mass, but they tend to be more sedentary than lean subjects. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH]
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Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinoids: Derivatives of vitamin A. Used clinically in the treatment of severe cystic acne, psoriasis, and other disorders of keratinization. Their possible use in the prophylaxis and treatment of cancer is being actively explored. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Rhythm Method: A contraceptive method whereby abstinence is practiced a few days before and after the estimated day of ovulation. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickettsiae: One of a group of obligate intracellular parasitic microorganisms, once regarded as intermediate in their properties between bacteria and viruses but now classified as bacteria in the order Rickettsiales, which includes 17 genera and 3 families: Rickettsiace. [NIH]
Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Risperidone: A selective blocker of dopamine D2 and serotonin-5-HT-2 receptors that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of schizophrenia. [NIH] Rubella: An acute, usually benign, infectious disease caused by a togavirus and most often affecting children and nonimmune young adults, in which the virus enters the respiratory
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tract via droplet nuclei and spreads to the lymphatic system. It is characterized by a slight cold, sore throat, and fever, followed by enlargement of the postauricular, suboccipital, and cervical lymph nodes, and the appearances of a fine pink rash that begins on the head and spreads to become generalized. Called also German measles, roetln, röteln, and three-day measles, and rubeola in French and Spanish. [EU] Rye: A hardy grain crop, Secale cereale, grown in northern climates. It is the most frequent host to ergot (claviceps), the toxic fungus. Its hybrid with wheat is triticale, another grain. [NIH]
Saline: A solution of salt and water. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcolemma: The plasma membrane of a smooth, striated, or cardiac muscle fiber. [NIH] Satiation: Full gratification of a need or desire followed by a state of relative insensitivity to that particular need or desire. [NIH] Saturated fat: A type of fat found in greatest amounts in foods from animals, such as fatty cuts of meat, poultry with the skin, whole-milk dairy products, lard, and in some vegetable oils, including coconut, palm kernel, and palm oils. Saturated fat raises blood cholesterol more than anything else eaten. On a Step I Diet, no more than 8 to 10 percent of total calories should come from saturated fat, and in the Step II Diet, less than 7 percent of the day's total calories should come from saturated fat. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Sclera: The tough white outer coat of the eyeball, covering approximately the posterior fivesixths of its surface, and continuous anteriorly with the cornea and posteriorly with the external sheath of the optic nerve. [EU] Sclerae: A circular furrow between the sclerocorneal junction and the iris. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Sebaceous gland: Gland that secretes sebum. [NIH]
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Sebum: The oily substance secreted by sebaceous glands. It is composed of keratin, fat, and cellular debris. [NIH] Second Messenger Systems: Systems in which an intracellular signal is generated in response to an intercellular primary messenger such as a hormone or neurotransmitter. They are intermediate signals in cellular processes such as metabolism, secretion, contraction, phototransduction, and cell growth. Examples of second messenger systems are the adenyl cyclase-cyclic AMP system, the phosphatidylinositol diphosphate-inositol triphosphate system, and the cyclic GMP system. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Sedentary: 1. Sitting habitually; of inactive habits. 2. Pertaining to a sitting posture. [EU] Sediment: A precipitate, especially one that is formed spontaneously. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Self Care: Performance of activities or tasks traditionally performed by professional health care providers. The concept includes care of oneself or one's family and friends. [NIH] Sella: A deep depression in the shape of a Turkish saddle in the upper surface of the body of the sphenoid bone in the deepest part of which is lodged the hypophysis cerebri. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Septum: A dividing wall or partition; a general term for such a structure. The term is often used alone to refer to the septal area or to the septum pellucidum. [EU] Septum Pellucidum: A triangular double membrane separating the anterior horns of the lateral ventricles of the brain. It is situated in the median plane and bounded by the corpus callosum and the body and columns of the fornix. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH]
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Sertraline: A selective serotonin uptake inhibitor that is used in the treatment of depression. [NIH]
Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sexual Abstinence: Refraining from sexual intercourse. [NIH] Sharks: A group of elongate elasmobranchs. Sharks are mostly marine fish, with certain species large and voracious. [NIH] Sharpness: The apparent blurring of the border between two adjacent areas of a radiograph having different optical densities. [NIH] Shivering: Involuntary contraction or twitching of the muscles. It is a physiologic method of heat production in man and other mammals. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Sibutramine: A drug used for the management of obesity that helps reduce food intake and is indicated for weight loss and maintenance of weight loss when used in conjunction with a reduced-calorie diet. It works to suppress the appetite primarily by inhibiting the reuptake of the neurotransmitters norepinephrine and serotonin. Side effects include dry mouth, headache, constipation, insomnia, and a slight increase in average blood pressure. In some patients it causes a higher blood pressure increase. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Simethicone: A mixture of dimethyl polysiloxanes and silica gel used as an antiflatulent. Without the addition of silica gel (dimethicone), it is used as an ointment base ingredient and skin protectant. [NIH]
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Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Snoring: Rough, noisy breathing during sleep, due to vibration of the uvula and soft palate. [NIH]
Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Channels: Cell membrane glycoproteins selective for sodium ions. Fast sodium current is associated with the action potential in neural membranes. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solitary Nucleus: Gray matter located in the dorsomedial part of the medulla oblongata associated with the solitary tract. The solitary nucleus receives inputs from most organ systems including the terminations of the facial, glossopharyngeal, and vagus nerves. It is a major coordinator of autonomic nervous system regulation of cardiovascular, respiratory, gustatory, gastrointestinal, and chemoreceptive aspects of homeostasis. The solitary nucleus is also notable for the large number of neurotransmitters which are found therein. [NIH] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic cells: All the body cells except the reproductive (germ) cells. [NIH] Spastic: 1. Of the nature of or characterized by spasms. 2. Hypertonic, so that the muscles are stiff and the movements awkward. 3. A person exhibiting spasticity, such as occurs in spastic paralysis or in cerebral palsy. [EU]
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Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrin: A high molecular weight (220-250 kDa) water-soluble protein which can be extracted from erythrocyte ghosts in low ionic strength buffers. The protein contains no lipids or carbohydrates, is the predominant species of peripheral erythrocyte membrane proteins, and exists as a fibrous coating on the inner, cytoplasmic surface of the membrane. [NIH]
Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Spermatogenesis: Process of formation and development of spermatozoa, including spermatocytogenesis and spermiogenesis. [NIH] Spermatozoa: Mature male germ cells that develop in the seminiferous tubules of the testes. Each consists of a head, a body, and a tail that provides propulsion. The head consists mainly of chromatin. [NIH] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] Spices: The dried seeds, bark, root, stems, buds, leaves, or fruit of aromatic plants used to season food. [NIH] Spina bifida: A defect in development of the vertebral column in which there is a central deficiency of the vertebral lamina. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spirometry: Measurement of volume of air inhaled or exhaled by the lung. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Spores: The reproductive elements of lower organisms, such as protozoa, fungi, and cryptogamic plants. [NIH] Sprue: A non febrile tropical disease of uncertain origin. [NIH] Stabilization: The creation of a stable state. [EU] Stabilizer: A device for maintaining constant X-ray tube voltage or current. [NIH]
