A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R EFERENCES
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 Ó2003 by ICON Group International, Inc. Copyright Ó2003 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., 1960Anemia: 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: 0-597-83551-9 1. Anemia-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 anemia. 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 ANEMIA .................................................................................................... 3 Overview ....................................................................................................................................... 3 The Combined Health Information Database ................................................................................ 3 Federally Funded Research on Anemia ....................................................................................... 14 E-Journals: PubMed Central ....................................................................................................... 54 The National Library of Medicine: PubMed................................................................................ 62 CHAPTER 2. NUTRITION AND ANEMIA ........................................................................................ 289 Overview ................................................................................................................................... 289 Finding Nutrition Studies on Anemia ...................................................................................... 289 Federal Resources on Nutrition................................................................................................. 294 Additional Web Resources......................................................................................................... 295 CHAPTER 3. ALTERNATIVE MEDICINE AND ANEMIA .................................................................. 301 Overview ................................................................................................................................... 301 The Combined Health Information Database ............................................................................ 301 National Center for Complementary and Alternative Medicine ............................................... 302 Additional Web Resources......................................................................................................... 309 General References..................................................................................................................... 320 CHAPTER 4. DISSERTATIONS ON ANEMIA.................................................................................... 321 Overview ................................................................................................................................... 321 Dissertations on Anemia ........................................................................................................... 321 Keeping Current ........................................................................................................................ 324 CHAPTER 5. CLINICAL TRIALS AND ANEMIA .............................................................................. 325 Overview ................................................................................................................................... 325 Recent Trials on Anemia ........................................................................................................... 325 Keeping Current on Clinical Trials ........................................................................................... 351 CHAPTER 6. PATENTS ON ANEMIA .............................................................................................. 353 Overview ................................................................................................................................... 353 Patents on Anemia .................................................................................................................... 353 Patent Applications on Anemia................................................................................................. 387 Keeping Current ........................................................................................................................ 395 CHAPTER 7. BOOKS ON ANEMIA .................................................................................................. 397 Overview ................................................................................................................................... 397 Book Summaries: Federal Agencies ........................................................................................... 397 Book Summaries: Online Booksellers ........................................................................................ 398 The National Library of Medicine Book Index........................................................................... 404 Chapters on Anemia .................................................................................................................. 405 Directories ................................................................................................................................. 407 CHAPTER 8. MULTIMEDIA ON ANEMIA ....................................................................................... 409 Overview ................................................................................................................................... 409 Video Recordings....................................................................................................................... 409 Audio Recordings ...................................................................................................................... 410 Bibliography: Multimedia on Anemia ....................................................................................... 410 CHAPTER 9. PERIODICALS AND NEWS ON ANEMIA .................................................................... 413 Overview ................................................................................................................................... 413 News Services and Press Releases ............................................................................................. 413 Newsletters on Anemia.............................................................................................................. 417 Newsletter Articles .................................................................................................................... 418 Academic Periodicals covering Anemia..................................................................................... 419 APPENDIX A. PHYSICIAN RESOURCES.......................................................................................... 423 Overview ................................................................................................................................... 423
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Contents NIH Guidelines ..........................................................................................................................423 NIH Databases ...........................................................................................................................425 Other Commercial Databases .....................................................................................................428 The Genome Project and Anemia ...............................................................................................428 APPENDIX B. PATIENT RESOURCES ...............................................................................................435 Overview ....................................................................................................................................435 Patient Guideline Sources ..........................................................................................................435 Associations and Anemia ...........................................................................................................450 Finding Associations ..................................................................................................................453 APPENDIX C. RESEARCHING MEDICATIONS .................................................................................455 Overview ....................................................................................................................................455 U.S. Pharmacopeia .....................................................................................................................455 Commercial Databases ...............................................................................................................458 Researching Orphan Drugs .......................................................................................................458 APPENDIX D. FINDING MEDICAL LIBRARIES ................................................................................461 Overview ....................................................................................................................................461 Preparation .................................................................................................................................461 Finding a Local Medical Library ................................................................................................461 Medical Libraries in the U.S. and Canada .................................................................................461
ONLINE GLOSSARIES ................................................................................................................467 Online Dictionary Directories ...................................................................................................470 ANEMIA DICTIONARY ..............................................................................................................471 INDEX...............................................................................................................................................577
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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 anemia 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 anemia, 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 anemia, 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 anemia. 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 anemia, 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 anemia. 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 ANEMIA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on anemia.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and anemia, 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 “anemia” (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: ·
Diagnosis of Iron Deficiency in Patients With Rheumatoid Arthritis and Anemia: An Algorithm Using Simple Laboratory Measures Source: Journal of Rheumatology. 23(2):237-240; 1996. Summary: This journal article for health professionals describes a study that sought to develop an easily recalled algorithm that identified iron deficiency in anemic patients with rheumatoid arthritis (RA) using readily available laboratory tests. Anemia of chronic disorders ( ACD ) and iron deficiency are common features in RA; however, they may be difficult to distinguish without marrow sampling, which is invasive, time consuming, and expensive. Forty-five anemic patients with RA underwent marrow sampling in addition to a complete blood count and serum ferritin and iron saturation measurements. Results indicate that 47 percent of the patients had iron deficiency. These patients had significantly lower mean corpuscular volume ( MCV ), serum ferritin , and
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iron saturation. A three-step algorithm was developed using these laboratory variables to identify iron deficiency. This algorithm correctly classified 94 percent of the patients with iron deficiency and 85 percent with ACD. Results demonstrate that iron deficiency may be reliably identified by measuring serum ferritin , MCV , and iron saturation in many patients with RA, thereby avoiding the trauma and expense of marrow sampling. 24 references, 2 figures, and 1 table. (AA-M). ·
Anemia of Gastrointestinal Origin in the Elderly Source: Practical Gastroenterology. 26(9): 22-24, 29-31, 35-36. September 2002. Contact: Available from Shugar Publishing. 12 Moniebogue Lane, Westhampton Beach, NY 11978. (516) 288-4404. Fax (516) 288-4435. Summary: Physiological alterations in the gastrointestinal (GI) system in older individuals may predispose to the development of anemia. In more than half the cases an underlying cause can be established. This article reviews the pathophysiology, diagnosis and treatment of anemia of GI origin in the elderly. The increased prevalence of gastric hypochlorhydria (reduced amounts of hydrochloric acid in the stomach's gastric juice, thus reduced digestion) in the elderly as a result of disease or medications affects bioavailability of several micronutrients predominantly iron, folate, and cobalamin. Though GI blood loss is by far the most common cause of iron deficiency anemia, poor dietary intake, coupled with impaired absorption contributes to deficiency and anemia. Patient evaluation identifies an etiological basis (cause) for anemia and a basis for treatment. For example, folate fortification of food has been implemented to minimize nutritional folate deficiency and prevent harmful consequences. 7 tables. 40 references.
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Diagnosis and Treatment of Anemia in Inflammatory Bowel Disease Source: Inflammatory Bowel Diseases. 3(3): 204-216. Fall 1997. Contact: Available from Raven Press, Ltd. 1185 Avenue of the Americas, New York, NY 10036. (800) 777-2836 or (212) 930-9500. Fax (212) 869-3495. Summary: This article reviews the diagnosis and treatment of anemia in inflammatory bowel disease (IBD), a problem caused in more than 80 percent of the cases by iron or vitamin deficiency. The reported incidence of anemia in IBD varies between 30 and 70 percent and fluctuates with disease activity or with complicating factors such as gastrointestinal bleeding. The exact mechanisms of the anemia are unknown. Laboratory test results are often unclear because of the immunologic activity of the inflammatory disorder itself. Recent studies have shown that the proinflammatory cytokines produced in IBD can suppress erythropoiesis by the inhibition of erythropoietin secretion and action. In therapeutic trials, it has been shown that coadministration of recombinant erythropoietin can substantially improve therapy in those with refractory anemia in IBD. Significant drawbacks are the need for repetitive subcutaneous injections of erythropoietin as well as the high costs of the medication. Subgroups of patients in need of erythropoietin therapy need to be identified as do those most likely to improve with conventional substitution therapy (iron and vitamin supplementation). The authors present patient care algorithms to define the correct flow of diagnostic measures and therapeutic interventions in patients with IBD and anemia. 5 figures. 3 tables. 70 references. (AA-M).
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Rational Approach to the Anemia Workup Source: Patient Care. 30(7): 158-160, 165-168, 171, 174-175, 178-179. April 15, 1996. Contact: Available from Medical Economics. 5 Paragon Drive, Montvale, NJ 07645. (800) 432-4570. Fax (201) 573-4956. Summary: In this article, the author provides a rational approach to the workup for a patient with anemia. Topics include iron deficiency anemia; the anemia of chronic disease; distinguishing among anemias; anemia risk factors; screening; symptoms of anemia; the anemia workup; and hypoproliferative anemia. The author provides practical tips and strategies throughout for working with older patients. The author includes a patient care flowchart for the diagnostic process. 2 figures. 4 tables. 11 references.
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Anemia: A Risk Factor for Diabetic Retinopathy? Source: Practical Diabetology. 20(4): 32-34. December 2001. Contact: Available from R.A. Rapaport Publishing, Inc. 150 West 22nd Street, New York, NY 10011. (212) 989-0200 or (773) 777-6801. Summary: Diabetic retinopathy (eye disease associated with diabetes) continues to be a major problem in the United States. This article reviews the risk factors for diabetic retinopathy and then presents a case report that supports the idea that anemia needs to be added to the list of risk factors. Retinal hypoxia (reduced amounts of oxygen being delivered to the retina) has long been associated with the development of diabetic retinopathy; anemia is one of the conditions that can contribute to retinal hypoxia. The authors discuss the clinical features, mechanism of injury from anemia, and relationship between retinopathy and hemoglobin level. The authors conclude by suggesting laboratory evaluation for anemia in patients with diabetes who may have an increased risk of developing anemia. This group includes pregnant women, women with menorrhagia (loss of large amounts of blood with their menstruation), postoperative patients, patients with renal (kidney) failure, patients with neoplastic processes (including cancer), patients with gastrointestinal bleeding, and patients with poor blood glucose control. Normalization of hemoglobin levels may stabilize progressive retinopathy. 9 references.
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Just the FAQs: Frequently Asked Questions About Iron and Anemia in Patients with Chronic Kidney Disease Source: American Journal of Kidney Diseases. 39(2): 426-432. February 2002. Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Anemia in patients with chronic kidney disease is caused by insufficient production of erythropoietin (epoetin). Iron deficiency, chronic inflammation, hyperparathyroidism, and blood loss each may contribute to anemia in these patients. This article answers a series of frequently asked questions, many of which concern the patient who fails to respond to usual doses of epoetin. The authors provide the answers they have given at seminars held during meetings of the National Kidney Foundation (April 2000) and the American Society of Nephrology (October 2000). Questions and issues discussed include the best measure of iron status (hemoglobin tests), handling patients with low or normal transferrin saturation and high serum ferritin, diagnosing infection, patient selection for iron administration, administration and dosage of serum
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ferritin, the addition of vitamin C to drug regimens, maintenance iron protocols versus periodic iron therapy, maintenance iron therapy administered through dialysis facilities, total dose iron infusion, how to compare adverse reaction rates, and the use of iron and epoetin therapy in patients with chronic kidney disease who are not on dialysis. 3 figures. 33 references. ·
Trends in Anemia Management Among US Hemodialysis Patients Source: JASN. Journal of the American Society of Nephrology. 13(5): 1288-1295. May 2002. Contact: Available from Lippincott Williams and Wilkins. 12107 Insurance Way, Hagerstown, MD 21740. (800) 638-6423. Summary: This article reports on a study undertaken to describe the relationship between hematocrit (Hct, a measure of oxygen-carrying red blood cells) and changes in the prescribed dose of erythropoietin (EPO) as well as selected patient and process care measures across annual national samples of hemodialysis patients from 1994 to 1998. The study used statistics for each of these years, and patient demographic and clinical information was collected from October to December for each year. Surrogates of iron stores and patterns of iron and EPO administration were profiled from 1996 to 1998. Mean Hct and EPO dose increased each year. Increasing Hct was positively associated with male gender, more years on dialysis, older age, higher urea reduction ratio (URR) and transferrin saturation, prescription of intravenous iron, and lower ferritin and EPO dose. Male gender, older age, diabetes, higher Hct, and increasing weight, URR, and transferrin saturation were associated with lower EPO doses. Conversely, intravenous EPO and iron were associated with higher prescribed EPO doses. Although increasing Hct is associated with decreasing EPO dose at the patient level, the increase in Hct seen across years among the cohorts of hemodialysis patients in the United States has been associated with increasing doses of EPO at the population level. The authors conclude that to achieve still higher hematocrit values, as has been advocated by some clinicians, disproportionately greater EPO dose is likely, unless alternative routes of administration are used, or different patterns of iron administration are demonstrated to be safe, effective, and can be implemented. 3 figures. 5 tables. 56 references.
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Anemia in CKD: Prevalence, Diagnosis, and Treatment: Case Study of the Anemic Patient Source: Nephrology Nursing Journal. 29(4): 371-374. August 2002. 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: This article reports on a point-in-time observational study that was conducted in over 1,000 nephrology (kidney specialty) offices between November 1999 and December 2000 to determine the prevalence of anemia in patients with chronic kidney disease (CKD). Trends in hemoglobin (Hb) and serum creatinine (SCr, a measure of kidney function) levels were assessed among 4,831 evaluable patients to determine the relationship between renal (kidney) function and anemia. Results demonstrated that anemia is common in patients with CKD, with progressive increases in prevalence and severity as renal function deteriorates. Overall, 26.3 percent of these patients had Hb levels below 10 grams per deciliter, 46.7 percent had Hb levels below 11 grams per deciliter, and 63.9 percent had Hb levels below 12 grams per deciliter. Despite the high percentage of patients with anemia, only 31.3 percent were being treated for this
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condition. These data suggest that anemia is prevalent and undertreated in patients with CKD. The authors conclude that nephrology nurses can be influential in providing proactive management of anemia throughout the spectrum of CKD to improve anemiarelated outcomes. 2 figures. 14 references. ·
Meta-Analysis of Subcutaneous Versus Intravenous Epoetin in Maintenance Treatment of Anemia in Hemodialysis Patients Source: American Journal of Kidney Diseases. 40(3): 439-446. September 2002. Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Clinical and pharmacokinetics studies have shown that target hemoglobin or hematocrit levels can be maintained using a reduced recombinant human erythropoietin (epoetin) dosage by switching from intravenous (IV) to subcutaneous (SC) administration. This article reports on a meta-analysis of comparative studies of epoetin administered IV versus SC undertaken to assess the relative costs of these administration routes. Twenty-seven prospective clinical studies involving 916 patients were included in the analysis. Results indicate that the cost of epoetin is reduced substantially when administered SC in comparison to IV. Recommendations of current US and European guidelines, which encourage the use of SC administration, not only have a sound rationale in terms of efficacy and safety, but also have a sound economic basis. 2 figures. 3 tables. 53 references.
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Health Care Resource Utilization and the Impact of Anemia Management in Patients with Chronic Kidney Disease Source: American Journal of Kidney Diseases. 40(3): 539-548. September 2002. Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: Limited information exists on resource utilization patterns and overall patient management of chronic kidney disease (CKD) before the initiation of dialysis therapy. This article reports on a retrospective claims analysis from January 1997 to December 1999 that was conducted using a managed care database on 1,936 incident dialysis patients, examining the 12 months preceding dialysis initiation to evaluate whether managed are patients with CKD are receiving expected interventions and appropriate management of their disease. Despite high overall resource use, treatments for preparation for dialysis therapy, appropriate tests, and nutritional supplements were administered infrequently. Comorbid conditions, such as anemia and diabetes, were appropriate addressed with erythropoietin and ACE inhibitors in only a minority of cases. In preparation for dialysis therapy, only 20.8 percent underwent a vascular access procedure. Although patients consumed significant amounts of resources during the 12 months before dialysis initiation, many were not using expected resources for the appropriate management of CKD. The authors conclude that a number of opportunities exist to improve predialysis care through better management of these conditions. 2 figures. 5 tables. 33 references.
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Effects of Hemodialysis Dose on Anemia, Hypertension, and Nutrition Source: Renal Failure. 24(5): 615-621. 2002. Contact: Available from Marcel Dekker Journals. P.O. Box 5017, Monticello, NY 127015176. (212) 696-9000.
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Summary: There is good evidence that by improving dialysis adequacy, the morbidity (related illness) and mortality (death) of hemodialysis (HD) patients decrease. Dialysis adequacy has also been related to the better control of arterial blood pressure (BP), anemia, and improvement of patients' nutritional status. This article reports on a selfcontrol study of 34 patients on HD (23 males, 11 females), aged 52.6 years (plus or minus 15.5 years), HD duration 55.9 months (plus or minus 61.2 months), referring to the effect of increasing delivered dialysis dose, over a 2-year period, on their clinical and laboratory parameters. Delivered HD dose increased, statistical significance, the following: urea reduction ratio (URR), Kt per V, and Hb (hemoglobin); no difference was noticed in weekly EPO (erythropoietin) dose. Both systolic and diastolic BP decreased significantly. The authors conclude that increasing dialysis dose results in both clinical and laboratory improvement regarding hypertension, nutritional status, and control of HD patients' anemia. 2 tables. 25 references. ·
Anemia Treatment in Chronic Renal Insufficiency Source: Seminars in Nephrology. 22(6): 474-478. November 2002. Contact: Available from W.B. Saunders Company. Periodicals Department. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Summary: Anemia is a common complication of chronic renal insufficiency (CRI), one that leads to a reduced quality of life and an increased burden on the heart. In recent years, it has been shown that anemia is underrecognized and undertreated in these patients. The benefits of recombinant human erythropoietin (rHuEPO) treatment in this patient population have been well shown. The major side effect, hypertension (high blood pressure) is particularly important in CRI, requiring careful monitoring. In this review article, the author weighs the benefits of anemia therapy against the risks and costs. On balance, the author concludes that anemia treatment meets a basic and important health need in these patients. The author provides an abbreviated patient care algorithm for anemia monitoring in CRI. 1 figure. 44
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Anemia of Chronic Renal Insufficiency: Defining the Scope of the Challenge. Case Study of the Anemic Patient Source: Nephrology Nursing Journal. 28(1): 51-54. February 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: Chronic renal insufficiency (CRI) is a significant, often silent, disorder that affects more than 10 million patients in the United States. Anemia often develops early in the course of CRI, greatly increasing the risk of morbidity and mortality. Despite this risk, anemia of CRI is underrecognized and undertreated. This article helps nephrology nurses become aware of the laboratory indices and anemia management principles to help improve outcomes in patients with CRI. Creatinine clearance is an indirect measure of kidney function used by many clinicians to confirm the diagnosis of CRI. Even though creatinine levels can signal significant kidney impairment, the systemic manifestations of CRI are typically minimal, and most patients are asymptomatic. The author stresses that serum creatinine levels are not the best measure of early CRI; preferred tests include glomerular filtration rate (GFR), which provides the best overall index of kidney function. Anemia associated with CRI can have debilitating effects that compromise quality of life and are associated with significant morbidity and mortality. The article includes a case study of a 69 year old man with diabetes. The author
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concludes that anemia is often underrecognized and undertreated in the CRI population and that nurses can play an important role in rectifying this situation. 3 figures. 1 table. 20 references. ·
Management of Anemia in Chronic Kidney Disease (Predialysis) Patients: Nephrology Nursing Implications Source: Nephrology Nursing Journal. 28(3): 341-345. June 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: Anemia (shortage of red blood cells) is a frequent problem in patients with chronic kidney disease (CKD) who are not yet receiving dialysis and can lead to major health complications if left untreated. This article reviews the nephrology (kidney) nursing implications of managing patients with anemia in predialysis patients with CKD. Anemia can be caused by blood loss, decreased red blood cell (RBC) lifespan, uremia byproducts that inhibit erythropoiesis (the making of RBCs), decreased levels of erythropoietin (the hormone that helps the body gain access to iron), and deficiences in essential nutrients such as folate or iron. The successful management of these patients entails repletion of iron stores, often through use of intravenous iron, particularly in patients receiving erythropoietin therapy. Successful treatment of anemia is associated with reduced morbidity (complications and associated conditions) and mortality, and significant improvements in cardiovascular and brain function as well as in quality of life. To encourage patient compliance with anemia management protocols, the nephrology nurse can play a key role in patient education in reducing barriers to proper management and in raising the awareness of the benefits of treating this condition. A patient care algorithm is provided. 3 figures. 28 references.
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Anemia: An Early Complication of Chronic Renal Insufficiency Source: American Journal of Kidney Diseases. 38(4): 803-812. October 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. Summary: The strong association between anemia (low levels of oxygen carrying cells, hemoglobin, in the blood) and cardiovascular complications among patients with end stage renal disease (ESRD) suggests that anemia during chronic renal (kidney) insufficiency (CRI) may also have important consequences. This article reports on a retrospective cohort study undertaken to identify factors associated with severe anemia (hematocrit or Hct less than 30 percent) and to examine anemia management practices in CRI. The CRI cohort was composed of 604 adult patients with elevated serum creatinine levels (a blood test that measures kidney function). There was a direct correlation between predicted glomerular filtration rate (GFR) and hematocrit in CRI; 45 percent of patients with serum creatinine levels of 2 milligrams per deciliter or less had an Hct less than 36 percent, and 8 percent had an Hct less than 30 percent. During the course of the study, mean Hct decreased from 35.1 percent (plus or minus 5.6 percent) to 31.8 percent (plus or minus 5.6 percent). Iron studies were obtained in only 19 percent of patients, and among these, the prevalence of iron deficiency was 53 percent. Only 30 percent of patients were administered recombinant human erythropoietin (rHuEPO), and 26 percent of patients were administered iron. Multivariate analyses showed that diabetes as the cause of renal disease, greater serum creatinine level, and having a single nephrology (kidney specialist) visit were associated with greater odds for rHuEPO use.
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These results show that anemia begins early in the course of CRI, and present management of anemia is suboptimal, even among patients under the care of nephrologists. The authors also call for educational programs to optimize anemia management among patients with CRI. 3 figures. 5 tables. 32 references. ·
Vascular Effects of Erythropoietin and Anemia Correction Source: Seminars in Nephrology. 20(4): 356-363. July 2000. Contact: Available from W.B. Saunders Company. Periodicals Department. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Summary: Since its introduction for clinical use a decade ago, recombinant human erythropoietin (rHuEPO) has revolutionized the management of the anemia of end stage renal disease (ESRD). Soon after its release, it became evident that the biological targets of rHuEPO were not limited to the erythroid progenitor cells. Instead, numerous clinical and laboratory studies have shown the modulatory action of rHuEPO on a wide array of cell types and organ systems. This article provides an overview of the modulatory actions of rHuEPO on the production and action of vasoregulatory factors and its direct and indirect effects on vascular function and structure. Chronic rHuEPO administration can result in a hematocrit (red blood cell) independent rise in arterial blood pressure in humans and in experimental animals with CRF (chronic renal failure). This is associated with and, in part, mediated by up regulation of the tissue renin angiotensin system, increased ET 1 production, enhanced generation of vasoconstrictive and depressed production of vasodilatory prostaglandins, elevation of cytosolic and induction of NO resistance. In addition, in vitro studies point to stimulation of vascular cell growth by rHuEPO. Thus, rHuEPO exerts a broad modulatory action on various vasoregulatory factors in a manner favoring a rise in arterial blood pressure. 59 references.
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Impact of Anemia Correction on Cardiovascular Disease in End-Stage Renal Disease Source: Seminars in Nephrology. 20(4): 350-355. July 2000. Contact: Available from W.B. Saunders Company. Periodicals Department. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Summary: Cardiovascular disease (CVD) is a major cause of mortality and morbidity in patients with end stage renal disease (ESRD). This article explores the impact of anemia correction on CVD in patients with ESRD. Anemia, a result of erythropoietin deficiency, is associated with increased all cause and cardiovascular mortality in this population, and predisposes patients to the development of symptomatic heart disease. Anemia is also associated with the development and progression of left ventricular echocardiographic disorders, which strongly predict cardiac failure and death. Left ventricular dilatation with compensatory hypertrophy, the major pattern of echocardiographic disease progression in hemodialysis patients, is a particularly strong predictor of late mortality. Partial correction of anemia with recombinant human erythropoietin likely reduces left ventricular mass and volume. Complete correction of anemia may prevent progressive left ventricular dilatation in patients with normal left ventricular volumes. A recent trial, however, reports excess mortality and vascular access loss in patients with preexisting symptomatic heart disease when anemia was completely corrected. Consequently, hematocrit (red blood cells) target ranges above 32 to 36 percent cannot be recommended in this population. Despite improvements seen in echocardiographic disease in patients without symptomatic heart disease, it is not yet possible to conclude that potential benefits derived from a normalized hematocrit will
Studies 11
outweigh potential risks in this subgroup of dialysis patients. 1 figure. 5 tables. 34 references. ·
Current Concepts of Anemia Management in Chronic Renal Failure: Impact of NKFDOQI Source: Seminars in Nephrology. 20(4): 320-329. July 2000. Contact: Available from W.B. Saunders Company. Periodicals Department. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Summary: Since the introduction of recombinant human erythropoietin (rHuEPO) into clinical nephrology practice 10 years ago, there has been a slow increase in hemoglobin (Hgb) levels. However, most patients with the anemia of chronic renal (kidney) failure (CRF) are still moderately anemic and have not achieved the target Hgb (11 to 12 grams per dL) recommended by the National Kidney Foundation Dialysis Outcomes Quality Initiative (NKF DOQI) anemia guidelines. This article reviews current concepts for anemia management in patients with CRF. The author notes that functional iron deficiency, insufficient rHuEPO doses, and comorbid factors such as inflammation or infection have been the major reasons for not achieving this target. By optimizing iron stores with regular infusions of intravenous iron in the hemodialysis patient (who has significant blood iron losses related to the hemodialysis procedure) and giving adequate amounts of rHuEPO, preferably subcutaneously instead of intravenously, the NKF DOQI recommended target Hgb can be achieved in the majority of patients so treated. The author comments that the role of 'underdialysis' (dialysis inadequacy) as a cause of less than optimal responsiveness to rHuEPO remains controversial. Other unresolved issues include the role of ACE inhibitors and carnitine in the management of patients using rHuEPO. Periodic monitoring of Hgb (e.g., every 2 to 4 weeks) and of iron parameters (e.g., every 3 months) is essential to optimize anemia management. 2 figures. 2 tables. 47 references.
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Anemia Management in Patients with Chronic Renal Insufficiency Source: American Journal of Kidney Diseases. 36(6, Supplement 3): S39-S51. December 2000. Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452 or (407) 345-4000. Summary: The introduction of recombinant human erythropoietin (rHuEPO) more than a decade ago provided the first effective treatment for the anemia associated with chronic renal (kidney) insufficiency (CRI). Despite evidence of the positive impact of rHuEPO, the anemia of CRI remains highly prevalent, underrecognized, and undertreated. This article reviews the rationale for treatment of anemia, current management practices, proposed treatment strategies, and the economic implications of improved anemia treatment. The benefits of correction of anemia include significant improvements in health related quality of life, overall well being, energy level, work capacity, aerobic capacity, cognitive function, sexual function, and immune function; a decrease in the requirement for blood transfusions; and evidence of reduction in cardiovascular complications. The current practice guidelines recommend that patients with CRI and anemia should be investigated and treated for iron deficiency and other causes of anemia. The aggressive approach of investigation and treatment of anemia as soon as the hematocrit drops below the normal range is the ideal strategy; however, third party payers in the United States do not begin to cover the cost of rHuEPO until the hematocrit level has fallen below 30 percent. The authors conclude that the cost of
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treating the large population of patients with CRI and anemia in the United States with rHuEPO would undoubtedly be high. However, the reduced cardiovascular disease burden related to improved anemia management, and the deferred cost of dialysis, may offset the high cost of rHuEPO. 1 figure. 2 tables. 110 references. ·
'Common' Uncommon Anemias Source: American Family Physician. 59(4): 851-858. February 15, 1999. Contact: Available from American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211-2672. (800) 274-2237. Website: www.aafp.org. Summary: This article reviews the more often seen diagnoses among the uncommon anemias'; these include the anemia of renal disease, thalassemia, myelodysplastic syndrome, and the anemia of chronic disease. These conditions may be suggested by the clinical presentation, laboratory test values, and peripheral blood smear, or by failure of the anemia to respond to iron supplements or nutrient replacement. The principal cause of the anemia of renal disease is a decreased production of red blood cells related to a relative deficiency or erythropoietin. When treatment is required, erythropoietin is administered, often with iron supplementation. In the anemia of chronic disease, impaired iron transport decreases red blood cell production. Treatment is predominantly directed at the underlying condition. Since iron stores are usually normal, iron administration is not beneficial. Thalassemia minor results from a congenital abnormality of hemoglobin synthesis. The disorder may masquerade as mild iron deficiency anemia, but iron therapy and transfusions are often not indicated. In the myelodysplastic syndrome, blood cell components fail to mature, and the condition may progress to acute nonlymphocytic leukemia. The rate of progression depends on the subtype of myelodysplasia, but the leukemia is usually resistant to therapy. 5 figures. 3 tables. 16 references. (AA-M).
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Anemia Management in Pediatric Dialysis Patients: Case Study of the Anemic Patient Source: ANNA Journal. American Nephrology Nurses Association Journal. 26(3): 349352. June 1999. Contact: Available from American Nephrology Nurses' Association. East Holly Avenue, Box 56, Pitman, NJ 08071. (609) 256-2320. Fax (609) 589-7463. Website: www.annanurse.org. Summary: Anemia is equally devastating in children as it is in adults. This article examines the use of Epoetin alfa in the pediatric population, including the role of nurses in educating patients and ensuring prescribed outcomes. Decreased energy levels from anemia can lead to deterioration in the ability to exercise, to participate in the normal activities of childhood, and to learn. Moreover, these affects may make it difficult for children to engage in social interactions with their peers, thereby altering their development. Epoetin alfa (erythropoietin) therapy effectively ameliorates the anemia of end stage renal disease (ESRD) in pediatric dialysis patients and thus minimizes many of these negative effects. The author outlines the use of medical play as a way to education the pediatric patient and his or her family. Controlled hands on experience can help the child and family adjust to medical care and prevent the development of an overly stressful experience that could affect future behavior. The article includes an illustrative case study of a 15 year old girl with ESRD who is on peritoneal dialysis. The author stresses that nurses play a prominent role in devising innovative methods for educating patients and families, while proactively monitoring, assessing, and
Studies 13
intervening to ensure that hemoglobin (Hb) levels remain in the target range. 3 tables. 12 references. (AA-M). ·
Update on Anemia and Iron Management in Dialysis Patients Source: Contemporary Dialysis and Nephrology. 19(5): 31, 32, 34. May 1998. Summary: Maintaining adequate iron levels is critically important for the management of anemia in dialysis patients. This article provides an update on anemia and iron management in patients on dialysis. In addition to cardiovascular problems, anemia also impacts such critical outcome areas as morbidity, hospitalizations, and quality of life. The author reviews related studies, particularly Canadian research. Some of the studies highlighted the beneficial effects of improving anemia on hospitalization rates. Improving anemia led to a decrease in the number of hospital admissions and the length of hospital stays, decreasing the morbidity factor. The author also reports on work establishing and reviewing the target hematocrit (Hct) levels for this population. They conclude that improving anemia from a Hct of 25 percent (the level achieved prior to the use of erythropoietin) to the current upper target level of 36 percent significantly improves brain function. A new test (the reticulocyte hemoglobin concentration) is available that may replace the transferrin saturation and serum ferritin tests currently used to determine and define iron deficiency. An additional problem is the poor absorption and the side effects of oral iron taken with food or medication in this patient population; patient noncompliance is common. The author reports work discussing the best methods of administering erythropoietin (including subcutaneously and intravenously) and stresses the importance of individualizing the iron management strategy for each patient. A given dose of erythropoietin will cause a different rate of production of red blood cells in different patients; the demand side is also different in each patient.