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Staff Development: The process by which the employer promotes staff performance and efficiency consistent with management goals and objectives. [NIH] Standard therapy: A currently accepted and widely used treatment for a certain type of cancer, based on the results of past research. [NIH] Stapes: One of the three ossicles of the middle ear. It transmits sound vibrations from the incus to the internal ear. [NIH] Steatorrhea: A condition in which the body cannot absorb fat. Causes a buildup of fat in the stool and loose, greasy, and foul bowel movements. [NIH] Steatosis: Fatty degeneration. [EU] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Sterilization: The destroying of all forms of life, especially microorganisms, by heat, chemical, or other means. [NIH] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Steroid therapy: Treatment with corticosteroid drugs to reduce swelling, pain, and other symptoms of inflammation. [NIH] Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stomach Ulcer: An open sore in the lining of the stomach. Also called gastric ulcer. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stroke Volume: The amount of blood pumped out of the heart per beat not to be confused with cardiac output (volume/time). [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH]
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Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Sulfates: Inorganic salts of sulfuric acid. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Sulfuric acid: A strong acid that, when concentrated is extemely corrosive to the skin and mucous membranes. It is used in making fertilizers, dyes, electroplating, and industrial explosives. [NIH] Superstitions: A belief or practice which lacks adequate basis for proof; an embodiment of fear of the unknown, magic, and ignorance. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Suppositories: A small cone-shaped medicament having cocoa butter or gelatin at its basis and usually intended for the treatment of local conditions in the rectum. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]
Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Sweat: The fluid excreted by the sweat glands. It consists of water containing sodium chloride, phosphate, urea, ammonia, and other waste products. [NIH] Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's
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response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate through direct electrical connections which are sometimes called electrical synapses; these are not included here but rather in gap junctions. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Systolic blood pressure: The maximum pressure in the artery produced as the heart contracts and blood begins to flow. [NIH] Systolic pressure: The highest pressure to which blood pressure rises with the contraction of the ventricles. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late
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in appearing. [EU] Tellurium: Tellurium. An element that is a member of the chalcogen family. It has the atomic symbol Te, atomic number 52, and atomic weight 127.60. It has been used as a coloring agent and in the manufacture of electrical equipment. Exposure may cause nausea, vomiting, and CNS depression. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Temporal Lobe: Lower lateral part of the cerebral hemisphere. [NIH] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermogenesis: The generation of heat in order to maintain body temperature. The uncoupled oxidation of fatty acids contained within brown adipose tissue and shivering are examples of thermogenesis in mammals. [NIH] Thermoregulation: Heat regulation. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Third Ventricle: A narrow cleft inferior to the corpus callosum, within the diencephalon, between the paired thalami. Its floor is formed by the hypothalamus, its anterior wall by the lamina terminalis, and its roof by ependyma. It communicates with the fourth ventricle by the cerebral aqueduct, and with the lateral ventricles by the interventricular foramina. [NIH] Thoracic: Having to do with the chest. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thromboembolism: Obstruction of a vessel by a blood clot that has been transported from a distant site by the blood stream. [NIH] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone,
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which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroid Hormones: Hormones secreted by the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tobacco Use Cessation: Cessation of the habit of using tobacco products for smoking or chewing, including the use of snuff. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tonometry: The standard to determine the fluid pressure inside the eye (intraocular pressure). [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transcutaneous: Transdermal. [EU] Transdermal: Entering through the dermis, or skin, as in administration of a drug applied to the skin in ointment or patch form. [EU] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH]
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Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translocate: The attachment of a fragment of one chromosome to a non-homologous chromosome. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Trifluoperazine: A phenothiazine with actions similar to chlorpromazine. It is used as an antipsychotic and an antiemetic. [NIH] Trigger zone: Dolorogenic zone (= producing or causing pain). [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Truncal: The bilateral dissection of the abdominal branches of the vagus nerve. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH]
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Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH] Umbilical Arteries: Either of a pair of arteries originating from the internal iliac artery and passing through the umbilical cord to carry blood from the fetus to the placenta. [NIH] Umbilical Cord: The flexible structure, giving passage to the umbilical arteries and vein, which connects the embryo or fetus to the placenta. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Urinalysis: Examination of urine by chemical, physical, or microscopic means. Routine urinalysis usually includes performing chemical screening tests, determining specific gravity, observing any unusual color or odor, screening for bacteriuria, and examining the sediment microscopically. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]
Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic. [NIH] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterine Contraction: Contraction of the uterine muscle. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH]
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Uvula: Uvula palatinae; specifically, the tongue-like process which projects from the middle of the posterior edge of the soft palate. [NIH] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vagal: Pertaining to the vagus nerve. [EU] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Vaginal Discharge: A common gynecologic disorder characterized by an abnormal, nonbloody discharge from the genital tract. [NIH] Vagotomy: The interruption or removal of any part of the vagus (10th cranial) nerve. Vagotomy may be performed for research or for therapeutic purposes. [NIH] Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx). [NIH] Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. [NIH]
Valproic Acid: A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GABA levels in the brain or by altering the properties of voltage dependent sodium channels. [NIH] Valves: Flap-like structures that control the direction of blood flow through the heart. [NIH] Varices: Stretched veins such as those that form in the esophagus from cirrhosis. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular Resistance: An expression of the resistance offered by the systemic arterioles, and to a lesser extent by the capillaries, to the flow of blood. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vasomotor: 1. Affecting the calibre of a vessel, especially of a blood vessel. 2. Any element or agent that effects the calibre of a blood vessel. [EU] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venlafaxine: An antidepressant drug that is being evaluated for the treatment of hot flashes in women who have breast cancer. [NIH]
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Venous: Of or pertaining to the veins. [EU] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vesicoureteral: An abnormal condition in which urine backs up into the ureters, and occasionally into the kidneys, raising the risk of infection. [NIH] Vestibulocochlear Nerve: The 8th cranial nerve. The vestibulocochlear nerve has a cochlear part (cochlear nerve) which is concerned with hearing and a vestibular part (vestibular nerve) which mediates the sense of balance and head position. The fibers of the cochlear nerve originate from neurons of the spiral ganglion and project to the cochlear nuclei (cochlear nucleus). The fibers of the vestibular nerve arise from neurons of Scarpa's ganglion and project to the vestibular nuclei. [NIH] Vestibulocochlear Nerve Diseases: Diseases of the vestibular and/or cochlear (acoustic) nerves, which join to form the vestibulocochlear nerve. Vestibular neuritis, cochlear neuritis, and acoustic neuromas are relatively common conditions that affect these nerves. Clinical manifestations vary with which nerve is primarily affected, and include hearing loss, vertigo, and tinnitus. [NIH] Veterinarians: Individuals with a degree in veterinary medicine that provides them with training and qualifications to treat diseases and injuries of animals. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Villous: Of a surface, covered with villi. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virilism: Development of masculine traits in the female. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virulent: A virus or bacteriophage capable only of lytic growth, as opposed to temperate
Dictionary 363
phages establishing the lysogenic response. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Virus Diseases: A general term for diseases produced by viruses. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Afferents: The sensory fibers innervating the viscera. [NIH] Visceral fat: One of the three compartments of abdominal fat. Retroperitoneal and subcutaneous are the other two compartments. [NIH] Viscosity: A physical property of fluids that determines the internal resistance to shear forces. [EU] Visual Acuity: Acuteness or clearness of vision, especially of form vision, which is dependent mainly on the sharpness of the retinal focus. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the crystalline lens of the eye and in front of the retina. It is contained in a thin hyoid membrane and forms about four fifths of the optic globe. [NIH] Vitreous Hemorrhage: Hemorrhage into the vitreous body. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Vomeronasal Organ: A specialized part of the olfactory system located anteriorly in the nasal cavity within the nasal septum. Chemosensitive cells of the vomeronasal organ project via the vomeronasal nerve to the accessory olfactory bulb. The primary function of this organ appears to be in sensing pheromones which regulate reproductive and other social behaviors. While the structure has been thought absent in higher primate adults, data now suggests it may be present in adult humans. [NIH] Waist circumference: To define the level at which the waist circumference is measured, a bony landmark is first located and marked. The subject stands, and the technician, positioned to the right of the subject, palpates the upper hip bone to locate the right ileum. Just above the uppermost lateral border of the right ileum, a horizontal mark is drawn and then crossed with a vertical mark on the midaxillary line. The measuring tape is then placed around the trunk, at the level of the mark on the right side, making sure that it is on a level horizontal plane on all sides. The tape is then tightened slightly without compressing the skin and underlying subcutaneous tissues. The measure is recorded in centimeters to the nearest millimeter. [NIH] Wakefulness: A state in which there is an enhanced potential for sensitivity and an efficient responsiveness to external stimuli. [NIH] Weight Gain: Increase in body weight over existing weight. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
364
Weight Gain
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zearalenone: (S-(E))-3,4,5,6,8,10-Hexahydro-14,16-dihydroxy-3-methyl-1H-2benzoxacyclotetradecin-1,7(8H)-dione. One of a group of compounds known under the general designation of resorcylic acid lactones. Cis, trans, dextro and levo forms have been isolated from the fungus Gibberella zeae (formerly Fusarium graminearum). They have estrogenic activity, cause toxicity in livestock as feed contaminant, and have been used as anabolic or estrogen substitutes. [NIH] Zygote: The fertilized ovum. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
365
INDEX 5 5-alpha, 34, 271 A Abdomen, 243, 271, 283, 284, 303, 319, 322, 337, 353, 354, 357, 361, 363 Abdominal, 18, 58, 244, 248, 256, 271, 272, 319, 320, 322, 334, 336, 337, 341, 359, 360, 363 Abdominal fat, 58, 271, 363 Abdominal Pain, 244, 248, 271, 320, 337, 360 Abscess, 216, 271, 350 Absenteeism, 167, 271 Acceptor, 271, 334 Acetylcholine, 271, 289, 331 Acidosis, 199, 271 Acne, 34, 244, 253, 271, 348 Acne Vulgaris, 34, 271 Acoustic, 49, 271, 362 Actin, 161, 271, 328, 329 Actinin, 271, 301 Activities of Daily Living, 62, 271 Acuity, 55, 271 Adaptability, 271, 287 Adaptation, 13, 127, 155, 200, 271, 288 Adenosine, 272, 280, 285, 338 Adenovirus, 93, 272 Adipocytes, 16, 27, 60, 64, 182, 272, 321 Adipose Tissue, 15, 16, 27, 60, 271, 272, 300, 357 Adjustment, 7, 8, 23, 200, 246, 271, 272 Adjuvant, 138, 154, 158, 272, 308 Adolescence, 14, 63, 68, 226, 272 Adolescent Nutrition, 38, 272 Adrenal Cortex, 145, 272, 294, 304, 315, 332, 341, 347 Adrenal Medulla, 272, 286, 303, 331 Adrenergic, 16, 44, 72, 89, 94, 156, 179, 181, 272, 277, 278, 300, 303, 338, 342, 356 Adrenergic Agents, 272, 277 Adult-Onset Diabetes, 16, 272 Adverse Effect, 13, 23, 32, 52, 170, 185, 210, 211, 224, 272, 290, 351 Aerobic, 26, 229, 272, 304 Aerobic Exercise, 26, 229, 272 Afferent, 43, 272, 305, 321 Affinity, 91, 145, 186, 272, 273, 280, 290, 352
Age of Onset, 273, 359 Aggressiveness, 160, 273 Agonist, 273, 300, 329, 331, 338 Agoraphobia, 273, 316, 334 A-HA, 94, 273 Airway, 37, 59, 273, 352 Akathisia, 273, 278 Alanine, 158, 273 Albumin, 48, 157, 247, 252, 273, 339 Alertness, 273, 284 Algorithms, 66, 273, 283 Alimentary, 273, 298, 335, 336 Alkaline, 162, 172, 271, 273, 275, 285, 357 Alkaloid, 273, 285, 290, 331 Alleles, 45, 273, 313 Allergen, 150, 273 Allograft, 4, 274 Allylamine, 274 Alopecia, 34, 274 Alpha Particles, 274, 345 Alpha-fetoprotein, 274, 306 Alpha-Linolenic Acid, 128, 274 Alternative medicine, 227, 274 Alum, 176, 274, 290 Aluminum, 176, 274, 281 Alveoli, 274, 362 Amenorrhea, 274, 276, 339 Amine, 86, 179, 274, 314 Amino Acid Motifs, 274, 292 Amino Acid Sequence, 145, 274, 277, 292, 308 Amino Acid Substitution, 274, 313 Ammonia, 176, 274, 275, 310, 355, 360 Ammonium Sulfate, 176, 275 Amniocentesis, 200, 275 Amniotic Fluid, 275, 309 Amphetamines, 275, 290 Amygdala, 144, 275, 322 Amylase, 127, 168, 275 Anabasine, 38, 275 Anabolic, 135, 159, 275, 299, 334, 364 Anaemia, 77, 275, 325 Anaesthesia, 275, 317 Anal, 14, 24, 251, 275, 303, 323, 328 Analgesic, 159, 275, 321 Analog, 190, 275 Analysis of Variance, 55, 138, 275 Anaphylatoxins, 275, 291
366
Weight Gain
Anaphylaxis, 275, 320 Anastomosis, 275, 320 Anatomical, 276, 280, 292, 316, 330, 349 Androgenic, 34, 276, 334 Androgens, 92, 138, 272, 276, 294, 315, 325 Anemia, 40, 75, 209, 247, 253, 256, 276, 307, 312, 324 Anesthesia, 94, 164, 273, 276, 301 Angina, 276, 342 Angina Pectoris, 276, 342 Angiotensin converting enzyme inhibitor, 199, 276 Angiotensin-Converting Enzyme Inhibitors, 11, 97, 276 Angiotensinogen, 276, 347 Animal Husbandry, 163, 276 Animal model, 34, 59, 61, 153, 276 Anions, 273, 276, 320, 351 Anorexia, 75, 76, 80, 91, 110, 111, 131, 226, 275, 276 Anorexia Nervosa, 75, 76, 80, 91, 110, 111, 131, 226, 276 Anorexiant, 154, 276 Anovulation, 276, 339 Antagonism, 276, 285, 290 Anthropometry, 44, 49, 276 Antiallergic, 277, 294, 295 Antiangiogenic, 165, 277 Antibacterial, 173, 277, 353 Antibiotic, 155, 165, 179, 276, 277, 296, 300, 336, 353 Antibodies, 178, 180, 277, 280, 312, 314, 316, 324, 339 Antibody, 172, 180, 273, 277, 291, 303, 312, 314, 316, 317, 325, 353 Anticholinergic, 146, 183, 277, 288 Anticoagulant, 277, 343 Anticonvulsant, 277, 361 Antidepressant, 38, 100, 115, 146, 183, 277, 284, 294, 306, 316, 361 Antidiabetic, 211, 277 Antidiabetic Agent, 211, 277 Antidote, 277, 285 Antiemetic, 277, 278, 288, 315, 359 Antigen, 273, 275, 277, 291, 314, 315, 316, 317, 325 Antigen-Antibody Complex, 277, 291 Anti-inflammatory, 277, 280, 294, 310, 334, 341 Anti-Inflammatory Agents, 277, 280, 294 Antimicrobial, 163, 277 Antineoplastic, 277, 294, 300, 309, 318
Antineoplastic Agents, 277, 318 Anti-Obesity Agents, 146, 183, 277 Antioxidant, 127, 278, 279 Antipruritic, 278, 295 Antipsychotic Agents, 21, 278 Anus, 275, 278, 284, 306, 319, 336, 346 Anxiety, 38, 46, 70, 144, 145, 160, 164, 184, 201, 267, 273, 278, 315, 334, 342 Anxiety Disorders, 278, 334 Aorta, 58, 278, 312, 341, 362 Apathy, 278, 330 Apnea, 184, 278 Apolipoproteins, 14, 278, 322 Apoptosis, 34, 278 Appetitive Behavior, 65, 278 Aqueous, 279, 281, 296, 321, 322 Arachidonate 12-Lipoxygenase, 279, 322 Arachidonate 15-Lipoxygenase, 279, 322 Arachidonate Lipoxygenases, 279, 322 Arachidonic Acid, 279, 342 Arcuate Nucleus, 34, 155, 279 Arginine, 158, 160, 189, 275, 279, 331, 333 Aromatic, 279, 337, 353 Arterial, 30, 43, 144, 274, 279, 289, 293, 315, 343, 356 Arteries, 278, 279, 280, 283, 284, 293, 294, 312, 323, 326, 328, 329, 345, 360 Arteriolar, 279, 284, 347 Arterioles, 279, 283, 285, 329, 361 Arthralgia, 216, 279 Articular, 279, 333 Ascorbic Acid, 121, 122, 279, 314 Aspartic, 159, 279 Aspartic Acid, 159, 279 Aspirate, 53, 279 Aspiration, 279, 306 Aspirin, 199, 279 Assay, 14, 23, 280 Astrocytes, 280, 327 Asymptomatic, 280, 313 Atherogenic, 14, 19, 280 Atopic, 193, 280 ATP, 32, 280, 294, 299, 309, 338, 343 Atrial, 280, 293, 359 Atrioventricular, 280, 293 Atrium, 280, 293, 359, 362 Atrophy, 208, 280, 322 Attenuated, 280 Atypical, 32, 70, 72, 74, 80, 89, 91, 179, 280, 290, 348 Auditory, 55, 280, 315, 361 Autoantibodies, 109, 280
Index 367