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Anemia Following Renal Transplantation Source: Transplantation Proceedings. 30(7): 3025-3026. November 1998. Contact: Available from Appleton and Lange. P.O. Box 86, Congers, NY 10920-0086. (203) 406-4623. Summary: Anemia observed in long term surviving renal transplant recipients has tended to receive weak attention from transplant physicians since it is not a life threatening complication such as infection. However, this complication can have a significant impact on the quality of life for recipients after renal transplantation. This article reports on a study undertaken to gain insight into the disorders of the red blood cell (RBC) observed in the recipients with stable allograft function after successful renal transplantation. Sixty patients (39 male, 21 female) were included in the study. Twelve (10 male, 2 female) were diagnosed with anemia; the authors conclude that 10 of the 12 had anemia related to their renal allograft dysfunction. The authors call for further examination to determine long term effects of cyclosporine A on red cell disorder associated with erythropoietin production of the renal allografts. The authors also note that progressing normocytic anemia is a common feature in patients with chronic rejection; therefore, physicians should pay more attention to anemia following successful renal transplantation. 1 figure. 1 table. 7 references.
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Anemia, Hypertension, and Myocardial Dysfunction in End-Stage Renal Disease Source: Seminars in Nephrology. 17(4): 257-269. July 1997.
14 Anemia
Contact: Available from W.B. Saunders Company. Periodicals Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Summary: Cardiovascular disease remains the major cause of mortality in patients with end-stage renal disease (ESRD). This article addresses myocardial dysfunction in patients with ESRD. The pathophysiology of cardiac dysfunction in ESRD is complex and not fully understood. However, it appears that the two major determinants of left ventricular (LV) hypertrophy and dysfunction are anemia and hypertension, both of which are very common in ESRD patients. Early and aggressive correction of anemia and hypertension may have a significant impact on cardiac disease in ESRD patients. The authors' discussion focuses on the management of anemia and hypertension, and the current information available on the pathogenesis and management of LV dysfunction in ESRD. The authors report on the use of various hypertensive agents, summarizing the side effects of these agents, as well as comorbid conditions influencing choice of drugs. The most current recommendation for treating anemia is to administer erythropoietin (EPO) to all anemic patients with advanced renal failure. The most likely etiology for a suboptimal response to EPO is iron deficiency. It is recommended that iron stores be checked and supplemented before EPO therapy is started. Even in the presence of adequate stores at the start of therapy, patients may rapidly deplete their iron stores during the hematopoietic response to EPO. The authors conclude that, due to the complexity of the pathogenesis of cardiac dysfunction in uremic patients, a multidimensional approach is necessary. Control of hypertension and correction of anemia are important in the longterm management of heart failure. 4 tables. 125 references. (AA-M). ·
Anemia, Dialysis, and Dollars (editorial) Source: New England Journal of Medicine. 334(7): 461-463. February 15, 1996. Summary: In this editorial, the author addresses the issue of dialysis adequacy and morbidity and mortality related to dialysis. Topics include the use of erythropoietin to treat dialysis-related anemia; the reasons why some patients do not respond well to erythropoietin therapy, including the role of inadequate dialysis, nutrition, and coexisting illness; how economic issues may contribute to suboptimal levels of dialysis; and the differences in mortality levels among dialysis facilities. The author concludes by challenging the dialysis facilities to offer concrete proof of the standard of care they provide. 13 references.
Federally Funded Research on Anemia The U.S. Government supports a variety of research studies relating to anemia. 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.
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).
2
Studies 15
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 anemia. 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 anemia. The following is typical of the type of information found when searching the CRISP database for anemia: ·
Project Title: ANEMIA NEPHROPATHY
AND
CLINICAL
OUTCOMES
IN
DIABETIC
Principal Investigator & Institution: Mohanram, Anupama; Internal Medicine; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002; Project Start 0-MAY-2003 Summary: (provided by applicant): Diabetic nephropathy (DN) is the leading cause of ESRD in the U.S. and cardiovascular (CV) morbidity and mortality are excessive in this population. Preliminary data from the Reduction in Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial indicate that anemia is a modifiable risk factor for ESRD and CV morbidity and mortality in type 2 DN. I hypothesize that hemoglobin (Hb) is an independent predictor of both renal and CV disease in this population. The specific aims of this project are to determine if anemia is an independent predictor of 1) ESRD; 2) cardiovascular morbidity (non-fatal CV events defined as hospitalization for heart failure, myocardial infarction, and unstable angina, and mortality (sudden cardiac death, death due to progressive heart failure, myocardial infarction, and other cardiac causes) and 3) hospitalization for revascularization (coronary, peripheral, cerebral, or renal), amputation, and stroke. I will use the RENAAL trial database involving 1,513 Type 2 diabetic patients with nephropathy followed on average for 3.4 years. Cox proportional hazards regression models using baseline and follow-up (Hb) will be employed as the independent variable, and renal disease, cardiovascular disease, and vascular disease outcomes as dependent variables. Power analysis based on observed event rates in the RENAAL trial indicate 95% power to detect a 30% reduction in risk of the primary composite endpoint of doubling serum creatinine, ESRD or death for patients in the highest compared to the lowest quartile of baseline Hb. I expect these results will establish anemia as an independent risk factor for ESRD and cardiovascular morbidity and mortality in type 2 diabetics with progressing renal disease. These data could change practice and lead to new clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ANEMIA MANAGEMENT AND SURVIVAL IN A HEMODIALYSIS COHORT Principal Investigator & Institution: Robinson, Bruce M. Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 1-JUL-2002; Project End 0-JUN-2004 Summary: (provided by applicant): Background: Despite numerous publications about the management of the anemia of chronic kidney disease (CKD) its best management remains controversial, and the need for continued improvement is a stated priority in the National Kidney Foundation-Kidney Disease Outcomes Quality Initiative (NKFKDOQI) Clinical Practice Guidelines for patients with CKD. Specific aim 1: In hemodialysis patients, determine the relation between hemoglobin concentration and
16 Anemia
dosing patterns of erythropoietin and parenteral iron. Hypothesis: The erythropoietin and iron doses most closely associated with target hemoglobin are consistent with the NKF-KDOQI guidelines recommended doses. Specific aim 2: In hemodialysis patients, determine the relation between hemoglobin concentration and survival.Hypothesis: Most favorable survival is associated with mean hemoglobins that include the NKFKDOQI guidelines' target range. We will address these aims using prospectively collected individual-level patient data from up to 10,000 hemodialysis patients in the American arm of the Dialysis Outcomes and Practice Patterns Study (DOPPS). Enrollment for the DOPPS began in 1996 and is ongoing. For both specific aims, we will investigate causality by controlling for time-varying and bidirectional associations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: CELL THERAPIES FOR COOLEY'S ANEMIA Principal Investigator & Institution: Ryan, Thomas M. Biochem & Molecular Genetics; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2003; Project Start 1-JUL-2003; Project End 0-JUN-2007 Summary: (provided by applicant): Cooley's anemia (CA) will be cured in an animal model of beta thalassemia major by therapeutic cloning, genome modification, and replacement cell therapy Therapeutic cloning will be used to derive primary beta/0 thalassemic embryonic stem (ES) cell lines that will be genetically modified to correct their defect. Corrected thalassemic ES cells will be used for replacement cell therapy after differentiation into hematopoietic progenitors and transplantation back into CA animals. Initial experiments will utilize a knockout mouse model of primary betathalassemia that reproduces most of the pathology of the disorder (PNAS 92 9259-9263). The model was created by targeted deletion of 16 kilobases of DNA that removes both adult mouse beta-globin genes. Later experiments will utilize a novel mouse model of CA generated by targeted gene replacement of the adult murine alpha-globin genes with human alpha-globin and the adult mouse beta-globin genes with a human gammato beta-globin gene switching cassette that contains a primary beta thalassemic allele. Newborn mice homozygous for the knockin allele will survive solely on human fetal hemoglobin at birth. The mice will succumb to CA during the first weeks of life once the fetal to adult hemoglobin switch is complete. Cooley's anemia ES cell lines will be established from developing blastocysts isolated from either heterozygous mating pairs or from nuclear transfer of fibroblast nuclei isolated from newborn CA mice into enucleated mouse eggs. Identical Cooley's anemia mice will be cloned from these ES cells by injection of CA ES cells into tetraploid blastocysts. Cloning after modification of the CA ES cells will be utilized to test genetic therapies designed to correct the thalassemia. Therapeutic benefit will be assessed by a direct comparison of the anemia in mice cloned from the modified ES cells to clones produced from the unmodified CA ES cells. Hematopoietic stem cells (HSCs) isolated from the bone marrow of cloned mice generated from the corrected CA ES cells will be used to cure sublethally conditioned isogeneic mice cloned from the diseased ES cells Finally, in vitro differentiation of the corrected CA ES cells will be used to generate hematopoietic progenitors in cell culture Conditioned CA mouse clones will be cured by the injection of these isogeneic corrected hematopoietic progenitors. Successful completion of these studies will delineate the basic steps required for curing many heritable hematopoietic disorders in humans, namely, therapeutic cloning to establish autologous ES cell lines, correction of diseased allele(s) in the ES cells, and hematopoietic progenitor replacement cell therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies 17
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Project Title: CLINICAL APPLICATIONS OF A NOVEL FANCONI ANEMIA ASSAY Principal Investigator & Institution: Shimamura, Akiko;; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 5-JUL-2002; Project End 1-MAY-2007 Summary: Congenital bone marrow failure syndromes are characterized by abnormal hematopoietic cell growth, differentiation, and survival. Bone marrow transplant is the only available curative treatment, but is associated with significant side effects and limited by donor availability. The development of new therapeutic modalities calls for investigators with: 1. Expertise in bone marrow failure syndromes, 2. An understanding of the clinical implications of new molecular discoveries, 3. Experience in the design and implementation of clinical trials. Dr. Shimamura is a pediatric hematologist/oncologist with a molecular background in signal transduction and apoptosis. The proposed training program is designed to allow her to develop expertise in bone marrow failure syndromes and to gain experience in the design and implementation of patient-oriented research. Her long-term goal is to become an independent investigatory applying our understanding of molecular mechanisms of bone marrow failure to solve clinical problems. Dr. Shimamura will pursue her career development under the co- mentorship of Dr. Alan D'Andrea and Dr. David Nathan. Dr. D'Andrea's studies have uncovered a novel Fanconi anemia (FA) biochemical pathway. She proposes to study the clinical applications of these findings as follows: 1. Investigate the FANCD activation assay as a new functional screen for the FA pathway, 2. Screen for pharmacological agents that augment FANCD activation, and 3. Assess the effect of FA gene replacement therapy on the restoration of FANCD activity as part of the on-going Dana-Farber/Children's Hospital FA gene therapy project directed by Dr. Nathan. Dr. Shimamura has assembled a committee of expert advisors and collaborators to assist her in this project. Her project will be supported by several local core facilities and programs including the Fanconi Anemia Center, the Harvard Vector Laboratory, the Cell Manipulation and Gene Transfer Laboratories, the Clinical Gene Therapy Program, and the General Clinical Research Center at Children's Hospital. To complete her training, she will attend a bone marrow failure clinic at Children's Hospital, build a bone marrow failure repository for future independent studies, and complete course work on clinical research design, implementation and analysis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORE--FANCONI ANEMIA CELL REPOSITORY Principal Investigator & Institution: Grompe, Markus C. Professor; Oregon Health & Science University Portland, or 972393098 Timing: Fiscal Year 2001 Summary: The OHSU Fanconi Anemia Cell Repository (Core C) serves as a local, national and internal source of cell lines for research on Fanconi Anemia. In addition, it provides information regarding complementation groups and/or mutations to A patients and their families. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CORRECTION OF RPS 19 DEFECTS IN DIAMOND BLACKFAN ANEMIA Principal Investigator & Institution: Sieff, Colin A. Associate Professor; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115
18 Anemia
Timing: Fiscal Year 2001 Summary: Diamond Blackfan anemia (DBA) is a congenital anemia that develops at birth or soon after, and is due to failure of production of erythrocytes and their precursors, with normal or near normal myeloid and platelet lineages. It is inherited in about 10% of cases, mostly as an autosomal dominant. Recent genetic studies have led to the surprising identification of mutations in a ribosomal protein gene, RP219, on chromosome 19q13.2, in about 25% of both familial and sporadic cases (DBA1), and there is evidence for involvement of at least 2 other genes. Patients can remit completely on corticosteroids or may become resistant to treatment, and then require regular blood transfusions, or bone marrow transplant if a histocompatible sibling donor is available. The long term objective of this proposal is to develop preclinical data for a gene therapy protocol for severe DBA1 patients who are not eligible for matched sibling stem cell transplantation. Therefore the specific aims are (1) to identify RPS19 mutant patients by PCRT-based sequence analysis and by characterization of mutant proteins using antibodies to RPS19; (2) to further characterize the in vitro erythroid defect in these patients and then use abnormality in the erythroid progenitor cells and precursors; and (3), to "knock-in" to embryonic stem (ES) cells a mutation that has occurred independently in 6 unrelated families. The mutant ES cells will be injected into blastocysts and reimplanted into pseudopregnant females to generate chimeric animals for developing heterozygotes and breeding to homozygosity. Transmitting heterozygotes will be cross-bred to observe the consequences of mutation of both alleles in vivo. The major objective here is to create a DBA1 mouse that can be used to evaluate retrovirus and lentivirus RPS19 gene correction. Accomplishment of these goals will lead to further in vivo evaluation and a clinical protocol (not part of this project but part of the research program). In addition to the practical benefit to severely affected DBA1 patients, we hope to gain insight into how mutations in RPS19 lead to a block in the development of early erythroid cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ANEMIA
CYTOKINE-MEDIATED
PATHOPHYSIOLOGY
IN
FANCONI
Principal Investigator & Institution: Chen, Ming; Pediatrics; Weill Medical College of Cornell Univ New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 1-JUL-2001 Summary: Fanconi anemia (FA) is an autosomal recessive disorder characterized by cellular hypersensitivity to DNA crosslinking agents such as mitomycin C (MMC) and diepoxybutane (DEB) (Auerbach 1993), bone marrow (BM) failure, diverse congenital anomalies, and a marked increased in the incidence of malignancies. Eight complementation groups (FA-A through FA-H) have been identified. The human genes defected in the FA-C, FA- A FA-G groups were recently cloned. Fancc-deficient mice have been created by targeted mutations of the murine Fancc gene. Cells from France -/mice showed hypersensitivity to MMC and DEB. Surprisingly, however, no gross hematologic defects or congenital anomalies were detected, although the homozygous mice showed decreased fertility. Evidence has been collected indicating that certain cytokines are involved in Fanconi anemia. TNF-alpha and IFN-gamma are inhibitory cytokines that can induced deregulated. Progenitor growth and apoptosis in Fancc-/hematopoietic progenitor cells (HPC). FANCC transgene protected HPC FANCC transgene protected HPC from Fas-mediated apoptosis. IL-6, TNF-alpha and IFNgamma, among others, are known to mediate immune-neuro-endocrine interactions. More recently, multiple endocrine abnormalities were discovered in FA patients,
Studies 19