Autoantigens, 280 Autoimmune disease, 244, 280, 328 Autonomic, 51, 160, 271, 278, 280, 331, 352, 355 Autonomic Nervous System, 51, 280, 352, 355 Autopsy, 201, 280 Auxin, 163, 280 Axons, 281, 297, 333, 345 B Back Pain, 248, 281 Bacterial Infections, 201, 281 Bacterial Physiology, 272, 281 Bacteriophage, 281, 339, 358, 362 Bacteriuria, 281, 360 Balloon Dilatation, 84, 281 Baroreflex, 29, 281 Basal Ganglia, 278, 281, 289, 322 Base, 41, 44, 109, 147, 177, 281, 297, 308, 320, 345, 351, 357 Basement Membrane, 162, 281, 305, 321 Bed Rest, 202, 281 Behavior Therapy, 128, 281 Benign, 19, 281, 312, 348 Bentonite, 170, 281 Benzamides, 179, 282 Benzene, 282, 320 Bilateral, 282, 339, 359 Bile, 158, 244, 282, 288, 307, 308, 320, 323, 341, 354, 360 Bile Acids, 282, 354 Bile Acids and Salts, 282 Bile Ducts, 282, 308, 341 Bile Pigments, 282, 320 Biliary, 244, 281, 282, 285 Biliary Atresia, 244, 282 Biliary Tract, 282, 285 Bilirubin, 273, 282, 308, 315 Binding Sites, 64, 148, 282 Bioassay, 105, 282 Biochemical, 16, 17, 54, 273, 282, 306, 333, 350 Biological response modifier, 282, 318 Biological therapy, 282, 311 Biomarkers, 13, 49, 51, 282 Biopsy, 208, 244, 247, 255, 282 Biosynthesis, 145, 279, 282, 333, 338, 350 Biotechnology, 69, 71, 127, 150, 207, 227, 237, 283 Biotransformation, 283, 337 Bipolar Disorder, 73, 110, 169, 283
Bladder, 153, 183, 212, 283, 307, 317, 328, 330, 343, 360 Blastocyst, 283, 292, 302, 338 Bloating, 283, 308, 317, 320 Blood Cell Count, 283, 312 Blood Coagulation, 283, 285, 357 Blood Platelets, 283, 350 Blood transfusion, 75, 251, 283 Blood Volume, 283, 305 Body Fluids, 282, 283, 284, 300, 306, 332, 352, 359 Body Image, 33, 53, 69, 98, 283, 297 Bone Density, 23, 283 Bone Marrow, 182, 282, 284, 295, 316, 323, 324, 327, 352, 354 Bowel, 208, 215, 216, 217, 275, 284, 298, 317, 319, 330, 337, 354, 360 Bowel Movement, 284, 298, 354 Brachial, 284, 345 Brachial Artery, 284, 345 Bradykinin, 284, 331, 339 Brain Stem, 284, 287 Branch, 90, 265, 284, 324, 335, 337, 344, 353, 357 Breakdown, 153, 284, 298, 308 Breast Feeding, 246, 257, 284 Breeding, 152, 276, 284 Bronchial, 281, 284, 314 Buccal, 57, 284, 323 Buffers, 67, 281, 284, 353 Bupropion, 38, 43, 156, 181, 284 Burns, 229, 284 Burns, Electric, 284 Bypass, 97, 223, 242, 284, 320 C Cachexia, 70, 94, 284 Caffeine, 200, 249, 284, 345 Calcium, 20, 23, 57, 173, 176, 199, 215, 222, 247, 252, 257, 285, 291, 315, 335, 351, 357 Calcium channel blocker, 199, 215, 285 Calcium Channel Blockers, 199, 285 Calcium Channels, 20, 285 Calcium Chloride, 176, 285 Calculi, 281, 285 Caloric intake, 60, 65, 85, 154, 169, 178, 200, 222, 250, 285 Calorimeter, 40, 285 Capillary, 284, 285, 325, 340, 362 Capsaicin, 43, 199, 285 Capsules, 191, 285, 300, 308 Carbon Dioxide, 285, 296, 308, 338, 347 Carcinogen, 57, 285
368
Weight Gain
Carcinogenesis, 58, 285, 288 Carcinogenic, 282, 285, 318, 342, 354 Carcinoma, 73, 285, 286 Cardiac, 27, 28, 40, 51, 94, 161, 274, 281, 284, 286, 293, 303, 308, 329, 348, 349, 354 Cardiac Output, 40, 281, 286, 354 Cardiomyopathy, 151, 286 Cardiopulmonary, 67, 286 Cardiorespiratory, 26, 45, 272, 286 Cardioselective, 286, 342 Cardiotoxicity, 125, 286 Carotene, 163, 286, 348 Carrier Proteins, 286, 339 Case report, 106, 110, 286, 290 Case series, 72, 102, 119, 286, 290 Castration, 147, 177, 286 Catabolism, 40, 286 Catalytic Domain, 160, 189, 286 Cataracts, 228, 244, 253, 286 Catecholamine, 286, 300, 337 Catheterization, 281, 286 Catheters, 281, 286 Cations, 287, 320 Caudal, 287, 298, 315, 340 Causal, 31, 34, 287, 303, 319 Cause of Death, 26, 41, 61, 167, 287 Cecum, 287, 321 Celiac Disease, 10, 71, 118, 287 Cell Adhesion, 161, 287 Cell Death, 127, 190, 278, 287, 329 Cell Differentiation, 287, 351 Cell Division, 281, 287, 309, 311, 325, 327, 339, 342, 350 Cell Lineage, 182, 287 Cell membrane, 285, 286, 287, 297, 308, 338, 352 Cell proliferation, 287, 351 Cell Survival, 287, 311 Cellulose, 287, 307, 339 Centrifugation, 287, 312 Cerebellum, 145, 287, 307 Cerebral Palsy, 244, 287, 352 Cerebrospinal, 288, 289 Cerebrospinal fluid, 288, 289 Cerebrovascular, 61, 210, 285, 286, 288 Cerebrum, 287, 288 Cervical, 288, 349 Cervix, 201, 288 Cetirizine, 288, 315 Character, 198, 276, 288, 296, 310 Chemopreventive, 44, 288 Chemoreceptor, 278, 288
Chemotactic Factors, 288, 291 Chemotherapy, 85, 138, 163, 288 Chenodeoxycholic Acid, 288, 360 Child Behavior, 39, 288 Chlorpromazine, 179, 288, 306, 359 Cholecystectomy, 186, 288 Cholecystokinin, 43, 181, 288 Choleretic, 288, 360 Cholesterol, 7, 9, 14, 97, 121, 123, 131, 166, 200, 206, 223, 245, 255, 282, 289, 293, 301, 308, 315, 322, 323, 349, 354 Cholesterol Esters, 289, 322 Cholinergic, 278, 289, 331 Chorea, 278, 289 Choroid, 145, 289, 348 Choroid Plexus, 145, 289 Chromatin, 278, 289, 353 Chromium, 121, 122, 144, 186, 289 Chromosome, 31, 289, 312, 313, 320, 322, 350, 359 Chronic, 11, 13, 15, 22, 25, 34, 37, 42, 45, 47, 49, 51, 68, 83, 104, 125, 126, 127, 153, 164, 169, 170, 182, 183, 184, 186, 190, 193, 202, 209, 217, 228, 243, 244, 251, 271, 281, 284, 288, 289, 298, 302, 307, 313, 315, 317, 320, 323, 339, 341, 355, 356, 360 Chronic Disease, 22, 25, 42, 47, 154, 186, 284, 289 Chronic renal, 289, 307, 339 Chylomicrons, 289, 322 Ciliary, 59, 70, 289, 328 Cimetidine, 191, 289 Circadian, 13, 289 Circulatory system, 169, 289, 302 Claviceps, 289, 349 Cleft Palate, 246, 289 Clinical study, 290, 293 Clone, 222, 290 Cloning, 154, 283, 290 Clozapine, 71, 78, 79, 107, 108, 179, 191, 290 Coagulation, 283, 290, 313, 339 Coca, 290 Cocaine, 184, 290 Cofactor, 290, 343, 357 Cognition, 20, 149, 290, 330 Cohort Studies, 290, 303 Colitis, 132, 290, 320 Collagen, 252, 281, 290, 306, 308, 333, 339, 342 Collapse, 59, 275, 284, 291, 352
Index 369
Colloidal, 273, 281, 291, 351 Colorectal, 57, 126, 291 Colorectal Cancer, 57, 291 Colostomy, 217, 291 Combination Therapy, 211, 291, 304 Comorbidity, 79, 98, 210, 291 Complement, 44, 55, 275, 291, 309, 320, 324, 339 Complementary and alternative medicine, 125, 134, 291 Complementary medicine, 125, 291 Compress, 3, 292 Computational Biology, 237, 292 Conception, 206, 214, 292, 293, 306, 341, 354 Concomitant, 17, 52, 170, 292 Confounding, 25, 292 Confusion, 292, 330, 360 Congestion, 278, 292, 303 Congestive heart failure, 15, 292 Conjugated, 79, 119, 129, 282, 288, 292, 295 Connective Tissue, 279, 284, 290, 292, 306, 308, 323, 348, 354, 356 Consciousness, 275, 292, 296, 297, 299, 348 Consensus Sequence, 64, 274, 292 Conserved Sequence, 274, 292 Constipation, 202, 212, 245, 251, 252, 256, 267, 278, 292, 320, 337, 351 Constriction, 292, 320, 361 Constriction, Pathologic, 292, 361 Consultation, 44, 246, 292 Consumption, 12, 18, 57, 63, 136, 171, 179, 192, 198, 268, 292, 297, 331, 334 Contamination, 170, 292, 332 Contraception, 23, 80, 293 Contraceptive, 23, 200, 293, 302, 325, 348 Contractility, 276, 293 Contraindications, ii, 257, 293 Contralateral, 35, 293, 332 Control group, 5, 9, 11, 18, 26, 28, 29, 33, 42, 63, 67, 69, 293, 341, 345 Controlled clinical trial, 41, 293 Controlled study, 23, 62, 68, 74, 94, 106, 108, 293 Conventional therapy, 7, 109, 185, 293 Conventional treatment, 8, 185, 293 Coordination, 68, 287, 293, 328 Cor, 70, 79, 144, 145, 293, 294 Coronary, 7, 8, 9, 30, 38, 58, 68, 76, 149, 166, 178, 186, 276, 286, 293, 294, 326, 328, 329 Coronary Disease, 166, 293
Coronary heart disease, 8, 30, 68, 76, 149, 178, 186, 286, 293 Coronary Thrombosis, 294, 326, 328, 329 Coronary Vessels, 293, 294 Corpus, 206, 294, 323, 341, 350, 357 Corpus Luteum, 206, 294, 323, 341 Corrosion, 153, 294 Cortex, 145, 294, 306, 313, 345 Cortical, 294, 304, 345, 350 Corticosteroid, 294, 341, 354 Corticotropin-Releasing Hormone, 70, 294 Cortisol, 51, 54, 181, 273, 294 Cortisone, 294, 341 Cotinine, 42, 294 Courtship, 279, 294 Creatine, 121, 122, 128, 166, 294 Creatine Kinase, 166, 294 Creatinine, 92, 294 Cribriform, 294, 332 Criterion, 18, 294 Critical Care, 48, 94, 295 Crossing-over, 295, 346 Cross-Sectional Studies, 295, 303 Cultured cells, 60, 295 Curative, 295, 331, 357 Cutaneous, 295, 323 Cyanosis, 295, 313 Cyclic, 285, 295, 311, 331, 338, 343, 350 Cyclosporine, 244, 253, 295 Cyproheptadine, 179, 295 Cyst, 279, 295 Cysteine, 159, 160, 189, 295, 355 Cystine, 295 Cytochrome, 32, 289, 295, 334 Cytokine, 108, 182, 295 Cytokinin, 163, 295 Cytomegalovirus, 153, 244, 295 Cytoplasm, 278, 287, 295, 296, 302, 311, 327, 329, 348 Cytoskeletal Proteins, 296, 301 Cytoskeleton, 161, 296 Cytotoxic, 138, 255, 285, 296, 351 D Dairy Products, 197, 245, 256, 296, 349 Data Collection, 14, 49, 53, 69, 296 Databases, Bibliographic, 237, 296 Daunorubicin, 296, 300 Deamination, 296, 360 Decarboxylation, 296, 314 Decidua, 296, 338 Decision Making, 69, 246, 249, 296 Defecation, 224, 296
370
Weight Gain
Defense Mechanisms, 180, 296 Degenerative, 296, 313, 328, 333, 348 Deletion, 175, 278, 296 Delirium, 278, 296 Delivery of Health Care, 297, 309 Delusions, 297, 344 Dementia, 146, 183, 278, 297 Dendrites, 297, 330, 332, 345 Density, 7, 9, 12, 14, 23, 25, 81, 283, 287, 297, 301, 322, 332 Dental Care, 209, 297 Dentate Gyrus, 127, 297, 313 Dentists, 209, 297 Depersonalization, 297, 334, 349 Depolarization, 297, 351 Depressive Disorder, 297, 322 Derealization, 297, 334 Dermatitis, 151, 297, 315 Detoxification, 164, 297 Deuterium, 297, 314 Developed Countries, 52, 183, 210, 297 Developing Countries, 52, 297 Dextrorotatory, 156, 181, 298 DHEA, 133, 298 Diabetes Insipidus, 298, 339 Diabetic Retinopathy, 210, 298 Diagnostic procedure, 143, 227, 298 Dialysate, 5, 298 Dialyzer, 298, 312 Diarrhea, 94, 97, 105, 202, 208, 209, 243, 245, 251, 256, 298, 320, 321 Diastolic, 298, 315, 325 Diastolic pressure, 298, 315, 325 Diencephalon, 298, 315, 357 Dietary Fats, 52, 255, 298, 322 Dietary Fiber, 200, 247, 298 Dietetics, 218, 219, 298 Dietitian, 199, 213, 245, 254, 255, 298 Diffusion, 298, 317 Digestion, 54, 147, 208, 224, 273, 282, 284, 298, 308, 317, 319, 322, 323, 336, 354 Digestive system, 141, 223, 252, 298, 308 Digestive tract, 298, 352 Digital photography, 12, 69, 299 Dihydrotestosterone, 34, 271, 299, 346 Dihydroxy, 299, 364 Dilation, 30, 284, 299, 361 Dimethyl, 157, 179, 184, 299, 351 Diploid, 299, 339 Direct, iii, 17, 48, 61, 135, 171, 231, 299, 300, 323, 338, 345, 346, 356 Disaccharides, 168, 299
Disease Outbreaks, 299 Disease Reservoirs, 163, 299 Disease Transmission, 299 Disparity, 61, 299 Disposition, 15, 20, 299 Dissection, 16, 89, 299, 359 Dissociation, 272, 299, 319 Distal, 299, 320, 336, 344 Diuresis, 48, 284, 299 Diuretic, 48, 165, 285, 299, 307 Diurnal, 86, 104, 299 Dizziness, 299, 334 DNA Topoisomerase, 299, 309 Dogfish, 165, 300 Dopamine, 21, 146, 156, 184, 278, 284, 288, 290, 300, 327, 338, 348 Dosage Forms, 184, 191, 300 Dosage schedule, 66, 223, 300 Dose-dependent, 15, 300 Double-blinded, 45, 50, 51, 300 Doxorubicin, 125, 300 Drive, ii, vi, 4, 6, 17, 95, 117, 188, 203, 208, 214, 244, 246, 255, 300, 321 Drug Interactions, 199, 232, 300 Drug Residues, 179, 300 Drug Tolerance, 300, 358 Duct, 286, 300, 304, 349 Dumping Syndrome, 256, 295, 300 Duodenal Ulcer, 192, 300, 331 Duodenum, 282, 300, 301, 308, 320, 354 Dyskinesia, 278, 301 Dyslipidemia, 68, 186, 205, 211, 301 Dyspareunia, 301, 304 Dyspnea, 301, 334 Dystonia, 278, 301 Dystrophin, 161, 301 Dystrophy, 162, 301 E Eating Disorders, 41, 80, 91, 131, 136, 156, 184, 186, 205, 224, 242, 301 Ectopic, 31, 301 Edema, 48, 268, 298, 301, 307, 330 Effector, 271, 291, 301, 330, 338 Effector cell, 301, 330 Ego, 301, 332, 346 Elastin, 291, 301 Electroacupuncture, 126, 301 Electrolyte, 211, 294, 297, 300, 301, 306, 327, 332, 340, 352 Electrons, 278, 281, 301, 319, 320, 334, 345 Embryo, 30, 283, 287, 301, 302, 306, 317, 332, 333, 341, 353, 360
Index 371
Embryo Transfer, 30, 302, 341 Emesis, 278, 302 Empirical, 39, 302 Enanthate, 62, 302 Encapsulated, 302, 322 Encephalocele, 302, 330 Endemic, 209, 302, 324, 353 Endocrine System, 302, 330 Endocrinology, 84, 87, 93, 107, 118, 119, 145, 302 Endometrial, 75, 186, 302 Endometrium, 296, 302, 326, 331 Endoscopy, 209, 302 Endothelial cell, 165, 302, 357 Endothelium, 302, 331 Endothelium-derived, 302, 331 Endotoxic, 302, 322 Endotoxins, 291, 302 End-stage renal, 212, 289, 302, 339 Energy balance, 4, 34, 40, 46, 60, 85, 303, 321, 338 Energy Intake, 13, 25, 33, 42, 55, 63, 74, 138, 222, 303 Enhancer, 190, 303 Environmental Health, 236, 238, 303 Enzymatic, 160, 189, 285, 286, 291, 303, 314, 348 Enzyme Inhibitors, 303, 339 Ependyma, 279, 303, 357 Epidemic, 62, 183, 303, 353 Epidemiologic Studies, 13, 303, 309 Epidemiological, 35, 41, 303 Epidermal, 159, 303, 326 Epidermis, 303, 345 Epigastric, 303, 334 Epinephrine, 272, 300, 303, 331, 359 Epithelial, 59, 296, 303, 313, 321 Epithelial Cells, 303, 313, 321 Epithelium, 159, 281, 302, 303, 308 Epitope, 16, 303 Ergot, 303, 349 Erythema, 303, 360 Erythrocytes, 275, 276, 283, 284, 304, 346 Escalation, 163, 304 Esophagus, 84, 224, 298, 304, 308, 312, 346, 354, 361 Estradiol, 14, 23, 53, 64, 138, 304 Estrogen, 22, 23, 52, 58, 65, 147, 149, 177, 229, 304, 325, 342, 364 Estrogen Replacement Therapy, 65, 304 Ethanol, 304, 306 Ethmoid, 304, 332
Ethnic Groups, 38, 47, 304 Ethnobotany, 174, 304 Evacuation, 292, 304, 308 Excipient, 165, 304 Excitatory, 304, 310 Excrete, 11, 244, 304, 320 Exercise Test, 42, 304 Exercise Tolerance, 45, 62, 304 Exhaustion, 276, 304, 324 Exocrine, 288, 304, 334 Exogenous, 27, 43, 64, 171, 172, 180, 194, 283, 304, 359 Expiration, 148, 304, 347 Extracellular, 60, 161, 215, 280, 292, 304, 305, 306, 352, 357 Extracellular Matrix, 161, 292, 305, 306 Extracellular Space, 305 Extraction, 162, 174, 305 Extrapyramidal, 66, 273, 278, 300, 305 Extrarenal, 215, 305 Extravascular, 48, 305 Extravascular Lung Water, 48, 305 Eye Infections, 272, 305 F Facial, 246, 253, 305, 315, 352 Facial Nerve, 305, 315 Facial Nerve Diseases, 305, 315 Family Planning, 204, 237, 305 Famotidine, 191, 305 Fathers, 202, 305 Fatigue, 10, 172, 218, 268, 305, 312 Fatty acids, 27, 159, 166, 273, 305, 310, 322, 342, 357 Fatty Liver, 242, 305 Febrile, 305, 324, 353 Feces, 292, 305, 354 Feeding Behavior, 185, 186, 305 Femoral, 23, 306 Femur, 306 Fermentation, 147, 173, 306 Ferritin, 247, 252, 306 Fertilization in Vitro, 306, 341 Fetal Development, 306, 330 Fetal Monitoring, 200, 202, 306 Fetoprotein, 200, 306 Fetus, 214, 274, 306, 307, 338, 341, 353, 354, 360 Fibrin, 283, 306, 337, 357 Fibrinogen, 88, 306, 339, 357 Fibroblasts, 64, 306, 319 Fibrosis, 15, 24, 39, 45, 84, 105, 139, 274, 306, 349
372
Weight Gain
Fissure, 289, 297, 306, 334 Flatulence, 208, 306 Flatus, 306, 308 Fluid Therapy, 306, 332 Fluoxetine, 88, 106, 113, 306 Fluphenazine, 179, 306 Foetal, 96, 306 Foetoplacental, 307, 332 Folate, 257, 307 Fold, 7, 27, 52, 145, 161, 306, 307 Folic Acid, 201, 209, 214, 255, 307 Follicles, 307 Food Deprivation, 144, 307 Food Habits, 28, 307 Food Preferences, 307 Forearm, 283, 307, 345 Fossa, 287, 307 Fourth Ventricle, 289, 307, 357 Fractionation, 275, 307 Fructose, 17, 61, 88, 127, 250, 307, 309, 311 Fundus, 307, 332 Fungi, 170, 289, 305, 307, 311, 326, 327, 328, 353, 364 Fungus, 303, 307, 349, 364 Furosemide, 48, 307 G Galactosemia, 79, 307 Galanin, 34, 70, 307 Gallbladder, 178, 186, 224, 271, 282, 288, 298, 307, 308 Gallstones, 186, 282, 288, 308, 360 Ganglia, 271, 308, 330, 355 Gap Junctions, 308, 356 Gas, 45, 208, 256, 275, 285, 298, 306, 308, 314, 317, 320, 331, 347, 361, 362 Gas exchange, 45, 308, 347, 362 Gastrectomy, 256, 295, 308 Gastric, 54, 126, 154, 224, 281, 289, 300, 305, 308, 312, 314, 331, 336, 346, 354 Gastric Acid, 289, 308, 331 Gastric Emptying, 224, 308 Gastric Juices, 308, 336 Gastric Mucosa, 308, 336 Gastrin, 289, 308, 314 Gastroenterology, 92, 105, 113, 208, 308 Gastrointestinal tract, 179, 188, 224, 304, 306, 308, 321, 350, 359 Gastroparesis, 246, 308 Gelatin, 191, 308, 310, 355, 357 Gene, 16, 17, 30, 40, 41, 45, 47, 57, 60, 72, 73, 89, 107, 126, 128, 153, 155, 160, 161, 162, 166, 175, 176, 183, 189, 194, 207,
222, 228, 243, 272, 273, 283, 301, 308, 309, 314, 350 Gene Expression, 16, 17, 31, 41, 126, 128, 194, 228, 308 Genetic Code, 308, 331 Genetic Counseling, 243, 308 Genetic Engineering, 283, 290, 309 Genetic testing, 200, 201, 309 Genetics, 11, 21, 32, 44, 80, 95, 222, 309, 337 Genistein, 23, 309 Genital, 309, 361 Genotype, 21, 32, 150, 309, 337 Geographic Locations, 61, 309 Geriatric, 94, 104, 106, 108, 309 Germ Cells, 166, 309, 325, 333, 352, 353, 357 Gestation, 9, 30, 53, 55, 67, 89, 200, 309, 336, 338, 353 Gestational Age, 9, 54, 109, 309 Gibberellin, 163, 309 Ginger, 178, 309 Gingival Hyperplasia, 253, 309 Ginseng, 134, 309 Gland, 35, 272, 294, 300, 309, 315, 323, 334, 335, 338, 343, 349, 350, 354, 357, 358 Glomerular, 309, 347 Glomeruli, 309, 332 Glomerulonephritis, 248, 255, 309, 323 Glomerulus, 309, 310, 329 Glucocorticoid, 181, 182, 228, 310, 341 Glucose Intolerance, 4, 31, 298, 310 Glucose tolerance, 24, 44, 49, 51, 92, 111, 175, 205, 249, 310 Glucose Tolerance Test, 44, 49, 205, 249, 310 Glucosidases, 168, 310 Glutamate, 310, 337 Glutamic Acid, 159, 307, 310, 342 Glutamine, 61, 159, 310 Gluten, 10, 71, 118, 121, 122, 208, 287, 310 Glycerol, 310, 338 Glycerophospholipids, 310, 338 Glycine, 159, 282, 288, 310, 350 Glycogen, 126, 193, 310 Glycogen Synthase, 193, 310 Glycoprotein, 161, 306, 311, 321, 357 Glycoside, 299, 311, 349 Glycosidic, 311, 332 Goats, 144, 171, 296, 311 Gonad, 311 Gonadal, 206, 311, 354
Index 373
Gonadotropin, 110, 311 Governing Board, 311, 340 Grade, 28, 152, 162, 186, 248, 311 Grading, 152, 311 Graft, 4, 311, 314 Graft Survival, 4, 311 Grafting, 311, 316 Gram-positive, 311, 354 Granule, 297, 311, 348 Granulocytes, 311, 328, 351, 363 Grasses, 162, 289, 307, 311 Growth factors, 53, 138, 172, 176, 311 Guanylate Cyclase, 311, 331 H Habitual, 35, 49, 69, 288, 312 Hair follicles, 35, 312 Half-Life, 146, 184, 312 Haloperidol, 179, 312 Haploid, 312, 339 Haptens, 273, 312 Headache, 285, 312, 341, 351 Health Behavior, 67, 312 Health Education, 58, 248, 256, 312 Health Status, 38, 53, 312 Heart attack, 286, 312 Heart failure, 15, 276, 312 Heart Valves, 281, 312 Heartbeat, 312, 325 Heartburn, 251, 252, 312, 317 Hematocrit, 247, 252, 283, 312 Heme, 282, 295, 312, 313, 334 Hemodialysis, 5, 10, 11, 92, 97, 109, 210, 219, 246, 255, 298, 312, 320 Hemodynamics, 48, 312 Hemoglobin, 6, 7, 8, 10, 200, 211, 247, 252, 276, 283, 295, 304, 312, 313, 320, 321 Hemoglobin M, 200, 295, 313 Hemorrhage, 216, 312, 313, 354, 363 Hemostasis, 313, 350 Hepatic, 17, 19, 126, 127, 151, 214, 273, 297, 310, 313, 340 Hepatitis, 243, 313 Hepatitis C, 244, 313 Hepatocytes, 27, 313 Hereditary, 18, 243, 313, 328 Heredity, 223, 271, 308, 309, 313 Herpes, 163, 165, 313 Herpes Zoster, 313 Heterogeneity, 273, 313 Heterotrophic, 307, 313 Heterozygote, 153, 313 Hiccup, 288, 313
Hippocampus, 127, 297, 313, 322, 345 Hirsutism, 169, 314, 315 Histamine, 91, 191, 193, 275, 278, 288, 289, 295, 305, 314, 315, 320, 331, 346 Histidine, 159, 314 Histology, 314, 334 Holidays, 9, 216, 229, 314 Homeostasis, 61, 97, 160, 205, 215, 314, 352 Homologous, 160, 189, 273, 295, 313, 314, 350, 356, 359 Hormonal, 17, 23, 57, 138, 151, 280, 294, 304, 314 Hormone Replacement Therapy, 58, 149, 229, 314 Hormone therapy, 91, 229, 314, 325 Host, 59, 162, 281, 311, 314, 316, 328, 349, 361, 362 Human growth hormone, 105, 314 Hybrid, 290, 314, 349 Hybridomas, 314, 319 Hydrogen, 158, 271, 274, 281, 284, 285, 297, 314, 327, 330, 334, 337, 344 Hydrolysis, 176, 279, 283, 314, 338, 339, 343 Hydrophobic, 310, 314, 322 Hydroxylysine, 291, 314 Hydroxyproline, 159, 291, 314 Hydroxyzine, 193, 315 Hyperacusis, 253, 305, 315 Hyperandrogenism, 50, 51, 169, 315 Hyperbilirubinemia, 315, 320 Hypercalcemia, 253, 315 Hypercholesterolemia, 131, 301, 315 Hyperemesis, 204, 315 Hyperglycemia, 19, 24, 106, 180, 208, 210, 213, 315 Hyperlipidemia, 4, 187, 211, 219, 301, 315 Hypersensitivity, 273, 275, 315, 348 Hypertension, 4, 8, 15, 19, 22, 28, 30, 68, 94, 110, 111, 113, 153, 169, 178, 182, 183, 186, 187, 210, 211, 219, 248, 276, 285, 286, 312, 315, 329, 342 Hyperthyroidism, 85, 115, 315, 342 Hypertrichosis, 314, 315 Hypertriglyceridemia, 301, 315 Hypertrophy, 293, 315, 359 Hypoglycemia, 109, 185, 199, 200, 208, 211, 213, 214, 215, 219, 246, 247, 250, 315 Hypoglycemic, 200, 208, 214, 315 Hypoglycemic Agents, 200, 208, 315 Hypophyseal, 315, 325 Hypotension, 210, 278, 315