including deficiencies in growth hormone, thyroid and gonads function. We hypothesize that the endocrine abnormalities be due to aberrant response to cytokines, particularly TNF-alpha and IFN-gamma, in the endocrine glands. The proposed project will use Fancc-deficient mice and cell lines derived from endocrine glands, along with certain cytokines, to test this hypothesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: DETECTION OF HYPOXIA IN SICKLE CELL ANEMIA BY BOLD MRI Principal Investigator & Institution: Fabry, Mary E.; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2001 Summary: (Adapted from Applicant's Abstract) Treatment of sickle cell painful crisis has suffered from a lack of objective criteria for detecting progression of crisis and use in evaluating treatment protocols. To date, MRI of painful crisis has yielded results which are intriguing but difficult to evaluate. Detection of hypoxia in regions with acute pain may yield a useable marker. The technology for in vivo observation of blood perfusion and tissue oxygenation by blood oxygen level dependent (BOLD) magnetic resonance imaging (MRI) has matured into a sensitive technique an can be applied to these problems. The investigators will test the hypothesis that painful crisis of the limbs is accompanied by areas of blood hypoxia due to partial obstruction of the circulation which can be detected by BOLD MRI. The investigators also test the hypothesis that the stereotypical repetition of painful crisis as the same sight might be the consequence of congenital or acquired alteration (by previous crises or other effects) in the microcirculation that predispose to repeat crises in the same site. The investigators will also examine the hypothesis that HU will reduce the extent of the area affected and/or the degree of blood hypoxia in areas prone to crisis. The investigators have demonstrated in transgenic mice expressing the BetaS-globin gene that BOLD-MRI can detect the presence of high levels of deoxy hemoglobin (blood hypoxia) in tissues such as the medulla of the kidney which have been shown to have very low oxygen tension by other means. Highly deoxygenated sickle cell blood is at risk of polymer formation and the microcirculation is a risk of vaso- occlusion. The investigators propose here to use BOLD-MRI to detect blood deoxygenation in adult patients with sickle cell painful crisis. A goal of these studies to separate acute, ongoing events during sickle cell painful crisis from the results of previous episodes of ischemia. Previous approaches to detection of pathological changes occurring during the course of sickle cell painful crisis such as 99mTc bone scans and MRI are too sensitive to the presence of old infarcts to allow detection of new infarcts without prior baseline studies. If successful, this approach may allow the unique visualization of poorly perfused regions without reference to baseline studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DEVELOPMENT AND ANALYSIS OF MURINE MODELS FOR SICKLE CELL ANEMIA Principal Investigator & Institution: Rubin E.; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001 Summary: The long range objective of this proposal is to further our understanding of the molecular basis for sickle cell anemia with particular emphasis on examining genetic factors that contribute to the variable clinical expression of the disease. The specific
20 Anemia
goals are: (1) to characterize sickle cell disease and the factors which impact on its severity in our recently developed mouse model of sickle cell anemia, whose red cells contain exclusively human HbS; and (2) to apply genome-wide mapping tools and quantitative trait analyses to identify genetic loci unlinked to the globin cluster that modify the severity of sickle cell disease. Our first goal relates to the transgenic/gene knockout mouse model of sickle cell anemia which we generated during the previous funding period. These animals, possessing exclusively human hemoglobin HbS and no adult murine hemoglobins, are born with extensive red cell sickling and associated morbidity. We will exploit this unique model to perform detailed investigations of the pathophysiology of the disease, unavailable for study in humans. We will examine the effectiveness of agents predicted to lessen disease severity. These studies will analyze factors which have an impact on gamma-globin gene expression (i.e., hydroxyurea) and vascular tone (i.e., nitrous oxide). The second goals will employ a genome-wide scan to identify loci that alter sickle cell disease severity and globin chain switching using inbred strains of mice. These studies are divided into two parts. They will identify modified loci, using different mouse genetic backgrounds, that: (1) affect the severity of murine sickle cell disease resulting from the expression of the same human sickle transgene; and (2) affect gamma-to beta-globin switching of the same human betaglobin YAC transgene. In both of these studies, we seek to identify genes unlinked to the globin cluster in mice which are likely to impact on the severity of sickle cell disease in humans. The studies are anticipated to contribute to our improved understanding of the molecular mechanisms responsible for variable clinical expression of sickle cell disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: DNA REPAIR DEFECT IN FANCONI ANEMIA, GROUP A Principal Investigator & Institution: Lambert, Muriel W. Professor; Pathology and Lab Medicine; Univ of Med/Dent Nj Newark 30 Bergen St Newark, Nj 07107 Timing: Fiscal Year 2001; Project Start 1-JUL-1995; Project End 1-MAY-2003 Summary: The goal of this proposal is to delineate the relationship between the FAA and FAC gene products and the DNA repair defect in Fanconi anemia, complementation groups A (FA-A) and C (FA-C). It has been hypothesized that an underlying mechanism for this disorder may involve a DNA repair defect. We have isolated a DNA endonuclease complex from the nuclei of FA-A and FA-C cells and shown that it is defective in ability to incise DNA at sites of interstrand cross- links. Levels of a 230 kDa protein, associated with this complex and which binds to crosslinked DNA, are decreased in FA-A and FA-C cells. This protein has recently been identified as nonerythroid alpha spectrinllsigma* (alphaSpIIsigma*). The deficiency in alphaSpIIsigma* is corrected in FA-A cells transduced with a retroviral vector expressing the FAA cDNA, indicating that the FAA gene plays a role in its expression or stability. alphaSpIIsigma* also forms a complex with the FAA and FAC proteins in the nucleus which suggests that this complex may play role in DNA repair. It is possible that alphaSpllsigma* acts as a scaffold to help align or enhance interaction between proteins involved in the repair of interstrand cross-links and proteins that interact with FAA and FAC. The present proposal will address this by first determining the isoform of the alphaSpllsigma* we have identified and producing a recombinant protein that can be used in further studies. Exactly what proteins are associated with the FAA-FACalphaSpllsigma* complex, whether any of these proteins have binding affinity for DNA containing interstrand cross-links, and whether there is a deficiency in any of these proteins in FA-A and FA-C cells will be determined. The role of the FAA and FAC proteins in regulating the expression or stability of alphaSpllsigma* will be assessed as
Studies 21
will the role of each of these three proteins in the repair of DNA interstrand cross-links. If alphaSpllsigma* is acting as a scaffolding protein, to help align and allow interactions between these as well as other proteins, this could have far reaching implications in a number of different processes, in addition to DNA repair, which have been associated with this protein, such as signal transduction and cell growth and development. A deficiency in alphaSpllsigma* in FA cells could thus ultimately affect hematopoietic differentiation and development. Isolation and identification of proteins associated with the FAA-FAC- alphaSpllsigma* complex and determination of their interactions with each other, other nuclear proteins, and DNA repair should help elucidate the basis of bone marrow failure and the development of aplastic anemia and leukemia in FA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: FANCONI ANEMIA Principal Investigator & Institution: D'andrea, Alan D. Professor; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2001 Summary: Fanconi Anemia (FA) is an autosomal recessive cancer susceptibility disorder characterized by multiple congenital abnormalities, progressive bone marrow failure, and cellular sensitivity to DNA crosslinking agents. FA is characterized by hematopoietic stem cell dysfunction, and the treatment of choice for the disease is an allogeneic bone marrow transplant. Since most FA patients do not have a suitable donor, FA is also a candidate disease for gene therapy. The purpose of the current project is to focus on various of the basic biology of FA related to our ongoing gene therapy trials. The specific aims for the five year study period are (1) To develop and characterize a mouse model for Fanconi Anemia Complementation Group G (FANCG knock-out mouse). Our recent studies demonstrate that FA-G patients have more severe disease than FA-A patients. Therefore, a mouse model for FA-G may demonstrate distinct pathology, compared to the previously describe FA- C mouse. The subaims of this section are to generate a colony of FANCG (-/-, -/+, and +/+) mice, to characterize the hematopoietic system in the FANCG knock-out mouse, to characterize the stem cell population in FANCG knock-out, and to perform competitive repopulation studies, comparing the relative engraftment of FANCG (-/-) cells versus FANCG (+/+) cells. In specific aim 2, we will further develop murine models for Fanconi Anemia Gene Therapy in order to compare the transduction of bone marrow cells from FANCC, FANCA, and FANCG knockout mouse models with either pMMP (murine) retroviral vectors or lentiviral vectors. A significant strength of this specific aim will be our ability to assay infection efficiency of transduced bone marrow, by using PCR of cDNA integrations and immunofluorescence of expressed heterologous FA proteins. In specific aim 3, we will systematically compare cell lines and primary cells derived from patients from all nine complementation groups of FA for distinct cellular abnormalities. This aim will be closely aligned with our new Fanconi Anemia Diagnostic and Clinical Center at the DFCI, which has provided us with the opportunity to collect and subtype cell lines from many FA patients. We will compare the ionizing radiation (IR) sensitivity and bleomycin sensitivity of all FA complementation groups, and will examine these cell lines for defects in Non-Homologous End joining (NHEJ) and Homologous Recombination (HR). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
22 Anemia
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Project Title: FANCONI ANEMIA GENE PATHWAY IN RADIATION RESPONSES Principal Investigator & Institution: Thompson, Lawrence H. Senior Scientist; Biology & Biotechnology Res; University of Calif-Lawrnc Lvrmr Nat Lab Lawrence Livermore National Lab Livermore, Ca 94550 Timing: Fiscal Year 2001; Project Start 4-JAN-2001; Project End 1-DEC-2004 Summary: The project's objective is to understand the molecular regulatory processes cells use to minimize genetic damage and genetic instability associated with reactive oxygen species (ROS) arising from endogenous processes or ionizing radiation (IR). This goal is addressed through studies of FANCG/XRCC9, the gene that is defective in. group G of the cancer-prone disorder Fanconi anemia (FA). Because FancG protein confers IR resistance in hamster cells, the human homolog is expected to participate in IR responses in human cells. Historically, a link between the FA genes and radiation responses has been unclear, with some studies suggesting that the primary defect in FA lies in removing DNA interstrand crosslinks. The general hypothesis to be tested is that the FANCG protein, as a member of a multiprotein complex, protects mammalian cells against endogenous and IR-generated oxidative damage and maintains genomic integrity by coordinating homeostasis processes that include regulation of ROS levels, apoptosis, and cell cycle progression. The proposed studies will provide a highly quantitative characterization of FANCG protein's contribution to biochemical and cellular endpoints associated with both normal cell proliferation and responses to IR exposure. Isogenic pairs of mutant and FANCG-complemented cells will be derived in both hamster CHO cells and human lymphoblasts. These pairs will be analyzed with respect to chromosomal aberrations, cell survival, hprt gene mutations, apoptosis, ROS, and cell cycle parameters with and without IR exposure. The FANCG-complemented FA-G lymphoblasts will be used to examine gene and protein regulation during the cell cycle as well as the subcellular localization of the protein with and without IR damage. Three proteins that are candidate interactors with FANCG from preliminary studies will be evaluated for possible involvement in the FA pathway. Finally, already identified high-frequency human allelic variants of FANCG in the US population will be evaluated for degree of dysfunction. The results of these studies will lead to more specific models of the nature of the FA protein "pathway" and its quantitative contributions to multiple biological effects associated with IR-mediated oxidative damage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DETECTION
FANCONI
ANEMIA--HETEROGENEITY
AND
Principal Investigator & Institution: Auerbach, Arleen D. Genetics/Hematology; Rockefeller University New York, Ny 100216399
CARRIER Lab/Human
Timing: Fiscal Year 2001; Project Start 1-MAY-1985; Project End 0-JUN-2002 Summary: The purpose of this study is to determine the genetic basis of Fanconi anemia (FA), an autosomal recessive disorder characterized by diverse congenital abnormalities, and a predisposition to bone marrow failure and malignancy, particularly acute myelogenous leukemia (AML The specific objectives of this project are: (1) To identify mutations in the genes for FA complementation group A (FA-A) and group C (FA-C) and other FA genes when they are isolated, and to make genotype-phenotype correlations; (2) To develop screening methods using DNA technology, for FA diagnosis and carrier detection. (3) To isolate and clone other FA genes by a combination of positional and functional complementation; (4) To study the structure and expression of these other genes. A major resource and unique feature of this proposal is our access to a
Studies 23
large number of patients with FA exhibiting the full spectrum of its diverse features, through the International Fanconi Anemia Registry (IFAR) maintained by us at the Rockefeller University. This provides us with phenotypic information on FA patients as well as a source of cells for molecular studies; we currently have DNA samples from a total of 422 patients affected with FA. Understanding the genetic defect in FA should lead to a better understanding of birth defects and cancer predisposition in general, and the interaction of genetic and epigenetic factors in their pathogenesis. Mutation screening will initially be performed by sizing PCR amplified fragments from cDNA, by genomic DNA blot hybridization and by restriction endonuclease fingerprinting (REF). As mutations are characterized at the genomic level and sequenced, ARMS assays will be developed to permit rapid DNA based screening methods for (1) assignment of FA patients to complementation group, (2) prenatal diagnosis in FA families, and (3) identification of carriers in FA families and in populations at risk. It is an objective of this project to extend our ability to define the FA genotype of all patients and to make genotype-phenotype correlations. This would enable physicians to better predict clinical outcome and aid decision-making regarding major therapeutic modalities for this clinically heterogeneous disorder. A positional cloning approach will be used to clone the FAB and FAE genes, made feasible by the detailed physical mapping information that is rapidly becoming available through the Human Genome Project. Linkage analysis will be used to map these loci; cDNAs will be isolated by direct selection from cosmid contigs from the appropriate region. This will be combined with functional complementation in an effort to accelerate the identification of these genes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: FANCONI ANEMIA--ROLE OF THE C PROTEIN Principal Investigator & Institution: Hoatlin, Maureen E. Medicine; Oregon Health & Science University Portland, or 972393098 Timing: Fiscal Year 2001; Project Start 1-MAY-1997; Project End 1-MAR-2004 Summary: Fanconi anemia (FA) is a cancer susceptibility syndrome associated with developmental abnormalities and bone marrow failure. Because of the unique cellular hypersensitivity to DNA crosslinking agents FA is considered to be a DNA repair disorder. The first (of at least eight) of the known FA complementation group genes, FANCC, was cloned more than seven years ago. Despite substantial efforts to discover the function of the FANCC protein, and functions of the proteins encoded by the other more recently cloned FA genes (FANCA and FANCG), the basic defect is still unknown. We used a yeast two hybrid screen to identify a new POZ-zinc finger protein (termed FAZF) which interacts with FANCC. We recently showed that FAZF is a transcriptional repressor similar to the promyelocytic zinc finger protein (PLZF). PLZF represses transcription of target genes by recruitment of histone deacetylase through the SMRTmSin3-HDAC co-repressor complex and tethering the complex to specific DNA target sequences. The FANCC/FAZF interaction is intriguing because it suggests that the FANCC protein may be interacting with components of the histone deacetylase complex. We propose to investigate FAZF and its relationship to FA by: (1) Analyzing FAZF/FANCC interaction in response to DNA damage, determine if FAZF is an FA complementing protein, compare the expression of FAZF and FANCC in primary hematopoietic cells (2) Analyze the consequences of enforced expression of FAZF, identify FAZF's binding partners, determine if FAZF is phosphorylated in response to DNA damage (3) Produce and examine the phenotype of FAZF nullizygous mice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
24 Anemia