374
Weight Gain
Hypothalamic, 17, 23, 31, 43, 144, 145, 315 Hypotonia, 95, 289, 315 Hypoxemia, 49, 316 Hypoxia, 297, 316 I Id, 120, 130, 258, 264, 266, 301, 316 Idiopathic, 208, 316 Ileum, 287, 316, 320, 363 Imidazole, 314, 316, 346 Imipramine, 88, 316 Immersion, 126, 152, 316 Immune adjuvant, 274, 316 Immune function, 162, 316 Immune response, 162, 272, 274, 277, 280, 294, 312, 316, 324, 355, 361, 362, 363 Immune system, 162, 282, 301, 316, 324, 328, 361, 363 Immunity, 273, 316, 332 Immunization, 316, 341 Immunodeficiency, 223, 251, 316 Immunogenic, 316, 322 Immunoglobulins, 316, 339 Immunologic, 288, 309, 316 Immunology, 272, 273, 316 Immunosuppressant, 244, 316 Immunosuppressive, 4, 219, 255, 310, 316, 356 Impairment, 17, 29, 48, 296, 301, 305, 316, 319, 326, 344 Implantation, 148, 149, 292, 316, 331, 332 Impotence, 224, 316 In vitro, 15, 30, 59, 60, 146, 184, 302, 316, 356 In vivo, 13, 30, 31, 59, 60, 175, 176, 193, 316, 328, 356 Incision, 217, 317, 319 Incontinence, 104, 146, 149, 183, 184, 212, 317 Incubator, 158, 317 Indicative, 205, 317, 335, 361 Indigestion, 317, 321 Induction, 17, 30, 57, 61, 64, 70, 193, 276, 278, 317, 342 Infancy, 4, 7, 99, 109, 112, 243, 253, 317 Infant Behavior, 288, 317 Infantile, 317, 322 Infarction, 317 Infertility, 30, 201, 317 Infiltration, 242, 309, 317 Inflammatory bowel disease, 216, 217, 317 Informed Consent, 18, 317 Infuse, 317, 318
Infusion, 15, 43, 204, 211, 216, 219, 317, 318, 359 Infusion Pumps, 211, 318 Infusion Pumps, Implantable, 211, 318 Ingestion, 70, 170, 224, 310, 318, 328, 339, 357 Initiation, 59, 210, 214, 318, 358 Inlay, 318, 347 Inoculum, 147, 318 Inorganic, 188, 318, 328, 338, 355 Inositol, 187, 188, 318, 350 Inotropic, 300, 318 Inpatients, 86, 318 Insight, 60, 139, 318 Insomnia, 164, 206, 268, 318, 341, 351 Insulator, 318, 328 Insulin Infusion Systems, 318 Insulin-dependent diabetes mellitus, 6, 180, 318 Insulin-like, 83, 138, 211, 318 Intensive Care, 54, 77, 108, 318 Interferon, 183, 318, 319 Interferon-alpha, 319 Interleukin-6, 23, 319 Intermittent, 49, 306, 319, 323, 337 Internal Medicine, 8, 10, 302, 308, 319 Interstitial, 305, 319, 329, 347 Intervention Studies, 5, 41, 63, 319 Intestinal, 43, 128, 150, 168, 172, 178, 209, 216, 217, 223, 242, 286, 287, 288, 310, 319, 324 Intestinal Obstruction, 216, 319 Intoxication, 170, 296, 319, 364 Intracellular, 31, 160, 176, 189, 285, 305, 317, 319, 331, 340, 343, 346, 348, 350, 351 Intramuscular, 151, 152, 319, 335 Intraocular, 319, 358 Intraocular pressure, 319, 358 Intraperitoneal, 211, 319 Intravenous, 43, 144, 219, 244, 317, 318, 319, 335 Intrinsic, 273, 281, 319 Introspection, 202, 319 Invasive, 138, 154, 316, 319 Ion Channels, 280, 319, 330, 356 Ionization, 172, 319 Ions, 176, 281, 284, 285, 299, 301, 314, 319, 327, 352 Irritable Bowel Syndrome, 184, 320 Ischemia, 280, 320 Islet, 113, 194, 320 Isoenzyme, 294, 320
Index 375
Isoflavones, 149, 320 Isoleucine, 158, 320 J Jaundice, 244, 315, 320, 329 Jejunoileal Bypass, 154, 320 Jejunum, 320 Joint, 38, 224, 228, 279, 320, 333, 356 K Karyotype, 275, 320 Kb, 236, 320 Ketotifen, 193, 320 Kidney Failure, 302, 320 Kidney stone, 320, 360 Kidney Transplantation, 4, 211, 247, 255, 320 Kinetic, 15, 321 L Labile, 291, 321 Lactation, 80, 203, 204, 214, 215, 257, 321, 332, 334, 342 Lactose Intolerance, 168, 202, 245, 251, 321 Laminin, 161, 281, 321 Large Intestine, 224, 287, 291, 298, 319, 321, 346, 352 Latent, 321, 340 Lens, 286, 321, 363 Lesion, 321, 323, 356, 359 Lethal, 162, 321 Lethargy, 251, 321 Leucine, 158, 321, 336 Leukemia, 165, 300, 321 Leukocytes, 283, 284, 288, 311, 319, 321, 327 Levo, 321, 364 Libido, 276, 321 Library Services, 264, 321 Life cycle, 272, 307, 321 Ligament, 151, 321, 343 Ligands, 185, 186, 321 Limbic, 275, 321 Limbic System, 275, 321 Linear Models, 55, 322 Linkage, 31, 44, 155, 322 Linoleic Acids, 159, 322 Lip, 246, 322 Lipase, 19, 184, 322 Lipid A, 17, 78, 322 Lipodystrophy, 175, 322 Lipopolysaccharides, 322 Lipoprotein, 7, 9, 14, 19, 81, 169, 301, 322, 323 Liposomal, 34, 322
Liposome, 34, 322 Lipoxygenase, 70, 279, 322 Lithium, 50, 98, 179, 278, 322 Litter, 176, 322 Liver, 27, 119, 126, 165, 166, 197, 199, 219, 224, 242, 243, 244, 252, 253, 271, 273, 274, 279, 282, 295, 298, 300, 305, 307, 308, 310, 313, 322, 323, 329, 341, 347, 360 Liver Transplantation, 243, 323 Lobe, 314, 323 Localization, 145, 323 Localized, 145, 162, 166, 216, 301, 302, 314, 315, 317, 321, 322, 323, 339, 359, 360 Locomotion, 323, 339 Locomotor, 60, 323 Longitudinal study, 23, 40, 52, 71, 94, 99, 118, 323 Long-Term Care, 32, 323 Loop, 17, 161, 318, 323 Low-density lipoprotein, 166, 301, 322, 323 Lucida, 321, 323 Lumbar, 23, 281, 323 Lumen, 30, 168, 323 Lupus, 132, 254, 255, 323, 356 Lupus Nephritis, 255, 323 Lutein Cells, 323, 342 Lymph, 251, 288, 289, 302, 323, 324, 349 Lymph node, 251, 288, 323, 324, 349 Lymphatic, 302, 317, 323, 324, 349, 352, 353 Lymphatic system, 323, 324, 349, 352, 353 Lymphocyte, 182, 277, 324, 325 Lymphoid, 182, 277, 324 Lysine, 158, 314, 324 Lytic, 324, 362 M Macronutrients, 57, 324 Macrophage, 182, 324 Maintenance therapy, 66, 324 Major Histocompatibility Complex, 228, 324 Malabsorption, 208, 287, 324 Malaise, 216, 324 Malaria, 77, 324 Malaria, Falciparum, 324 Malaria, Vivax, 324 Malignant, 106, 172, 277, 324 Malnutrition, 16, 211, 273, 280, 284, 324 Mammary, 52, 159, 324, 331 Mammography, 18, 324 Mania, 324, 325
376
Weight Gain
Manic, 50, 146, 183, 278, 283, 322, 325, 344 Manic-depressive psychosis, 325, 344 Manifest, 31, 35, 199, 218, 325 Mean blood pressure, 9, 11, 325 Meat, 155, 162, 167, 197, 200, 245, 298, 325, 349 Meat Products, 167, 298, 325 Medial, 103, 145, 304, 325, 332 Median Eminence, 34, 325 Mediate, 161, 189, 300, 301, 325, 346 Mediator, 29, 52, 182, 288, 325, 350 Medical Records, 325, 348 Medical Staff, 300, 325 MEDLINE, 237, 325 Medroxyprogesterone, 107, 325 Medroxyprogesterone Acetate, 107, 325 Megaloblastic, 307, 325 Megestrol, 62, 84, 94, 102, 108, 325 Megestrol Acetate, 62, 84, 94, 108, 325 Meiosis, 325, 356 Melanin, 326, 338, 359 Melanocytes, 326 Melanoma, 165, 326 Memory, 44, 276, 296, 297, 326 Menarche, 52, 326 Meninges, 287, 326 Menopause, 5, 23, 132, 147, 149, 177, 222, 229, 326, 332, 340, 341, 342 Menstrual Cycle, 326, 332, 341, 342 Menstruation, 5, 274, 296, 326, 332, 341 Mental Disorders, 141, 326, 341, 344 Mental Health, iv, 11, 39, 113, 141, 223, 236, 239, 326, 341, 344 Mental Processes, 299, 326, 344 Mental Retardation, 176, 244, 253, 326 Mentors, 32, 39, 46, 48, 326 Mesolimbic, 278, 326 Metabolic disorder, 161, 218, 298, 326 Metabolite, 283, 299, 315, 326, 341 Methionine, 159, 299, 326, 355 MI, 88, 127, 144, 202, 250, 269, 326 Microbe, 326, 358 Microbiological, 163, 326 Microbiology, 119, 272, 280, 281, 326 Micronutrients, 144, 327 Microorganism, 171, 290, 327, 335, 363 Microscopy, 281, 327 Midaxillary line, 327, 363 Migration, 55, 161, 327 Milliliter, 283, 327 Millimeter, 327, 363 Mineralocorticoids, 272, 294, 327
Minority Groups, 28, 327 Miscarriage, 201, 327 Mitosis, 278, 327 Mobility, 224, 252, 327 Modeling, 29, 53, 209, 327 Modification, 52, 58, 219, 309, 327, 345 Molecular Structure, 327, 359 Monitor, 152, 211, 247, 294, 327 Monoamine, 157, 184, 327 Monocytes, 319, 321, 327, 328 Monotherapy, 20, 50, 51, 328 Mood Disorders, 115, 328 Morphological, 59, 302, 307, 326, 328 Morphology, 90, 328 Motility, 54, 328, 350 Motion Sickness, 328, 329 Movement Disorders, 278, 328 Mucins, 328, 349 Mucociliary, 59, 328 Mucociliary Clearance, 59, 328 Mucosa, 287, 288, 308, 323, 328, 342, 354 Mucus, 59, 328, 360 Multiple sclerosis, 190, 328 Multivariate Analysis, 6, 328 Muscle Contraction, 301, 328 Muscular Dystrophies, 162, 301, 328 Mycotoxicosis, 170, 328 Mycotoxins, 170, 328 Mydriatic, 299, 328 Myelin, 328 Myeloid Cells, 182, 328 Myocardial infarction, 278, 294, 326, 328, 329, 342 Myocardial Ischemia, 276, 293, 329 Myocardium, 276, 326, 328, 329 Myofibrils, 301, 329 N Nadir, 63, 329 Naloxone, 164, 329 Naltrexone, 164, 329 Narcolepsy, 184, 329 Narcotic, 329 Nasogastric, 226, 329 Natriuresis, 276, 329 Nausea, 126, 202, 212, 245, 256, 277, 278, 300, 308, 317, 329, 334, 341, 357, 360 NCI, 1, 138, 140, 202, 235, 244, 245, 329 Necrosis, 278, 317, 326, 328, 329 Neonatal, 9, 30, 54, 59, 67, 77, 89, 93, 98, 101, 108, 130, 172, 201, 226, 243, 329 Neonatal Hepatitis, 243, 329 Neonatal period, 172, 329
Index 377