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Project Title: FAS/FASL MEDIATED APOPTOSIS IN GVHD AND APLASTIC ANEMIA Principal Investigator & Institution: Civin, Curt I. Professor of Cancer Research; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 0-SEP-2002; Project End 1-MAR-2003 Summary: The ability to stably transduce lympho-hematopoietic stem-progenitor cells (HSCs) allows us to genetically engineer HSCs and their progeny to serve as improved cellular tools to treat disease and complications. In Specific Aim 1, we propose preclinical studies in mouse and human models to confirm the concept and elucidate the principal cellular and molecular mechanisms by which Fas ligand-transduced (FasL*) dendritic cells (DCs) or HSCs may selectively kill the T and NK cells that mediate GVHD. The results of Aim 1 will also provide modeling information on the application of transduced FasL+ cells to reduce immune attack against HSCs in severe aplastic anemia (SAA) (Specific Aim 3). Since it is expected that transduced FasL+ cells may be toxic in potential future translational in vivo applications, we will investigate technologies to limit potential FasL toxicity, eg by eliminating the transduced cells (or their FasL expression) after tolerance to HSCs has been generated. A novel transduced FasL+ cell therapy approach to reduce effector lymphocytes attacking host cells in GVHD (Aim 1) and SAA (Aim 3) may eventually be used in transplants for SAA, PNH and other diseases, and a potential clinical trial is outlined in Aim 1. In addition, our accompanying mechanistic studies on apoptotic pathways in alloimmune cells will increase information on the fundamentals of the Fas pathway in the effector cells mediating GVHD (and SAA), which in turn, should increase understanding of death pathways in the biology of (a) alloimmune responses, (b) hematologic malignancies that evade immune surveillance, and (c) transplanted organs (or pluripotent stem cells). In Specific Aim 2, Projects 1, 2 and 4 will cooperate to investigate the potential role of the Fas pathway in the pathophysiology of HSCs from SANPNH patients. Specific Aim 1: To engineer FasL+ host DCs or HSCs to selectively kill the cellular effectors of GVHD. Specific Aim 2: To investigate the role of the Fas pathway in the pathogenesis of SAA and PNH. Specific Aim 3: To investigate whether FasL+ HSCs selectively kill autologous anti-HSC CTLs in SAA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
·
Project Title: FETAL HEMOGLOBIN SYNTHESIS IN CHILDREN WITH SICKLE CELL ANEMIA Principal Investigator & Institution: Dover, George J. Professor of Pediatrics; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001 Summary: This research proposal is designed to test whether sodium phenylbutyrate (SPB) will increase fetal hemoglobin (HbF) in children with sickle cell anemia and thereby ameliorate complications from their disease. Increases in Hbf lessens the severity of disease and enhances survival. Several fatty acids, including butyrate analogues, have been shown to stimulate HbF production, suggesting that these agents may be beneficial in treating patients with sickle cell anemia. The purpose of this study is to determine if oral SPB will induce HbF synteiss in children with sickle cell anemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies 25
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Project Title: GENE THERAPY FOR PATIENTS WITH FANCONI ANEMIA Principal Investigator & Institution: Kiem, Hans-Peter; Member; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001 Summary: Gene therapy for patients with Fanconi anemia. The overall goal of this project is to develop gene therapy for patients with Fanconi Anemia (FA). FA is an autosomal recessive syndrome which is characterized by congenital abnormalities, predisposition to malignancy and bone marrow failure. Current treatment options for patients with FA include supportive care, growth factor treatment with G-CSF, and hematopoietic stem cell transplantation for patients with HLA-matched siblings; transplantation from unrelated donors has been less successful in a number of different protocols are currently being studied. Gene therapy has also been described, however, gene transfer efficiency has been low and the detection of genetically modified cells in patients has only been transient.. Thus, this project will incorporate a number of recently developed technologies to improve CD34+ peripheral blood stem cell (PBSC) mobilization and transduction. Specifically we propose to 1) study mobilization with a combination of G-CSF and SCF to improve CD34+ mobilization in patients with FA, 2) evaluate hematopoietic stem ell gene transfer efficiency using fibronectin assisted transduction in patients with FA, 3) develop improved retroviral packaging cells and vectors for gene transfer into hematopoietic repopulating cells, 4) evaluate novel transduction conditions, vectors and multiple infusions of transduced CD34+ cells in future gene therapy protocols for patients with FA. Other advances from other projects of this RFA and from ongoing stem cell transduction studies in our baboon model will be incorporated into future gene therapy protocols for patients with FA. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
·
Project Title: GENE THERAPY TREATMENT FOR SEVERE ANEMIA Principal Investigator & Institution: Lewis, David L. Senior Scientist; Mirus Corporation 505 S Rosa Rd, #104 Madison, Wi 53711 Timing: Fiscal Year 2002; Project Start 1-APR-2002; Project End 0-SEP-2002 Summary: (provided by the applicant): Gene therapy holds a promise for the treatment of both acquired and genetic diseases. Patients with diseases including end-stage kidney disease, acquired immunodeficiency syndrome and patients who are treated for cancer with high dose chemotherapy and bone marrow transplantation often develop anemia that can be treated or prevented by injection of recombinant EPO protein. EPO delivery via gene therapy would provide a significant treatment benefit. EPO is normally expressed in the kidney, which is a poor target for gene therapy in most patients because of severe organ failure. Yet, serum proteins such as EPO can be produced at ectopic sites and secreted to the serum. A novel method of intra-vascular injection of plasmid DNA expression vector results in highly efficient tranfection of skeletal muscle. This project will use this simple and innovative approach to develop a gene therapy protocol for the treatment of severe anemia. In this Phase 1 application, experiments are proposed to optimize EPO expression following intra-vascular delivery of plasmid DNA expression vectors and test this gene therapy protocol in a severe anemia model. During the Phase II studies, intra-vascular delivery techniques will be optimized to target small, defined muscle groups in a safe clinically applicable protocol. PROPOSED COMMERCIAL APPLICATION: The intravascular delivery methodology will be used in Phase III for the internal development of gene therapy protocols for severe anemia and applications such as clotting factor abnormalities, phenylketonuria, a1-antitrypsin
26 Anemia
deficiency, complement factor deficiencies, and other hematologic or metabolic disorders within Mirus and licensed to other companies for use within their ene therapy applications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GENETIC DETERMINANTS OF ANEMIA IN FALCIPARUM MALARIA Principal Investigator & Institution: Looareesuwan, Sornchai;; Mahidol University C/O Siriraj Hospital, Dhonburi Bangkok, Timing: Fiscal Year 2001; Project Start 5-JUL-2001; Project End 0-JUN-2002 Summary: The proposed research project is designed to identify and determine the clinical role of genetic determinants of host susceptibility to anemia with falciparum malaria in Thailand. Malaria provides the paradigm for a disease that has shaped the human genome through natural selection of protective genetic traits. More genes have now been implicated in variability of susceptibility to malaria than to any other infectious or non- infectious disease of humans. Genes now recognized as affecting the host response to malaria include those for hemoglobin variants, for red blood cell enzymes, components of the membrane cytoskeleton, membrane receptors and blood group proteins, as well as loci that modulate immune responses or are involved in underlying pathophysiologic processes. The proposed research will seek to identify and characterize the clinical consequences of genetic determinants of a specific complication of malaria infection-anemia-in three prospective trials, designed to detect a variety of types of protection against falciparum malarial infection- anemia-in three prospective trials, designed to detect a variety of types of protection against falciparum malaria in population-based, case-control and hospital-based studies. Project 1 has three specific aims: (1) to conduct a prospective, population-based study of the hemoglobin levels and genotypes of children and adults with malarial infection as detected by monthly mass blood survey and permanent passive case detection at a field site in western Thailand (Suan Phung); (2) to conduct a prospective, case-control study of the genotypes of children and adults who present with symptomatic episodes of falciparum malaria at another field site in western Thailand (Bongti); and (3) to conduct a prospective, hospital-based study of the genotypes of children and adults with severe anemia in falciparum malaria who are admitted to the Hospital for Tropical Disease, Bangkok. DNA from all participants will be stored in a repository. The special characteristics of Thai populations may facilitate the identification of a variety of unrecognized genetic forms of "innate", non-immune modes of host resistance, and lead to new prevention and treatment strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC MODIFIERS IN CHILDREN WITH SICKLE CELL ANEMIA Principal Investigator & Institution: Ware, Russell E. Professor; Pediatrics; Duke University Durham, Nc 27706 Timing: Fiscal Year 2001; Project Start 1-JUL-2001; Project End 0-JUN-2006 Summary: (provided by applicant) The beta6 (Glu toVal) mutation in the beta globin gene that leads to sickle cell anemia (SCA) has been known for many years, and the biophysical characteristics of intracellular sickling are well described, but the clinical heterogeneity in patients with SCA is poorly understood. Patients with SCA have a wide variability of clinical disease expression that is puzzling, despite efforts to identify globin gene modifiers such as alpha thalassemia, beta globin haplotype, or enhanced
Studies 27
gamma globin expression. Our preliminary data suggest that genetic modifiers outside the globin gene loci can alter clinical disease expression in SCA, and we hypothesize that these genetic modifiers can predict the development of cerebrovascular and hepatobiliary disease in children with SCA. To test our hypothesis, we will analyze DNA samples from over 400 pediatric patients enrolled in two completed NHLBIsponsored multicenter trials: (1) the Cooperative Study of Sickle Cell Disease (CSSCD) and (2) the Study to Prevent Stroke (STOP). We also include the upcoming Phase III infant hydroxyurea trial (BABY-HUG) that will add 200 additional DNA samples and the opportunity for direct patient contact and clinical research experience by trainees. We will test DNA samples from these unique pediatric cohorts for genetic polymorphisms (DNA mutations) in genes that collectively are important in thrombosis (e.g. methylenetetrahydrofolate reductase, platelet glycoprotein IIIa, plasminogen activator inhibitor, prothrombin, Factor V, and Factor VII genes), brain injury repair (apolipoprotein E), bilirubin metabolism (the UDP-glucuronosyltransferase), and iron accumulation (hereditary hemochromatosis gene). After determining the prevalence of each DNA mutation, we will correlate specific polymorphisms with patient data including laboratory measurements, clinical events, and radiological studies. The longterm goal is to identify genetic risk factors that influence the development of cerebrovascular and hepatobiliary disease, and to develop a prospective interventional clinical trial for children with SCA. Trainees will study laboratory techniques, statistical analysis, IRB protocol design, informed consent, ethical issues related to participation in clinical trials, and have direct patient contact with families participating in BABY-HUG. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GENETIC MODIFIERS OF SEVERITY IN SICKLE CELL ANEMIA Principal Investigator & Institution: Platt, Orah S. Associate Professor of Pediatrics; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001; Project Start 0-SEP-2001; Project End 1-JUL-2006 Summary: (provided by applicant): Despite the fact that all individuals with sickle cell anemia (SS) have the identical genetic defect (homozygous beta 6 glu to val), there is a wide variation in clinical severity. While clinicians have long been aware of this variability, it was the epidemiologic data amassed by the NHLBI's Cooperative Study of Sickle Cell Disease (CSSCD) that allowed objective measurement of this variability and identification of key risk factors for severity. In this proposal we focus on one of the key risk factors for severity identified by the CSSCD - baseline white blood cell count (baseline WBC). This initially unanticipated risk factor is becoming more obviously relevant as new investigations into the pathophysiology of the disease increasingly emphasize the importance of white cells and inflammation. At the same time, baseline WBC and other markers of inflammation are emerging as risk factors for mortality in the general population, making the exploration of genetic determinants of baseline WBC of interest not only to the SS population, but also to the population at large. Our strategy for locating the genes that are responsible for the variability in baseline WBC involves three unique populations: inbred strains of mice (Jackson Labs, Bar Harbor), baboon pedigrees (Southwest Foundation for Biomedical Research, San Antonio), and nuclear and extended families of ~300 probands with SS (Boston, Creteil). The animals will be useful in determining quantitative trait loci (QTLs) and ultimately individual genes that influence baseline WBC. The SS probands and their families will allow quantification of the relative importance of genetic and environmental modifiers of baseline WBC in the probands (SS), as well as their normal heterozygous (AS) and unaffected (AA) relatives. Genotyping, and phenotyping using baseline WBC and more specific markers of
28 Anemia
inflammation (e.g. cytokines, adhesion molecules, hematopoietic growth factors) in these families will allow not only QTL mapping and gene identification, but also an analysis of how genetically interrelated the inflammatory markers are. We anticipate that these studies will provide new insights into the genetics of inflammation that will be of benefit to patients with SS as well as the general population of African heritage. In addition, the data and sample resource we will create is designed to continue to answer questions well beyond the inflammation issue that we focus on in this proposal. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GLOBIN GENE TRANSFER FOR THERAPY OF SICKLE CELL ANEMIA Principal Investigator & Institution: Sadelain, Michel; Associate Professor & Director; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 0-SEP-1996; Project End 0-MAY-2005 Summary: (Applicant's Description Verbatim): Sickle cell anemia is one of the commonest inherited diseases in humans, characterized by a severe chronic hemolytic anemia with an unpredictable course. While current forms of chemotherapy do not represent a radical treatment, the use of bone marrow replacement is limited by complications of allogeneic transplantation and the need for aggressive conditioning regimens. Thus, the goal of this proposal is to develop a treatment for severe hemoglobinopathies that integrates a genetic correction in autologous hematopoietic stem cells (HSC) with a reasonable transplantation strategy. The approach we propose is based on efficient lentiviral-mediated transfer of a wild-type globin gene in cord blood or peripheral blood stem cells, together with a selection for genetically modified cells that is applied in vivo after transplantation. In vivo selection is useful for two purposes: (1) to increase the relative representation of genetically corrected blood cells and (2) to decrease the toxicity associated with the transplantation conditioning regimen. Our recent results establish that efficient gene transfer of a modified beta-globin gene and large elements of the beta-globin LCR can be achieved using recombinant lentiviruses. We have demonstrated that (1) a large LCR greatly increases mean globin expression compared to the core elements of the LCR that were previously investigated and (2) incorporation of an insulator element into a retroviral vector increases the probability of expression at random integration sites and decreases vector silencing. The major goals of this project are: (a) to improve erythroid-specific gene expression from a virally encoded beta-globin transcription unit; (b) to compare the betaAand gammaAglobin genes in terms of their level of expression in bone marrow chimeras and their therapeutic activity in mouse models of sickle cell disease; (c) to confer a competitive advantage to the transduced HSC for repopulation of the host marrow using resistance to methotrexate as a model. We propose a detailed analysis of the function of the LCR and of the chicken globin insulator in stringent in vitro and in vivo assays that are relevant to the critical evaluation of their therapeutic potential. These studies are based on investigations in murine models of sickle cell disease and in primary human CD34+ cells of normal subjects and patients. To analyze globin gene expression and the effectiveness of drug resistance in selecting out corrected cells that express therapeutic levels of the globin transgene, we will capitalize on our ability to efficiently derive erythroid progeny from long-term cultured CD34+ cells and our mouse/human xenochimeras based on NOD-scid/scidmice. We ultimately aim to establish by direct experimental evidence that expression of the lentivirus-encoded human globin gene is sustained over time in murine and human cells in vivo and that expression of the
Studies 29
mutant dihydrofolate reductase methotrexate/trimetrexate.
permits
efficient
in
vivo
selection
with
Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: GROWTH FAILURE IN FANCONI ANEMIA Principal Investigator & Institution: Wajnrajch, Michael;; Weill Medical College of Cornell Univ New York, Ny 10021 Timing: Fiscal Year 2001 Summary: Children with Fanconi anemia (FA) are being studied hormonally to determine the cause of their growth failure. Aspects of endocrine and somatic abnormality are being related to accumulated data regarding the mutations responsible for FA. Two papers relating to this protocol have been accepted for publication in peerreviewed journals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HEPCIDIN EXPRESSION IN THE ANEMIA OF CHRONIC DISEASE Principal Investigator & Institution: Weinstein, David A.; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2003; Project Start 1-AUG-2003; Project End 1-JUL-2008 Summary: (provided by applicant): The pathogenesis of the anemia of chronic disease is not understood. A recently identified peptide, hepcidin, has been found to be aberrantly expressed in hepatic adenomas in GSD (GSD), resulting in an iron-resistant irondeficiency anemia similar to that seen in the anemia of chronic disease. Hepcidin is postulated to be involved in the pathogenesis of the anemia of chronic disease, and these investigations are aimed at characterizing the role of hepcidin in both normal iron homeostasis and in subjects with the anemia of chronic disease. The specific aims are the following: 1) To evaluate the relationship between adenoma tumor burden and anemia; 2) To characterize iron absorption and distribution in normal controls, anemic patients, and patients with GSD Type 1 at (GSD1a; 3) To compare hepcidin expression in normal individuals and patients with GSD1a, and 4) To determine the role of hepcidin as a mediator of the anemia of chronic disease in patients with other inflammatory conditions. Methodology: The relationship between iron homeostasis and hepcidin expression will be studied in normal and pathologic states including GSD1a, juvenile rheumatoid arthritis, and inflammatory bowel disease. As inappropriate hepcidin expression has been demonstrated in hepatic adenomas in patients with GSD, direct observational studies in this population will be performed to allow further clinical correlation between these lesions and indices of erythropoiesis and iron status. Oral absorption of iron will be investigated in all subjects to define the relationship between hepcidin and iron absorption. For the inflammatory disorders, the oral iron challenge tests and direct measurement of hepcidin will be performed during periods of disease remission and exacerbation. The relationship between hepcidin and inflammatory markers will also be investigated. Through these studies, the role of hepcidin as a mediator of anemia of chronic disease will be elucidated. Improved understanding of the pathophysiology of the anemia of chronic disease will lay the foundation for new treatments for anemia and disorders of iron homeostasis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
30 Anemia
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Project Title: LENTIVIRUS
IMMUNE
CONTROL
OF
EQUINE
INFECTIOUS
ANEMIA
Principal Investigator & Institution: Mcguire, Travis C. Professor; Vet Microbiology and Pathology; Washington State University Pullman, Wa 99164 Timing: Fiscal Year 2001; Project Start 0-SEP-1986; Project End 1-MAR-2003 Summary: The principal investigator proposes to test the hypothesis that conserved equine infectious anemia virus (EIAV) protein epitopes identified by CTLm from carrier horses can be used to induce protective immune responses in naive horses. The research will focus on experiments that may provide conclusive evidence for the role of CD8+ CTL in EIAV control. Most immunocompetent horses terminate the initial viremia and recurrences of viremia to eventually become inapparent carriers with very low levels of virus. Termination of viremia requires lymphocyte responses; these appear to be more concordant with virus downregulation than do neutralizing antibodies, which appear after viremia has been terminated. With the intent of providing data concerning a cause/effect relationship between MHC class I-restricted CD8 CTL and control of EIAV infection, the principal investigator will address four specific aims: (1) To identify conserved EIAV epitopes recognized by alloantigen ELA-A5-restricted memory CTL (CTLm) from carrier horses; (2) to induce CTLm in horses with a retroviral vector expressing conserved CTL epitopes; (3) to determine whether or not co- expression of equine IL-12 and CTL epitopes by a retroviral vector will increase the frequency of CTLm; and (4) to determine whether or not immunized horses expressing at least one ELA-A5 allele are protected from or more efficiently control EIAV infection and disease following virus challenge. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: INTENSIVE NUTRITION THERAPY IN PATIENTS WITH SICKLE CELL ANEMIA Principal Investigator & Institution: Harmatz, Paul;; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INTERNATIONAL MALARIAL ANEMIA RESEARCH TRAINING PROGRAM Principal Investigator & Institution: Brittenham, Gary M. Professor of Medicine; Pediatrics; Columbia University Health Sciences Ogc New York, Ny 10032 Timing: Fiscal Year 2003; Project Start 1-MAR-2003; Project End 8-FEB-2007 Summary: (provided by applicant): This application requests support for a new International Malarial Anemia Research Training Program that builds upon an established, long-term partnership between Mahidol University , Bangkok, in Thailand, and Columbia University, New York, in the U.S. This Training Program will prepare Thai physicians, scientists and other health professionals for careers in basic and clinical research on the pathogenesis of severe malarial anemia, utilizing the clinical and laboratory facilities of the Faculty of Tropical Medicine at Mahidol University and of the College of Physicians and Surgeons at Columbia University. Taking advantage of the opportunities for active research experiences offered by our new joint project, "Pathogenesis of Severe Malarial Anemia in Thailand" (NIB Grant ROI AI5131O), the
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proposed Program will combine long- and short-term multidisciplinary training to ready Trainees for independent study of the mechanisms responsible for the profound anemia associated with infection by Plasmodium falciparum. The distinctive features of the new International Malarial Anemia Research Training Program proposed in this application are: (i) an active transdisciplinary research experience on a specific research project on malarial anemia under the direction of a member of the Program Faculty at Mahidol University, (ii) a programmatic requirement for rigorous training in a major basic science area (such as in hematology, genetics, immunology or associated areas) combined with experience in clinical tropical medicine and related disciplines, (iii) didactic exercises leading to a scholarly, comprehensive understanding of current concepts of the pathophysiology of the anemia associated with malarial infection, and (iv) an investigative focus on hematologic disease in falciparum malaria, with emphases on the immunobiology of infection, effects on erythropoiesis and red cell destruction, and interactions with thalassemia, hemoglobinopathies and red cell enzyme deficiencies. The overall goal of this new Training Program is to provide basic and clinical research training in the fundamental aspects of hematology and related disciplines to equip Trainees with the knowledge, skills and aptitudes needed for effective investigation of severe malarial anemia in Thailand. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: IRON DEFICIENCY AND ANEMIA IN HIV AND HCV INFECTED WOMEN Principal Investigator & Institution: Semba, Richard D. Ophthalmology; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 0-SEP-2001; Project End 1-JUL-2005 Summary: (provided by applicant): Anemia is common during human immunodeficiency virus (HIV) infection and is associated with increased HIV disease progression and higher mortality. Consequences of anemia include fatigue, a decreased sense of well-being, and a greater need for expensive recombinant human erythropoietin therapy, transfusions, and hospitalizations. Our studies show that the cumulative incidence of anemia is 100 percent among HIV-infected female injection drug users, and that iron deficiency anemia accounts for about half of the anemia. Iron deficiency is a major neglected problem of women, and no progress has been made in reducing the prevalence of iron deficiency among women in the U.S. over the last 30 years. Although iron supplementation can be used to prevent and treat iron deficiency anemia, concerns have been raised since iron supplementation and iron overload have been associated with increased HIV disease progression, higher mortality, and progression of hepatitis C (HCV) infection. These concerns have led to a dilemma about the use of iron supplements for iron deficiency and anemia in women with HIV and HCV. The prevalence of HCV is especially high among injection drug users in urban settings. Research is needed to determine whether the benefits of iron supplementation in this population outweigh the potential risks. Our specific aims are to determine whether a multivitamin and iron supplement can effectively reduce iron deficiency and anemia among HIV-positive and HIV-negative female injection drug users without worsening HIV or HCV infection. To address these aims, we propose to conduct a randomized controlled clinical trial of daily multivitamin and iron supplementation for 600 female injection drug users. Outcome measures include hemoglobin, indicators of HIV and HCV disease severity, and iron status, and the trial will be monitored by a data and safety monitoring committee. If the proposed trial shows that a multivitamin and iron supplement reduces anemia and does not worsen HIV or hepatitis C infection, the
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findings could be used to establish evidence-based guidelines for the prevention and/or reduction of anemia among women in the U.S. and elsewhere. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ISOLATION OF THE FANCONI ANEMIA NUCLEAR PROTEIN COMPLEX Principal Investigator & Institution: Kupfer, Gary M. Microbiology; University of Virginia Charlottesville Box 400195 Charlottesville, Va 22904 Timing: Fiscal Year 2001; Project Start 0-SEP-2000; Project End 1-AUG-2004 Summary: Fanconi anemia (FA) is a genetic disease with defects in development and hematopoiesis and propensity to cancer, indicating a vital and basic cell biology process at work. The hallmark of FA is genomic instability, evidenced by gross chromosomal breakage and DNA alkylating agent hypersensitivity, which correlates strongly with cancer predilection in general. Studies of FA are important in several ways. First, FA biology is involved across a spectrum of scientific disciplines, including hematology, oncology, and development. Second, since the known FA proteins are found only in mammalian cells and have no previously described protein domain, their study will yield the description of a novel pathway which promotes the maintenance of gnomic stability. Third, work on other proteins derived from rare cancer susceptibility syndromes have proved to have wide applicability in science in general and cancer in particular, such as Li-Fraumeni syndrome (p53), xeroderma pigmentosum (DNA nucleotide excision repair), and ataxia telangiectasia (P13 kinase). Fourth, basic work on FA has already led to clinical use of reagents for diagnosis and genetic counseling, and gene therapy trials are currently underway for treatment of FA. This work focuses on FA protein interactions. Preliminary data have shown that two FA proteins FANCA (Fanconi anemia complementation group A) and FANCC interact in a 500 kD nuclear complex, an interaction that is absent in 7 of the 8 FA complementation groups. Within the nucleus the data reveal that these proteins localize to the DNA and nuclear matrixcontaining fractions and have an appearance that parallels that of other nuclear matrix proteins. Evidence is also presented for inducible localization to chromatin and for direct DNA binding on gel shift assay. The efforts in this proposal will be driven by and will directly test two hypotheses: l) that the FA nuclear complex functions as a multimeric complex whose isolation will yield additional binding partners which will enable us to clone FA complementation group genes, and 2) that the FA proteins are associated with the nuclear matrix and with DNA in a cell cycle-regulated, complementation group-dependent, and drug-inducible fashion and interact with DNA either directly or indirectly. First, the FA protein complex will be characterized with respect to size and inducibility. Second, The complex will be isolated and analyzed by mass spectroscopy in order to identify novel and known associated proteins. Third, the subcellular localization of the FA proteins and their interaction with DNA will be investigated in a number of ways, including those which can lead to further new protein isolation. Identification of new proteins and elucidation of FA pathway mechanisms will help uncover a new realm of cancer biology and directly provide clinical applicability. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ISOLATION OF THE GENE FOR DOMINANT BLACKFAN ANEMIA Principal Investigator & Institution: Gazda, Hanna;; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 1-MAY-1999
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Summary: Diamond Blackfan anemia (DBA) is a rare congenital pure red cell aplasia characterized by severe normochromic, macrocytic anemia that usually presents early in infancy. Although most reported cases are sporadic there is evidence of inheritance, both dominant and recessive in about 12 - 25 percent of cases. The goal of this proposal is to isolate the dominant DBA gene. Because of recent evidence of genetic linkage to chromosome 19q we will first use DNA that we have collected from 5 Polish and 7 American DBA families to test this association. If this report cannot be confirmed we will perform linkage analysis on the whole genome. If evidence for linkage is found, either to chromosome 19q or to another region of the genome, we will use further polymorphic markers to fine map the region. This map will be used for a positional candidate gene approach to determine whether any likely genes are present within the mapped domain(s). Finally, we plan to examine candidate genes for mutations in affected but not unaffected family members using Southern blotting, single stranded conformation polymorphism (SSCP), and sequencing of the putative dDBA genes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: LONG ACTING ERYTHROPOIETIN PROTEINS FOR TREATING ANEMIA Principal Investigator & Institution: Cox, George N.; Bolder Biotechnology, Inc. 4056 Youngfield St Wheat Ridge, Co 800333862 Timing: Fiscal Year 2001; Project Start 1-MAY-1998; Project End 0-SEP-2003 Summary: Erythropoietin (EPO) is a kidney-derived glycoprotein hormone that stimulates red blood cell formation. Recombinant human EPO is widely used to stimulate erythropoiesis in patients with anemia and had world-wide sales in excess of $3 billion during 1997. We propose to create modified EPO proteins that are equal or superior to natural EPO at stimulating erythropoiesis in vivo, but which require less frequent dosing, on the order of once per week to once per month. During Phase I we identified sites in EPO that can be modified without affecting the protein's in vitro bioactivity. During Phase II, we will manufacture sufficient quantities of the modified EPO proteins for testing in pharmacokinetic and animal efficacy experiments. The improved characteristics of the novel EPO proteins will reduce the amount of EPO required per patient, improve patient compliance and quality of life and result in considerable cost savings to patients and healthcare providers. EPO is a member of a large family of structurally related growth factors and cytokines. Information gained from these studies will aid in creating long-acting versions of other members of this gene family for use in treating cancer, infectious disease and hematopoietic disorders. PROPOSED COMMERCIAL APPLICATIONS: Recombinant human EPO is used to restore red blood cell production in patients with anemia resulting from renal failure, chemotherapy and drug complications. Recombinant EPO had worldwide sales in excess of $3 billion in 1997. The modified EPO proteins under development will require much less frequent dosing, providing significant cost savings to patients and healthcare providers. Additional benefits may include significantly lower manufacturing costs, improved drug efficacy and improved patient quality of life. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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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 1-AUG-2001; Project End 1-JUL-2006
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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 wholebody 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 ·
Project Title: MOLECULAR ANALYSIS OF FANCONI'S ANEMIA C PROTEIN Principal Investigator & Institution: Plon, Sharon E. Assistant Professor; Molecular and Human Genetics; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 1-JUL-1995; Project End 0-JUN-2004 Summary: The long term goals of this project are to elucidate both the 'logic' and molecules involved in the genomic stability of hematopoietic cells through studies of Fanconi anemia (FA). Three FA genes have now been cloned, and the investigator is poised to ask precise questions about the organization and function of their protein products. Although the cellular phenotype of FA implicates these proteins in drugsensitive pathways as "gatekeepers" of genomic stability, their molecular functions remain incompletely understood. FANCC has a role in cellular detoxification by virtue of its interaction with NADPH cytochrome P-450 reductase (RED) and regulation of a pre-DNA damage step. FANCA is homologous to peroxidases, interacts with FANCG, and functions in the nucleus. Using cell culture yeast and mouse models, the investigator proposes to test the hypothesis that cytoplasmic FANCC-RED and nuclear
Studies 35