Neoplasia, 57, 329 Nephritis, 255, 329 Nephrologist, 210, 329 Nephropathy, 8, 19, 185, 320, 330 Nephrosis, 330 Nephrotic, 126, 248, 330 Nephrotic Syndrome, 126, 248, 330 Nervous System, 15, 186, 190, 271, 272, 273, 275, 280, 281, 282, 284, 285, 287, 288, 290, 308, 310, 312, 325, 328, 330, 333, 337, 350, 355, 356 Neural, 28, 43, 100, 110, 201, 272, 277, 302, 306, 330, 352 Neural tube defects, 100, 201, 306, 330 Neuroendocrine, 34, 160, 330 Neuroendocrinology, 33, 88, 119, 330 Neuroleptic, 106, 273, 278, 290, 330 Neuronal, 157, 162, 184, 285, 330 Neurons, 34, 43, 55, 70, 290, 297, 304, 308, 330, 331, 345, 355, 356, 362 Neuropathy, 184, 185, 210, 330, 336 Neuropeptide, 34, 112, 153, 155, 186, 294, 330 Neurotransmitters, 65, 330, 351, 352 Neutrons, 274, 330, 345 Niacin, 331, 359 Nidation, 302, 331 Nipples, 3, 331 Nitric Oxide, 162, 228, 331 Nitrogen, 176, 273, 274, 276, 310, 331, 359 Nizatidine, 91, 104, 191, 331 Norepinephrine, 15, 65, 110, 146, 157, 184, 272, 300, 331, 338, 351 Normal Distribution, 153, 331 Nuclei, 55, 274, 275, 301, 305, 309, 322, 327, 330, 331, 333, 343, 349, 362 Nucleic acid, 185, 186, 308, 331, 345 Nucleus, 34, 70, 144, 145, 155, 176, 278, 279, 289, 295, 297, 325, 327, 330, 331, 342, 343, 352, 362 Nurseries, 54, 331 Nursing Care, 206, 331, 335 Nutrition Assessment, 199, 246, 331 Nutritional Status, 38, 61, 108, 114, 126, 211, 216, 331 Nutritional Support, 126, 190, 332 O Observational study, 63, 332 Obsession, 202, 332 Oestrogen, 206, 332 Ointments, 300, 332, 334 Olfactory Bulb, 145, 332, 363
Oligo, 168, 332 Oligomenorrhea, 332, 339 Oligosaccharides, 168, 332 Omega-3 fatty acid, 156, 332 On-line, 68, 267, 332 Opacity, 286, 297, 332 Optic Chiasm, 315, 332, 333 Optic Disk, 298, 332 Optic Nerve, 332, 333, 348, 349 Organ Transplantation, 218, 244, 333 Ornithine, 133, 158, 333 Orthostatic, 278, 333 Osmotic, 273, 333, 351 Ossification, 333 Osteoarthritis, 151, 153, 173, 178, 183, 184, 186, 187, 333 Osteogenesis, 252, 333 Osteogenesis Imperfecta, 252, 333 Osteoporosis, 92, 149, 153, 183, 219, 245, 254, 304, 332, 333 Outpatient, 50, 333 Ovarian Follicle, 294, 333 Ovariectomy, 147, 177, 333 Ovaries, 50, 51, 149, 169, 315, 333, 339, 351 Ovary, 31, 169, 294, 304, 311, 332, 333, 334, 354 Overall survival, 138, 333 Overexpress, 166, 333 Overweight, 4, 8, 9, 18, 21, 22, 25, 33, 38, 42, 47, 49, 52, 56, 65, 68, 90, 95, 107, 120, 139, 151, 154, 173, 178, 186, 206, 228, 229, 268, 334 Ovulation, 169, 276, 325, 334, 348 Ovum, 294, 296, 309, 321, 333, 334, 341, 342, 364 Oxandrolone, 135, 334 Oxidation, 61, 128, 138, 271, 278, 279, 283, 295, 313, 334, 357 Oxidative Phosphorylation, 60, 334 Oxygen Consumption, 31, 75, 175, 304, 334, 347 Oxygenase, 57, 334 Oxygenation, 48, 316, 334 Oxytocin, 54, 334 P Palatal Obturators, 246, 334 Palate, 289, 334, 352, 361 Palliative, 325, 332, 334, 357 Pancreas, 180, 223, 224, 271, 282, 298, 308, 318, 320, 322, 334, 359 Pancreatic, 31, 126, 168, 180, 194, 288, 334 Panic, 88, 201, 316, 334
378
Weight Gain
Panic Disorder, 88, 316, 334 Paraffin, 58, 334 Parathyroid, 247, 252, 334, 335, 357 Parathyroid Glands, 334, 335 Parathyroid hormone, 247, 252, 335 Parenteral, 190, 219, 303, 335 Parenteral Nutrition, 190, 219, 335 Paresthesias, 334, 335 Parietal, 80, 335, 337 Parietal Lobe, 335 Parkinsonism, 278, 335 Paroxetine, 110, 335 Particle, 322, 335, 358 Partnership Practice, 335, 341 Parturition, 335, 342 Patch, 38, 66, 164, 335, 358 Pathogen, 318, 335 Pathogenesis, 49, 205, 335 Pathologic, 271, 278, 282, 293, 315, 335, 361 Pathologic Processes, 278, 335 Pathophysiology, 154, 166, 194, 335 Patient Care Management, 211, 249, 335 Patient Care Team, 254, 335 Patient Compliance, 169, 335 Patient Education, 198, 210, 242, 255, 256, 262, 264, 269, 336 Patient Selection, 198, 217, 336 Pelvic, 212, 336, 343 Penicillin, 276, 336, 361 Pensions, 46, 336 Pepsin, 289, 336 Pepsin A, 289, 336 Peptic, 252, 336 Peptic Ulcer, 252, 336 Peptide, 15, 31, 34, 43, 145, 158, 159, 163, 180, 288, 321, 336, 339, 343 Perception, 80, 91, 297, 336, 349 Perennial, 336, 359 Perforation, 216, 336 Pericardium, 336, 356 Perinatal, 4, 38, 67, 73, 101, 201, 206, 336 Perineal, 151, 212, 336 Perineum, 336 Periodontal disease, 224, 336 Perioperative, 94, 336 Peripheral Neuropathy, 224, 336 Peristalsis, 224, 336 Peritoneal, 210, 255, 298, 319, 336, 337 Peritoneal Cavity, 319, 337 Peritoneal Dialysis, 210, 255, 298, 337 Peritoneum, 336, 337 Peritonitis, 210, 224, 337
Perspiration, 212, 337 Petroleum, 334, 337 PH, 111, 283, 337 Pharmaceutical Preparations, 287, 304, 308, 337 Pharmaceutical Solutions, 300, 337 Pharmacodynamic, 305, 337 Pharmacogenetics, 21, 337 Pharmacokinetic, 20, 337 Pharmacologic, 27, 30, 42, 43, 65, 104, 129, 139, 276, 312, 337, 358 Pharmacotherapy, 154, 337 Phenobarbital, 244, 337 Phenotype, 19, 27, 31, 44, 222, 337 Phenylalanine, 159, 336, 337, 359 Phenylpropanolamine, 139, 338 Pheromones, 159, 338, 363 Phosphates, 176, 338 Phosphodiesterase, 184, 338 Phosphodiesterase Inhibitors, 184, 338 Phospholipases, 338, 351 Phospholipids, 166, 305, 318, 322, 338 Phosphorus, 247, 252, 285, 335, 338 Phosphorylates, 161, 189, 338 Phosphorylation, 61, 176, 338, 343 Photoperiod, 58, 206, 338 Physical Examination, 309, 338 Physiologic, 13, 14, 15, 27, 32, 35, 54, 62, 138, 273, 282, 306, 312, 326, 327, 338, 342, 346, 351 Physiology, 11, 32, 42, 43, 60, 88, 95, 107, 144, 148, 161, 190, 212, 219, 224, 302, 308, 338 Pigment, 282, 326, 338 Pilot study, 18, 20, 40, 63, 68, 69, 80, 128, 338 Pituitary Gland, 145, 151, 294, 338 Placenta, 3, 53, 90, 304, 307, 338, 341, 344, 360 Plant Growth Regulators, 162, 338 Plaque, 280, 339 Plasma cells, 277, 339 Plasma protein, 95, 273, 339, 351 Platelet Activation, 339, 351 Platelet Aggregation, 275, 331, 339 Platelets, 279, 331, 339 Platinum, 323, 339 Poisoning, 285, 296, 303, 319, 328, 329, 339 Polyarthritis, 228, 339 Polycystic, 31, 50, 51, 169, 315, 339 Polycystic Ovary Syndrome, 169, 315, 339 Polydipsia, 180, 339
Index 379
Polymorphic, 20, 297, 339 Polymorphism, 16, 52, 73, 107, 339 Polypeptide, 274, 290, 292, 306, 336, 339, 342, 343, 364 Polyposis, 291, 340 Polyuria, 180, 340 Population Control, 147, 177, 340 Portal System, 325, 340 Positive pressure ventilation, 45, 340 Posterior, 275, 281, 287, 289, 327, 334, 340, 349, 361 Postmenopausal, 5, 18, 22, 58, 65, 92, 304, 333, 340 Postmenopause, 65, 340 Postnatal, 30, 129, 340 Postoperative, 256, 340 Postprandial, 151, 205, 208, 340 Postprandial Blood Glucose, 151, 340 Postsynaptic, 340, 351, 356 Potassium, 172, 212, 215, 247, 252, 327, 340 Potentiating, 153, 340 Potentiation, 340, 351 Practice Guidelines, 85, 213, 239, 340 Precancerous, 288, 340 Precursor, 276, 279, 300, 301, 303, 331, 337, 340, 341, 359, 360, 361 Predisposition, 34, 151, 340 Prednisolone, 341 Prednisone, 228, 244, 253, 341 Pregnancy Outcome, 67, 90, 101, 113, 238, 341 Pregnancy Tests, 309, 341 Premenopausal, 5, 31, 149, 341 Premenstrual, 26, 132, 184, 207, 341 Premenstrual Syndrome, 132, 184, 207, 341 Prenatal, 53, 67, 72, 99, 136, 199, 201, 204, 214, 242, 243, 254, 301, 341 Prenatal Care, 204, 242, 254, 341 Pressoreceptors, 281, 341 Presynaptic, 341, 356 Primary Biliary Cirrhosis, 113, 341 Primary endpoint, 20, 58, 69, 341 Primary Prevention, 39, 69, 209, 341 Private Practice, 86, 341 Problem Solving, 21, 341 Prodrug, 190, 341 Progesterone, 3, 64, 206, 325, 341, 342, 354 Prognostic factor, 33, 342 Progression, 19, 45, 58, 185, 211, 276, 342 Progressive, 54, 95, 255, 287, 289, 297, 300, 304, 311, 328, 329, 333, 339, 342, 347
Projection, 296, 331, 332, 333, 342, 345 Prolactin, 64, 138, 342 Proline, 159, 291, 314, 342 Promoter, 59, 60, 107, 153, 166, 342 Prone, 34, 137, 214, 342 Prophase, 342, 356 Prophylaxis, 163, 342, 348, 361 Proportional, 101, 335, 342 Propranolol, 156, 181, 342 Prospective Studies, 45, 342 Prospective study, 4, 13, 22, 38, 72, 84, 138, 323, 342 Prostaglandin, 182, 276, 342 Prostaglandins A, 342, 343 Prostate, 35, 132, 186, 282, 332, 343, 359 Protease, 147, 291, 343 Protective Agents, 285, 343 Protein C, 25, 80, 150, 157, 161, 173, 211, 273, 274, 278, 281, 306, 322, 343, 353, 360 Protein Conformation, 274, 343 Protein Kinases, 176, 343 Protein S, 24, 135, 150, 157, 173, 194, 207, 283, 292, 308, 314, 343, 348 Protein-Tyrosine Kinase, 309, 343 Proteinuria, 330, 343 Proteoglycans, 281, 343 Proteolytic, 291, 306, 343 Protocol, 20, 35, 62, 102, 119, 343 Protons, 274, 314, 343, 345 Protozoa, 326, 327, 344, 353 Proximal, 299, 320, 341, 344, 350 Pruritus, 192, 193, 278, 315, 344 Psychiatric, 37, 38, 44, 72, 80, 85, 111, 112, 114, 210, 326, 344 Psychic, 321, 344, 350 Psychology, 12, 39, 45, 46, 55, 93, 95, 103, 217, 299, 344 Psychomotor, 296, 302, 330, 344 Psychopathology, 79, 344 Psychosis, 43, 104, 115, 278, 309, 344 Psychotropic, 32, 72, 113, 168, 169, 344 Puberty, 10, 14, 17, 47, 49, 216, 229, 344 Public Health, 14, 22, 25, 27, 37, 39, 41, 43, 52, 61, 62, 64, 69, 72, 77, 115, 118, 187, 199, 239, 344 Public Policy, 41, 237, 344 Publishing, 70, 248, 250, 344 Puerperium, 344 Pulmonary Artery, 283, 344, 345, 362 Pulmonary Edema, 48, 305, 320, 344 Pulmonary Embolism, 153, 183, 345 Pulmonary hypertension, 293, 345
380
Weight Gain
Pulse, 58, 327, 345 Pupil, 299, 328, 345 Purines, 345, 350 Purulent, 271, 345 Pustular, 271, 345 Pylorus, 300, 345 Pyramidal Cells, 297, 345 Pyramidal Tracts, 305, 345 Q Quality of Life, 12, 15, 20, 32, 44, 45, 62, 92, 112, 114, 138, 203, 212, 214, 217, 345 R Race, 6, 40, 45, 49, 61, 146, 156, 181, 184, 320, 327, 345 Radial Artery, 58, 345 Radiation, 173, 276, 307, 345, 364 Radioactive, 312, 314, 316, 319, 328, 345 Radiography, 309, 345 Radius, 345 Random Allocation, 345 Randomization, 65, 66, 345 Randomized clinical trial, 5, 16, 28, 48, 346 Ranitidine, 191, 346 Reality Testing, 344, 346 Receptors, Serotonin, 346, 350 Recombinant, 31, 105, 166, 180, 346, 361 Recombination, 160, 189, 346 Rectal, 281, 300, 346 Rectum, 278, 284, 291, 296, 298, 306, 308, 317, 321, 343, 346, 355 Recurrence, 33, 283, 325, 346 Red blood cells, 40, 304, 334, 346, 349 Reductase, 34, 346 Refer, 1, 218, 284, 291, 299, 307, 313, 323, 330, 344, 346, 350 Reflux, 90, 346 Refraction, 346, 353 Refractory, 21, 216, 346 Regimen, 6, 20, 138, 149, 154, 169, 185, 191, 213, 215, 217, 301, 336, 337, 346 Regurgitation, 246, 312, 346 Relapse, 32, 37, 68, 74, 95, 164, 218, 346 Relaxation Techniques, 202, 346 Reliability, 66, 346 Remission, 283, 324, 325, 346, 347 Renal failure, 215, 297, 347 Renin, 30, 276, 347 Renin-Angiotensin System, 30, 276, 347 Reproduction Techniques, 341, 347 Reproductive cells, 309, 347 Research Design, 42, 66, 347 Research Support, 39, 347