FANCA-FANCG complexes perform detoxification functions in their respective cellular compartments. Thus, the investigator will (I) characterize the expression patterns of FA gene products during mouse embryogenesis, including hematopoietic and germ cell development, by in situ and biochemical strategies; (II) determine the oligomeric structure and regulation of FA proteins; (III) use genetic strategies to IocaIize the function of FA proteins to pre- or post-DNA damage steps, and, in this context, test the function of the FANCA peroxidase domain; and (IV) isolate genes that regulate the FANCC-RED pathway, and characterize the relationship of this pathway to that regulated by FANCA-FANCG. Our combined genetic, cellular and biochemical approaches should result in a comprehensive view of the regulation and function of FA gene products. Aside from improving our understanding of fundamental mechanisms of cellular detoxification and chromosomal stability relevant to hematopoiesis, the manipulation of drug-sensitive pathways controlled by FA genes will provide novel translational opportunities for chemosensitization of leukemias or solid tumors to bifunctional cross-linkers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: MOLECULAR GENETICS OF FANCONI ANEMIA Principal Investigator & Institution: Moses, Robb E. Professor and Chair; Molecular and Medical Genetics; Oregon Health & Science University Portland, or 972393098 Timing: Fiscal Year 2001; Project Start 1-JUL-1994; Project End 0-JUN-2004 Summary: Fanconi anemia (FA) is an autosomal recessive disease which manifests increased risk of leukemia, regressive bone marrow failure, skeletal abnormalities, altered skin pigmentation and developmental delay. Therefore FA presents alterations in growth and development with anemia, and is an autosomal recessive disease with increased risk of cancer. There are eight complementation groups identified, indicating the involvement of multiple genes in the disease. This Program Project will use a molecular genetic approach to define the genetic elements causing Fanconi anemia and the function of the gene products in order to improve diagnosis and treatment. The concept of this project is to take a multi-disciplinary approach to the definition of the causes of Fanconi anemia at the molecular and cellular level. The clinical disciplines represented by the Investigators include medicine, pediatrics, medical genetics, hematology and oncology. The scientific areas of the investigations include molecular hematology, molecular genetics, mouse genetics, gene therapy, stem cell biology and DNA repair. The proposed project will have three investigative components and three core components: Project 1 will participate in cloning the FA-D group gene and analyze the function of the FA-D protein. Pathogenesis of FA as a result of crosslink repair defects will be tested in mouse models. Project 2 will participate in cloning FA-D and will build mouse models deficient in FA-D and FA-A gene products. Project3 will asess the apoptotic cytokine response defects in FA and define the molecular hematological defects in the mouse models. The Cytogenetics Core will test chromosome breakage in new Fanconi anemia cell line candidates and help map candidate Fanconi anemia genes. The Fanconi Anemia Cell Repository will identify Fanconi anemia cell lines for complementation testing and establish permanent cell lines for investigators as well as provide diagnostic procedures for FA patients and their providers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NEONATAL ANEMIA--PATHOPHYSIOLOGY AND TREATMENT Principal Investigator & Institution: Strauss, Ronald G. Professor Pathology/Pediatrics; Pathology; University of Iowa Iowa City, Ia 52242
of
36 Anemia
Timing: Fiscal Year 2001; Project Start 1-JUL-1992; Project End 1-MAR-2004 Summary: This application is a competitive renewal of our previous Program Project Grant (PPG) entitled "Neonatal Anemia: Pathophysiology and Treatment." The renewal is based on hypotheses developed from findings of the original PPG plus new tissues arising in neonatal hematology and transfusion medicine. Although all objectives of the original PPG have been achieve with progress reported (512 manuscripts published, 7 submitted for review, and 15 in preparation), it is important to continue studies of neonatal anemia in a PPG setting because: 1) medical science has yet to achieve a comprehensive understanding of the physiology of neonatal erythropoiesis and the pathophysiology of the anemia of prematurity; and 2) severe, transfusion-dependent anemia continues to be a problem faced daily by preterm infants-for which the efficacy, toxicity and optimal use of therapies are not clearly defined. The theme of our PPG is to optimize management of neonatal anemia- particularly, severe anemia in preterm infants that requires red blood cell (RBC) transfusions. Two strategic goals and eight objectives will be met by three projects and a core. To optimize use of recombinant human erythropoietin (EPO) in treating neonatal anemia. Project #1 will continue to investigate the physiology, pharmacokinetics (PK) and pharmacodynamics (PD) of EPO-utilizing novel methods that employ biotinylated EPO. To investigate the role of iron (Fe) availability and protein nutrition in the pathophysiology of the anemia of prematurity and to define their requirements in treating and possibly preventing neonatal anemia, Project #2 will investigate the effect of protein and graded oral Fe intakes on erythropoiesis, the effects of RBC transfusions and EPO on Fe therapy, and the efficacy and safety of intravenous Fe therapy. To determine the benefits of autologous placental blood transfusions containing mature RBCs and hematopoietic/immunologic progenitor cells, Project #3 will study the effects of delayed umbilical cord clamping or the equivalent transfusions of placental blood on maintaining neonatal blood and RBC volumes and hematopoietic/immunological development. The Core will provide administrative, statistical and research support and biotinylation laboratory services to all projects. To accomplish these goals, additional investigators, with expertise in new areas, have been recruited to complement the ongoing efforts of our established PPG group. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: NEURODEVELOPMENTAL CONSEQUENCES OF SEVERE FETAL ANEMIA W/ HYDROPS Principal Investigator & Institution: Harper, Dennis C. Professor; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2001; Project Start 1-DEC-2000; Project End 0-NOV-2001 Summary: The goal of this study is to determine if the neurodevelopmental outcome of anemic fetuses treated with intravascular blood transfusion and associated hydrops is different from matched controls. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NM1054: A NEW MURINE IRON DEFICIENCY ANEMIA MUTANT Principal Investigator & Institution: Fleming, Mark D.; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2003; Project Start 1-JUL-2003; Project End 0-JUN-2007 Summary: (provided by applicant): The characterization of spontaneous and induced mutants has proven invaluable in understanding mammalian iron metabolism. In
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particular, positional cloning of genes mutated in mouse, rat, human, and zebrafish iron deficiency and iron overload phenotypes has led to the discovery of multiple proteins that directly participate in or modify iron transport in mammals, many of which are directly relevant to understanding the pathophysiology of human diseases. Over the past several years, the generation of dense genetic and physical maps and near-complete genome sequences of mice and humans has greatly facilitated positional cloning and the rapidity in which mutants can be cloned. Here, we describe the initial phenotypic characterization of a new murine autosomal recessive hypochromic, microcytic anemia mutation, nm1054 (Dew mutation 1054). The phenotype of these animals strongly suggests an underlying defect in erythroid intracellular iron metabolism. Genetic mapping localizes the trait to mouse chromosome 1, and demonstrates that the mutant phenotype is due to a large genomic deletion that includes at least 5 genes. In this grant, we propose to evaluate the hypothesis that nm1054 is a defect in intraerythroid iron metabolism using bone marrow transplantation studies and in vitro iron uptake assays. Furthermore, we will clone the nm1054 anemia gene using bacterial artificial chromosome (BAC) and cDNA transgenic complementation. We expect that determining which of the deleted genes is responsible for the anemia will provide insight into the pathway of iron delivery and utilization in mammalian cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: OLIGONUCLEOTIDE BASED GENE THERAPY FOR SICKLE CELL ANEMIA Principal Investigator & Institution: Wang, Gan; Associate Professor; University of South Alabama Mobile, Al 366880002 Timing: Fiscal Year 2001 Summary: (Adapted from the Applicant's Abstract) Sickle cell anemia is the prototype of a genetic disease caused by a single base-pair mutation, an A-to-T transversion in the sixth codon of the human globin gene. At low oxygen tensions, the substitution of a single amino acid (GLU>Val) in the beta-globin subunit of hemoglobin results in a polymerization of HB S and leads to irregular shaped erythrocyte cells. The sickled erythrocyte cells become trapped n the microcirculation, causing extreme pain and damage to multiple organs. The investigators propose to test the hypothesis that triplexforming oligonucleotides linked to mutagenic agents can be used to generate mutations in betaS and gamma-globin genes to inhibit the polymerization of HB S within erythrocyte cells and this may be utilized in gene therapy for sickle cell diseases. SV40based shuttle vectors carrying the target genes will be constructed; an improved mammalian cell mutation assay system will be developed to facilitate the study of triplex-directed mutagenesis of the genes in vivo; oligonucleotides that bind to target sites will be designed and synthesized; oligonucleotide characteristics (such as nucleotide composition, chemical modifications, and analog substitutions) and targeted mutagenesis will be examined. Finally, experiments will be carried out to direct test the hypothesis that targeted mutagenesis of betaS and gamma-globin genes mediated by triplex-forming oligonucleotides can be achieved in vivo in the chromosomal DNA of mammalian cells in culture. The ultimate goal is the delivery of mutagenic oligonucleotides to bone marrow cells and the introduction of permanent and inheritable mutations into desired sites of the betaS and/or gamma-globin gene so that the polymerization of Hb S within cells will be inhibited. Although it may be some time before this technology is applied clinically, this grant application proposes a body of work to establish the potential for the role of targeted mutagenesis in both clinical and scientific endeavors.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: OPTIMIZING STROKE PREVENTION IN SC ANEMIA CHILDREN Principal Investigator & Institution: Adams, Robert J. Neurology; Medical College of Georgia 1120 15Th St Augusta, Ga 30912 Timing: Fiscal Year 2001; Project Start 5-JUL-1994; Project End 0-JUN-2005 Summary: (Adapted from the applicant's abstract) Stroke occurs in approximately 11% of children with homozygous sickle cell anemia by 20 years of age. Recently, The Stroke Prevention Trial in Sickle Cell Anemia (STOP) showed that high-risk patients can be identified with transcranial Doppler (TCD) ultrasound and that periodic blood transfusions can reduce the annual incidence of first time stroke in high-risk patients from 10% to 200 cm/sec) or clinical stroke. Patients who revert to high risk will be offered return to transfusion. TCD, magnetic resonance studies, key laboratory measures and endpoints will be read and/or adjudicated using centralized blinded procedures proved successful in STOP. Assuming the annual endpoint rate on transfusion remains at 10% after halting transfusion. This research will optimize the primary prevention strategy proven effective in STOP with significant potential for children with sickle cell anemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: OPTIMIZING STROKE PREVENTION IN SICKLE CELL ANEMIA Principal Investigator & Institution: Brambilla, Donald J. Principal Research Scientist; New England Research Institutes, Inc. 9 Galen St Watertown, Ma 02472 Timing: Fiscal Year 2001; Project Start 5-JUL-1994; Project End 0-JUN-2005 Summary: (Adapted from the applicant's abstract) Stroke occurs in approximately 11% of children with homozygous sickle cell anemia by 20 years of age. Recently, The Stroke Prevention Trial in Sickle Cell Anemia (STOP) showed that high-risk patients can be identified with transcranial Doppler (TCD) ultrasound and that periodic blood transfusions can reduce the annual incidence of first time stroke in high-risk patients from 10% to 200 cm/sec) or clinical stroke. Patients who revert to high risk will be offered return to transfusion. TCD, magnetic resonance studies, key laboratory measures and endpoints will be read and/or adjudicated using centralized blinded procedures proved successful in STOP. Assuming the annual endpoint rate on transfusion remains at 10% after halting transfusion. This research will optimize the primary prevention strategy proven effective in STOP with significant potential for children with sickle cell anemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ORAL L GLUTAMINE THERAPY FOR SICKLE CELL ANEMIA Principal Investigator & Institution: Niihara, Yutaka;; Harbor-Ucla Research & Educ Inst 1124 W Carson St Torrance, Ca 90502 Timing: Fiscal Year 2001; Project Start 0-APR-1998; Project End 1-MAR-2002 Summary: Sickle cell anemia is one of the most common and devastating hereditary disorders with significant morbidity and mortality affecting individuals of African American heritage. No safe, effective therapy is yet available. Within the last few years, hydroxyurea has been used in an increasing number of sickle cell anemia patients. However, hydroxyurea is a chemotherapeutic agent with myelosuppressive effects and its long term safety is still unknown. An ideal agent would be one that is readily
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available, effective and safe even with chronic use. Based on previous data from this laboratory on sickle red blood cell metabolism, we have conducted a pilot study recently using L-glutamine as an oral agent. The four week open label study involving seven homozygous hemoglobin S patients showed promising results by demonstrating improvement in redox potential and decrease in chronic pain in all patients. In addition a subsequent 12 week study involving 4 patients showed significant decrease in the frequency of painful sickle crises. On the basis of these data we propose to expand the study of L-glutamine therapy for sickle cell anemia to a double blind study to observe objectively the effect of the amino acid in sickle cell anemia patients in terms of their clinical status and hematological parameters. Our long term goal is to establish the usefulness and safety of L-glutamine in therapy of sickle cell anemia. Our specific aims in this project are to determine the effect of oral L-glutamine on 1) sickle red blood cells at cellular and biochemical level, 2) clinical status of the sickle cell anemia patients including the incidence of painful crisis, narcotic requirement for acute or chronic pain, 3) sickle cell anemia patients' hematological parameters including hemoglobin, hematocrit, reticulocyte count,and hexokinase level, and 4) adverse effects attributable to L-glutamine. L-glutamine is an amino acid that has been used widely for other purposes and shown to be safe by others. It is also inexpensive and readily available. The pilot data are promising. This project will provide the pathophysiologic basis for the use of L-glutamine and will evaluate the efficacy of L-glutamine in the therapy of sickle cell anemia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: ORAL SODIUM PHENYLBUTYRATE THERAPY FOR CHILDREN WITH SICKLE CELL ANEMIA Principal Investigator & Institution: Resar, Linda;; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001 Summary: This research proposal is designed to test whether sodium phenylbutyrate (SPB) will increase fetal hemoglobin (HbF) in children with sickle cell anemia & thereby ameliorate complications from their disease. Red blood cell sickling occurs in patients with sickle cell anmia because deoxygenated hemoglobin S(HbS) aggregates into rigid, rod-like polymers. The normal bi-concave red blood cell disc assumes a sickle shape, which is much less deformable & tends to fragment in the circulation. Moreover, abnormal membraane properties cause adherence to the vascular endothelium. The combination of these physical abnormalities give rise to the anemia & vaso-occlusive phenomenon associated with the disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PATHOGENESIS AND THERAPY OF MALARIAL ANEMIA IN THAILAND Principal Investigator & Institution: Looaresuwan, Sornchai;; Mahidol University C/O Siriraj Hospital, Dhonburi Bangkok, Timing: Fiscal Year 2001; Project Start 5-JUL-2001; Project End 0-JUN-2002 Summary: The proposed Tropical Medicine Research Center (TMRC) will build upon an established, productive and internationally recognized research program in malaria at the Faculty of Tropical Medicine, Mahidol University, and the National Science and Technology Developmental Agency (NSTDA) in Bangkok, Thailand, in a multidisciplinary collaborative project designed to characterize the pathophysiology and
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therapy of malaria anemia in Thailand. Malaria provides the paradigm for a disease that has shaped the human genome through natural selection of protective genetic traits. More genes have now been implicated in variability of susceptibility to malaria than to any other infections or non- infectious disease of humans. Genes now recognized as affecting the host response to malaria include those for hemoglobin variants, for red blood cell enzymes, components of the membrane cytoskeleton, membrane receptors and blood group proteins, as well as loci that modulate immune responses or are involved in underlying pathophysiologic processes. To determine the roles of immunogenetic determinants of malaria anemia and of genetic factors altering response to anti-malarial therapy, a program of interrelated basic and clinical research projects has been developed. The specific aims of the three component projects are: Project 1: to assess the effect of genetic determinants of host response on malarial anemia in three prospective clinical investigations: (i) a population-based study in Suan Phung village, Ratchaburi Province, (ii) a case-control study in Bongti, Kanchanburi, and (iii) a hospital-based study in Bangkok; Project 2: to determine if excessive activity of the T helper lymphocyte type 1 (Th-1) immune response and decreased activity of the Th-2 immune response are involved in the pathogenesis of severe anemia and children and adults with Plasmodium falciparum malaria; and Project 3: to determine the role of host genetic factors in artemisinin action. The three component projects will share common resources provided by two scientific core facilities: the Genetic Core Unit and the Central Laboratory and Data Coordinating Core Unit. The overall goal of the proposed research is to provide fundamental new insights about genetic and immunological determinants of both host resistance to malaria and host response to anti-malarial therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PATHOGENESIS AND THERAPY OF SIDEROBLASTIC ANEMIA Principal Investigator & Institution: Friedman, Jeffrey S. Skirball Institute; New York University School of Medicine 550 1St Ave New York, Ny 10016 Timing: Fiscal Year 2003; Project Start 1-MAR-2003; Project End 0-JUN-2003 Summary: Abstract: Pathoqenesis and Therapy of Sideroblastic Anemia: We have recently reported on a novel murine anemia caused by deficiency of superoxide dismutase 2 (SOD2), that bears striking similarity to human sideroblastic anemia (SA). SA is a morphologically distinct group of disorders characterized by accumulation of excess iron within red cells during development. Genetic lesions responsible for several subtypes of SA have been recently elucidated, and in each case highlight the importance of mitochondria as a locus for heme biosynthesis, iron transport or iron homeostasis in developing red blood cells. SOD2, is a critical intra-mitochondrial catalytic ant/oxidant, and deficiency of this enzyme leads to late embryonic or neonatal lethality in mice, with pathologic evidence of widespread mitochondrial dysfunction including myopathy, neuropathy and metabolic derangement. In order to study cell-autonomous effects of SOD2 deficiency, we devised a transplantation system in which hematopeietic stem cells (HSC) from Sod2 null embryos were used to reconstitute the immune and hematopoietic tissues of lethally irradiated host animals, and found that a major phenotype resulting from loss of SOD2 is a hemolytic anemia. This result suggested that mitochondrial dysfunction secondary to increased oxidative stress, or perhaps direct oxidation of key target proteins during red cell development, may be central to the pathogenesis of SA. The importance of oxidative damage in this model of SA was further highlighted by the dramatic response to therapy with a novel class of ant/oxidants, catalytic SOD/catalase mimetics. A primary focus of this proposal is detailed characterization of pathology,