Respiration, 278, 285, 288, 327, 347, 348 Respirator, 340, 347 Respiratory distress syndrome, 94, 347 Respiratory failure, 45, 347 Respiratory Physiology, 347, 362 Respiratory System, 328, 347 Resting metabolic rate, 13, 47, 87, 138, 347 Restoration, 28, 167, 347, 348, 364 Resuscitation, 201, 348 Retina, 55, 289, 298, 321, 332, 333, 348, 363 Retinal, 298, 299, 332, 333, 348, 363 Retinoids, 348, 363 Retinopathy, 55, 185, 210, 298, 348 Retrospective, 6, 348 Retrospective study, 6, 348 Rheumatism, 348 Rheumatoid, 228, 244, 348 Rheumatoid arthritis, 228, 244, 348 Rhinitis, 288, 320, 348 Rhythm Method, 200, 348 Ribosome, 348, 359 Rickettsiae, 348 Rigidity, 335, 339, 348 Risperidone, 21, 32, 66, 104, 110, 179, 191, 348 Rubella, 244, 348 Rye, 209, 289, 303, 349 S Saline, 94, 349 Saliva, 14, 42, 349 Salivary, 224, 295, 298, 305, 349 Salivary glands, 224, 295, 298, 305, 349 Saponins, 349, 354 Sarcolemma, 161, 349 Satiation, 57, 349 Saturated fat, 198, 200, 349 Schizoid, 349, 364 Schizophrenia, 20, 32, 43, 66, 74, 79, 86, 100, 104, 106, 112, 278, 348, 349, 364 Schizotypal Personality Disorder, 297, 349, 364 Sclera, 289, 349 Sclerae, 333, 349 Sclerosis, 328, 349 Screening, 18, 23, 153, 201, 203, 290, 349, 360 Sebaceous, 34, 349, 350 Sebaceous gland, 34, 349, 350 Sebum, 271, 349, 350 Second Messenger Systems, 330, 350 Secretory, 180, 328, 350, 356 Sedative, 315, 316, 350
Index 381
Sedentary, 28, 42, 100, 151, 347, 350 Sediment, 350, 360 Segregation, 281, 346, 350 Seizures, 20, 169, 244, 297, 350 Self Care, 206, 255, 271, 350 Sella, 338, 350 Semen, 343, 350 Senile, 146, 183, 278, 333, 350 Sepsis, 94, 350 Septal, 322, 350 Septum, 145, 350, 363 Septum Pellucidum, 350 Serine, 159, 176, 350 Serotonin, 20, 65, 103, 107, 157, 184, 278, 290, 295, 306, 335, 337, 346, 348, 350, 351, 359 Sertraline, 20, 351 Serum Albumin, 219, 351 Sex Characteristics, 272, 276, 332, 344, 351, 357 Sexual Abstinence, 251, 351 Sharks, 300, 351 Sharpness, 351, 363 Shivering, 351, 357 Shock, 275, 351, 359 Sibutramine, 65, 156, 184, 351 Signal Transduction, 31, 318, 351 Signs and Symptoms, 164, 346, 347, 351 Simethicone, 190, 351 Skeletal, 17, 31, 60, 112, 151, 161, 276, 294, 315, 328, 329, 352 Skeleton, 271, 306, 320, 342, 352 Skull, 302, 330, 352, 357 Sleep apnea, 49, 95, 98, 178, 186, 205, 352 Small intestine, 168, 208, 224, 282, 287, 288, 289, 300, 301, 314, 316, 319, 320, 329, 352, 362 Smooth muscle, 161, 186, 274, 275, 284, 285, 314, 347, 352, 355 Snoring, 35, 49, 352 Social Environment, 345, 352 Social Support, 21, 38, 67, 222, 352 Sodium, 5, 50, 111, 169, 172, 179, 191, 200, 215, 245, 327, 329, 352, 355, 361 Sodium Channels, 352, 361 Soft tissue, 284, 352 Solid tumor, 300, 352 Solitary Nucleus, 280, 352 Soma, 345, 352 Somatic, 164, 166, 272, 322, 325, 327, 336, 352, 361 Somatic cells, 166, 325, 327, 352
Spastic, 320, 352 Specialist, 210, 258, 299, 353 Specificity, 150, 273, 279, 285, 353 Spectrin, 301, 353 Spectrum, 20, 58, 66, 203, 353 Sperm, 276, 289, 347, 353 Spermatogenesis, 81, 353 Spermatozoa, 350, 353 Sphincter, 211, 212, 353 Spices, 245, 353 Spina bifida, 330, 353 Spinal cord, 186, 280, 284, 287, 288, 289, 303, 326, 330, 345, 353, 355 Spirometry, 49, 353 Spleen, 243, 244, 295, 323, 324, 353 Spontaneous Abortion, 214, 341, 353 Sporadic, 18, 353 Spores, 171, 318, 353 Sprue, 208, 353 Stabilization, 42, 353 Stabilizer, 50, 51, 169, 353 Staff Development, 206, 354 Standard therapy, 68, 354 Stapes, 315, 354 Steatorrhea, 209, 354 Steatosis, 305, 354 Sterile, 334, 354 Sterility, 81, 317, 354 Sterilization, 200, 354 Steroid, 4, 14, 135, 179, 217, 228, 254, 282, 294, 332, 349, 354 Steroid therapy, 217, 354 Stillbirth, 101, 104, 201, 341, 354 Stimulant, 284, 294, 295, 314, 354, 361 Stimulus, 293, 300, 301, 319, 335, 354, 357 Stomach Ulcer, 253, 354 Stool, 317, 320, 321, 354 Streptococcus, 201, 354 Stroke, 8, 30, 61, 141, 153, 178, 182, 183, 224, 236, 253, 286, 354 Stroke Volume, 286, 354 Stromal, 64, 182, 354 Stromal Cells, 182, 354 Stupor, 321, 329, 355 Subacute, 317, 355 Subclinical, 58, 317, 350, 355 Subcutaneous, 89, 152, 204, 211, 216, 272, 301, 322, 335, 355, 363 Subspecies, 353, 355 Substance P, 326, 350, 355 Substrate, 44, 61, 148, 160, 189, 190, 286, 303, 355
382
Weight Gain
Sulfates, 176, 355 Sulfur, 326, 355 Sulfuric acid, 275, 355 Superstitions, 201, 355 Supplementation, 40, 64, 83, 88, 127, 128, 144, 188, 200, 355 Support group, 248, 249, 256, 355 Suppositories, 308, 355 Suppression, 26, 32, 81, 145, 170, 186, 294, 355 Surfactant, 147, 355 Survival Rate, 333, 355 Sweat, 337, 355 Sympathetic Nervous System, 15, 276, 280, 355, 356 Sympathomimetic, 300, 303, 331, 338, 356 Symphysis, 111, 343, 356 Symptomatic, 50, 84, 192, 356 Synapses, 330, 332, 356 Synapsis, 356 Synaptic, 166, 331, 351, 356 Synaptic Transmission, 166, 331, 356 Synergistic, 43, 206, 342, 356 Systemic lupus erythematosus, 244, 254, 255, 323, 356 Systolic, 7, 169, 315, 325, 356 Systolic blood pressure, 7, 356 Systolic pressure, 325, 356 T Tachycardia, 193, 356 Tacrolimus, 244, 356 Tardive, 278, 356 Tellurium, 192, 357 Temporal, 58, 275, 305, 313, 357 Temporal Lobe, 275, 357 Testis, 304, 332, 357 Testosterone, 14, 31, 62, 81, 84, 102, 271, 346, 357 Tetany, 335, 357 Therapeutics, 15, 79, 209, 232, 357 Thermogenesis, 31, 357 Thermoregulation, 338, 357 Thigh, 24, 306, 357 Third Ventricle, 279, 315, 325, 357 Thoracic, 281, 357, 364 Thorax, 76, 271, 323, 357, 361 Threonine, 159, 176, 350, 357 Threshold, 315, 357 Thrombin, 306, 339, 343, 357 Thromboembolism, 318, 357 Thrombomodulin, 343, 357 Thrombosis, 210, 343, 354, 357
Thyroid, 49, 138, 151, 315, 334, 335, 357, 358, 359 Thyroid Gland, 315, 334, 335, 358 Thyroid Hormones, 138, 358, 359 Thyroxine, 273, 338, 358 Tin, 218, 336, 339, 358 Tobacco Use Cessation, 209, 358 Tolerance, 66, 160, 189, 271, 310, 358 Tomography, 58, 283, 358 Tonometry, 58, 358 Tooth Preparation, 272, 358 Topical, 34, 192, 193, 304, 334, 358 Toxic, iv, 34, 282, 289, 296, 311, 316, 330, 331, 349, 358 Toxicity, 20, 125, 127, 286, 300, 331, 358, 364 Toxicology, 119, 126, 238, 358 Toxins, 244, 277, 285, 302, 317, 328, 358 Trace element, 163, 289, 358 Trachea, 357, 358 Transcription Factors, 64, 176, 358 Transcutaneous, 318, 358 Transdermal, 78, 210, 358 Transduction, 17, 31, 351, 358 Transfection, 283, 359 Transfusion, 313, 359 Translation, 59, 359 Translocate, 176, 359 Transmitter, 271, 280, 300, 319, 325, 331, 356, 359 Transplantation, 4, 6, 85, 86, 211, 218, 243, 244, 289, 302, 316, 324, 359 Trauma, 190, 297, 312, 329, 359 Trees, 163, 359 Tricuspid Atresia, 293, 359 Tricyclic, 146, 179, 183, 199, 316, 359 Trifluoperazine, 179, 359 Trigger zone, 278, 359 Triglyceride, 7, 17, 58, 315, 359 Truncal, 14, 359 Tryptophan, 159, 291, 350, 359 Tuberculosis, 105, 242, 292, 323, 359 Tumor marker, 282, 359 Tyrosine, 158, 160, 189, 300, 343, 359 U Ulcer, 300, 336, 354, 359 Ulcerative colitis, 216, 217, 317, 360 Ultrasonography, 44, 200, 309, 360 Umbilical Arteries, 360 Umbilical Cord, 201, 360 Unconscious, 296, 316, 360 Urea, 92, 333, 355, 360
Index 383
Uremia, 320, 347, 360 Ureters, 320, 360, 362 Urethra, 343, 360 Uric, 110, 345, 360 Urinalysis, 255, 360 Urinary, 25, 31, 104, 149, 211, 212, 248, 267, 281, 285, 317, 340, 360 Urinary tract, 212, 248, 281, 360 Urinary tract infection, 248, 281, 360 Ursodeoxycholic Acid, 113, 360 Urticaria, 193, 275, 288, 315, 360 Uterine Contraction, 334, 360 Uterus, 149, 275, 288, 294, 296, 302, 307, 326, 333, 341, 360, 361 Uvula, 352, 361 V Vaccination, 172, 361 Vaccine, 272, 274, 343, 361 Vagal, 43, 51, 54, 361 Vagina, 288, 326, 361 Vaginal, 23, 53, 112, 212, 251, 361 Vaginal Discharge, 212, 361 Vagotomy, 154, 361 Vagus Nerve, 352, 359, 361 Valine, 158, 361 Valproic Acid, 191, 361 Valves, 153, 281, 361 Varices, 281, 361 Vascular Resistance, 281, 361 Vasoconstriction, 30, 127, 224, 303, 361 Vasodilation, 276, 361 Vasodilator, 284, 300, 314, 361 Vasomotor, 149, 304, 361 VE, 118, 361 Vector, 31, 358, 361 Vein, 319, 360, 361 Venlafaxine, 146, 183, 361 Venous, 210, 219, 283, 343, 359, 362 Ventilation, 45, 102, 347, 362 Ventral, 145, 279, 315, 362 Ventricle, 275, 280, 293, 313, 344, 345, 356, 359, 362 Ventricular, 293, 359, 362 Venules, 283, 285, 362 Vertebrae, 353, 362 Vesicoureteral, 90, 362
Vestibulocochlear Nerve, 315, 362 Vestibulocochlear Nerve Diseases, 315, 362 Veterinarians, 151, 362 Veterinary Medicine, 237, 362 Villi, 208, 224, 362 Villous, 208, 287, 289, 362 Viral, 30, 163, 165, 172, 201, 358, 362 Viral vector, 30, 362 Virilism, 315, 362 Virulence, 280, 358, 362 Virulent, 50, 362 Virus, 31, 165, 172, 223, 243, 251, 281, 303, 309, 313, 319, 339, 348, 358, 362, 363 Virus Diseases, 172, 363 Viscera, 352, 363 Visceral, 28, 58, 280, 322, 337, 361, 363 Visceral Afferents, 280, 361, 363 Visceral fat, 29, 363 Viscosity, 59, 363 Visual Acuity, 55, 363 Vitamin A, 157, 199, 200, 214, 243, 318, 363 Vitreous Body, 348, 363 Vitreous Hemorrhage, 298, 363 Vitro, 30, 363 Vivo, 59, 363 Vomeronasal Organ, 332, 363 W Waist circumference, 58, 69, 363 Wakefulness, 45, 296, 363 White blood cell, 253, 277, 321, 324, 328, 339, 363 Windpipe, 357, 364 Withdrawal, 38, 42, 65, 70, 78, 79, 93, 103, 164, 166, 167, 208, 297, 364 Womb, 360, 364 Wound Healing, 159, 364 X Xenograft, 276, 364 X-ray, 23, 138, 283, 353, 364 Y Yeasts, 307, 337, 364 Z Zearalenone, 170, 364 Zygote, 292, 364 Zymogen, 343, 364
384
Weight Gain