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biochemistry and protein/gene expression profiles in order to identify key molecular targets affected by loss of SOD2. A secondary focus is to document how catalytic ant/oxidant therapy affects this 'pathogenetic profile.' In parallel, we will examine gene expression profiles from marrow erythroid progenitors of SA patients, in part to classify this heterogeneous disorder, and in part to look for overlap with SOD2 deficiency. These studies will help to elucidate whether increased oxidative stress is a characteristic of SA, and thereby provide guidance as to the potential role of ant/oxidants as therapy for this disorder. The techniques developed in the course of this study--evaluation of protein oxidation and methods for purification of oxidized proteins--will provide tools for answering more general questions regarding the role of protein oxidation in other types of hemolytic processes, and as a determinant of survival of normal erythrocytes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PATHOPHYSIOLOGY OF THIAMINE-RESPONSIVE ANEMIA SYNDROME Principal Investigator & Institution: Neufeld, Ellis J. Associate Professor of Pediatrics; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2002; Project Start 1-DEC-2001; Project End 0-NOV-2006 Summary: (provided by applicant): The goal of this proposal is to determine the pathophysiology of the autosomal recessive disorder. Thiamine-Responsive Megaloblastic Anemia (TRMA). Patients with TRMA exhibit unique, vitamin-responsive anemia, as well as progressive sensorineural deafness and non-type I diabetes responsive in part to pharmacologic doses of thiamine. Fibroblasts from TRMA patients are sensitive to thiamine deprivation in culture, and undergo apoptotic cell death in thiamine concentrations less than 9 nM. Normal fibroblasts exhibit high affinity (nanomolar) thiamine uptake, whereas mutant cells do not. The gene defective in TRMA was mapped and cloned. It encodes a high-affinity thiamine transporter, a member of the solute carrier family. designated SLC19A2. In all known TRMA patients, homozygous defects in the SLCI9A2 gene have been identified. However, the basis of the disease phenotype remains obscure. The anemia of TRMA reveals both megaloblastic changes and ringed sideroblasts, reminiscent of acquired Myelodysplastic Syndromes. The bases of anemia, deafness and diabetes in TRMA are obscure. Our working hypothesis is that the defective thiamine transporter of TRMA results in intracellular metabolic changes responsible for features of the disease. The goals of the current proposal are: (1) To characterize the high-affinity thiamine transporter and its role in thiamine dependent metabolic pathways in TRMA and control cells in tissue culture. Synthesis and distribution of SLC19A2 protein will be studied, and metabolic pathways assessed by GC/mass spectroscopy analysis of stable isotope-tagged glucose metabolites. (2) To characterize high affinity thiamine transport and its role in mice, targeted disruption of the SLCI9A2 gene will be used to create an animal model for human pathophysiology. (3) To examine the role of thiamine transport system in hematopoiesis, using murine marrow from normal and TRMA animals. Clearer understanding of the role of the thiamine transporter will help to elucidate the basis of multi-organ system disease in TRMA, and improve fundamental understanding of the role of thiamine and thiamine transport in normal hematopoiesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PEDIATRICS:CHLAMYDIA, SICKLE CELL ANEMIA AND STROKE RISK Principal Investigator & Institution: Styles, Lori A. Associate Heatologist; Children's Hospital & Res Ctr at Oakland Research Center at Oakland Oakland, Ca 94609 Timing: Fiscal Year 2001; Project Start 4-SEP-2001; Project End 0-JUN-2005 Summary: (provided by applicant): Infection with Chlamydia pneumoniae (C. pneumoniae) is associated with an increased risk of cerebrovascular disease in the general population. Children with sickle cell anemia (SCA) are 200 times more likely to have cerebrovascular disease than normal children and are known to have an altered immune response to many infectious pathogens. C. pneumoniae is the leading infectious cause of acute chest syndrome which, interestingly, is a well- established risk factor for stroke in children with SCA. Our preliminary data indicates that SCA patients with MRI-documented cerebral infarction are 12 times more likely to have C. pneumoniae infection than SCA patients with normal MRI scans. We hypothesize that SCA patients have an abnormal immune response to C. pneumoniae that results in persistent infection which, in turn, triggers the development of cerebrovascular disease. Sickle cell anemia patients with an elevated velocity on transcranial doppler ultrasound (TCD) are known to be at high risk to develop stroke and an elevated TCD likely reflects underlying vascular disease. In addition, the Stroke Prevention in Sickle Cell Anemia Trial (STOP) demonstrated that almost 40% of children with an elevated TCD have evidence of cerebral infarction on MRI. Children with abnormal TCDs are, therefore, an appropriated population to investigate an association between cerebrovascular disease and C. pneumoniae infection. As an ancillary study of the STOP II trial we propose 1) To determine if C. pneumoniae infection is associated with cerebral infarction in children with SCA; 2) To characterize the immunological response to C. pneumoniae infection in patients with SCA. Establishing a link between C. pneumoniae infection and cerebral infarction will open the door to novel, less toxic approaches to the treatment and prevention of stroke in SCA, including antibiotics and vaccines. The data gained in this proposal would provide the preliminary data necessary to justify further clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PHYSIPATOGENESIS OF MALARIA ANEMIA IN HUMANS & MONKEYS Principal Investigator & Institution: Herrera, Socrates;; University of Valle Apdo, Aereo 2188 Cali, Timing: Fiscal Year 2002; Project Start 7-JUN-2002; Project End 8-FEB-2006 Summary: (adapted from the application): The purpose of the training described in this proposal is to make optimal use of the possibility to conduct comparative studies between malaria developed by humans in natural conditions and anemia induced by experimental malaria infection in monkeys. Aotus monkeys represent a very valuable model to study the physio-pathogenesis of anemia, particularly when it is associated to vaccination. Previous studies conducted by our group and by others, indicate that severe anemia develops in Aotus monkeys during the course of pre-clinical malaria vaccine trials. Our TMRC program will include the study of human communities naturally exposed to both P. falciparum and P. vivax transmission. We plan to approach a lack of information concerning the prevalence of anemia in those communities, the factors associated to its production such as those related to nutrition and to genetic features (i.e. Hemoglobinopathies). We propose to carry out training activities that cover from long term training of Colombian and Latin American graduate and post-doc
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students to short term seminars, workshops and summer courses for basic - scientists, clinicians and health workers. Clinical rotations will be offered to clinicians from malaria endemic areas in order to improve their skills in diagnosis and management of severe malaria, particularly severe anemia. Furthermore, we plan to establish a Web Site for Anemia. One of the most cost-effective activities in this training program, may be the workshops planned to be organized jointly with the Ministries of Health and PAHO. These workshops will approach the most relevant issues selected by the RollBack Malaria program. The training sites and facilities include those of the TMRC program that comprises: a) A field-site with clinical and research laboratories, insectaries and a second level hospital. b) A set of laboratories for molecular biology, immunology, protein chemistry, and parasite in vitro cultures. c) A primate center with both Aotus and Saimiri monkeys. d) Two third-level hospitals located in Cali. All these facilities and the activities developed in them will be coordinated by the Administrative and Visiting Scientist Cores of the TMRC. The teaching staff involves immunologists, hematologists, epidemiologist, statisticians, infectious diseases - specialists, pediatricians and pathologists. We will combine expertise of well-known scientists from Colombia, Brazil, Venezuela and the USA. A number of collaborating scientists and institutions from Colombia and other malaria endemic countries of Latin America, have been contacted and will provide trainee candidates. Trainee candidates will be selected on a competitive basis and an evaluation of outcome is proposed at the end of each yearly period, during the Training Advisory Group (TAG) meeting. These activities will profit from a long tradition of international training developed at the School of Health of Universidad del Valle, in Cali. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PLASMODIUM FALCIPARUM-INDUCED ANEMIA IN AOTUS MONKEYS Principal Investigator & Institution: Jones, Trevor R. Captain, Medical Service Corps; Naval Medical Research Center 503 Robert Grant Ave Silver Spring, Md 20910 Timing: Fiscal Year 2002; Project Start 0-SEP-2002; Project End 0-JUN-2003 Summary: (provided by applicant): Long-Term Objective: In two recent Aotus monkey vaccine studies using DNA and/or recombinant protein vaccines based on P. falciparum blood stage antigens, an unexpectedly high incidence of severe anemia was noted in the animals after they were challenged with blood-stage P. falciparum parasites. A clear understanding of the mechanism of anemia induction in these studies is critical to evaluating the risk of immunizing humans exposed to malaria with vaccines based on P. falciparum blood stage antigens. Specific Aims: 1) Establish two anemia models in P. falciparum-immunized Aotus; one vaccine-related and one not. 2) Determine whether chronic parasitemia induced by partial drug treatment leads to the same degree of anemia as is seen in the immunized, challenged animals. 3) Determine the relative importance and mechanisms of increased erythrocyte destruction/sequestration versus decreased erythropoiesis in these models. 4) Determine whether there is any association between vaccine-induced immune responses and the risk of anemia after challenge. 5) Determine whether increasing the efficacy of the vaccines can reduce the risk of anemia. Research Design and Methods: 1) Develop a reliable P. falciparum malaria anemia model in Aotus monkeys immunized with bloodstage P. falciparum vaccines, and a control model using sub-optimal drug treatment to maintain a low-density parasitemia. 2) Characterize the anemia models to determine whether parasites cause bone marrow dysfunction by parasite density affecting reticulocyte count independently of hematocrit. Determine whether parasites cause
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bone marrow dysfunction that affects blood cells other than reticulocytes. Determine whether parasite density is important to any alternations to bone marrow function. Determine whether parasitized erythrocytes being sequestered, lysed, or both. 3) Discover correlates of anemia. Determine whether the presence and degree of anemia correlates with spleen size, the presence of erythrocyte surface IgG or complement C3d, serum antibodies to the vaccine, serum antibodies to whole blood-stage parasites, circulating levels of erythropoietin, TNF-a. and IL10. 4) Measure erythrocyte survival and erythrocyte volume studies by evaluating the life span of biotinylated Aotus erythrocytes in immunized and non-immunized anemic monkeys. 5) Evaluate the effect of splenectomy on maintenance of anemia. 6) Evaluate ability of heat-killed parasites to induce anemia. 7) Compare bone marrow responses in immunized animals to bone marrow responses in monkeys rendered anemic by phlebotomy (anemia unrelated to both immunity and P. falciparum infection). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: PLEIOTROPIC AND EPISTATIC EFFECTS IN SICKLE CELL ANEMIA Principal Investigator & Institution: Nagel, Ronald L. Professor and Head; Medicine; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2001; Project Start 0-SEP-2001; Project End 1-JUL-2006 Summary: (provided by applicant): Sickle cell anemia (SCA) is the paradigmatic monogenic disease, but the sickle mutation is not sufficient to define the phenotype. Pleiotropic effects influence complications. Secondly, SCA exhibits an intense interindividual variability, which is likely to be the effect of epistatic genes, since heritability of major determinants of severity exhibit high concordance in monozygote twins (89%). The aim of this project is to define the epistatic/pleiotropic genes involved in sickle-cell mediated vaso-occlusion in different organs, building on our years of working on the genetics and pathophysiology of this problem in mice and men. We will engage in the detection of genes involved in sickle cell-mediated vaso-occlusion in animal models, in the detection of genes involved in sickle cell-mediated vaso-occlusion in patients with sickle cell anemia and in the detection of genes involved in vaso-occlusive and vasoproliferative processes in sickle cell retina and choroid and in cerebrovascular complications in sickle cell anemia, which our previous work has defined as a special case. The experimental design is the following: Approach 1: Appropriate tissues in sickle transgenic mice and other animal models -+ RNA -+ expression chips -> select the higher express genes and the lower expressing genes vs control -+ BLAST --> the selected human genes will be analyzed for potential epistatic effects by SNP arrays and by sequencing to define polymorphism in appropriately defined human sickle cell anemia DNA samples. Approach 2: In the complications without animal models, but candidate genes based on human pathophysiological data, SNPs and sequencing analyzes will be performed in sickle cell anemia patients with a particular complication vs sickle cell anemia patients without it. Of course, appropriate matching age groups will be selected to assure that the complication is no longer possible in the control group. Genes defined by these two approaches will be followed in animal models when available (KO or over expression, or generated for further confirmation. Members of this proposal have special expertise in retinal, cerebro-vascular problems and statistical analysis. Our institution has well established expertise in transgenic mice, microcirculatory preparations, hemopoiesis and patient follow-up, as a well as experienced SNP, sequencing and CHIP expression facilities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PREVENTION OF ANEMIA IN PREMATURE INFANTS BY IN LINE MONITORING Principal Investigator & Institution: Madan, Ashima;; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001 Summary: This is a collaborative study with Dr. John A. Widness, the Associate Program Director of the GCRC at the University of Iowa and Drs. Stevenson and Madan at Stanford who all have a long-standing interest in anemia. The purpose of this study is to determine whether the use of an ex-vivo monitoring device, the VIA Low Volume Mode ( LVM ) Monitor, can prevent anemia and therefore reduce the blood transfusion rate in premature infants below a birthweight of 1000 grams ( VLBW ), compared to those who get conventional laboratory testing. Improvement will be manifest by a 50% decrease in 1.) the number of RBC transfusions received in the first two weeks of life while in-line monitor is in use (primary hypothesis ) and 2.) phlebotomy loss in the first week of life (secondary hypothesis ). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PRIMAQUINE-INDUCED HEMOLYTIC ANEMIA Principal Investigator & Institution: Mc Millan, David C. Pharmacology; Medical University of South Carolina 171 Ashley Ave Charleston, Sc 29425 Timing: Fiscal Year 2001; Project Start 1-JAN-2001; Project End 1-DEC-2004 Summary: (Adapted from the Applicant's Abstract): Malaria is recognized as the most widespread parasitic infection in humans. Primaquine has been a major antimalarial drug for over 40 years due to its unique effectiveness against exoerythrocytic forms of the parasite. Its therapeutic value has grown in recent years with the development of resistance to alternate antimalarial drugs such as chloroquine and because of its utility in the treatment of Pneumocystis carinii pneumonia in AIDS patients. However, primaquine therapy has been severely limited because of its capacity to induce methemoglobinemia and hemolytic anemia, particularly in patients with glucose-6phosphate dehydrogenase deficiency. It has long been known that the hemotoxicity of primaquine is due to the action of metabolites and not the parent compound. However, the toxic specie(s) have not been identified and little is known about the mechanism underlying red cell injury. In collaborative studies with individuals at Walter Reed, we have examined the hemotoxicity of known and putative phenolic metabolites of primaquine and have observed potent and direct-acting hemotoxicity. In other studies, we have synthesized 6-methoxy-8-hydroxylaminoquinoline (MAQ-NOH) and found that this metabolite was also a direct-acting hemotoxicant. We now propose to investigate the mechanism of red cell damage induced by these metabolites and examine their metabolic formation in vitro. The hypotheses under test in this proposal are: 1) that two pathways of oxidative damage, initiated by lipid peroxidation and protein thiol oxidation, occur in the red cell; and 2) that quinone/quinoneimine metabolites act via lipid peroxidation, whereas the N-hydroxy metabolite acts via protein thiol oxidation. Three aims are presented: 1) to characterize the hemolytic response and pattern of oxidative injury induced within red cells by each type of primaquine metabolite; 2) to elucidate the oxidative metabolism of primaquine in rat and human liver microsomes and hepatocytes, and identify GYP isoforms responsible for primaquine metabolism; and 3) to identify intracellular and external cell surface alterations that correlate with phagocytosis of primaquine metabolite-damaged red cells by cultured splenic macrophages.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen ·
Project Title: QUESTIONS TO DETERMINE RISK OF IRON DEFICIENCY ANEMIA IN YOUNG CHILDREN Principal Investigator & Institution: Wilson, Modena;; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001 Summary: Iron deficiency anemia (IDA) is an important issue for children because of its many serious health effects. It is associated with dimished cognitive function, delayed infant growth and development, decreased exercise tolerance, and impaired immune function. Iron deficiency anemia has been shown to cause changes in behavior and to lower developmental test scores in infance. Poverty is an important risk factor for IDA and, in Baltimore City, 32% of all children live in poverty. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RHESUS MONKEY MODEL FOR HUMAN B19 PARVOVIRUS INFECT: HEMOLYTIC ANEMIA Principal Investigator & Institution: Traina-Dorge, Vicki L.; Tulane University of Louisiana New Orleans, La 70118 Timing: Fiscal Year 2001 Summary: Parvovirus infection is responsible for erythema infectiosum (Fifth?s disease) in children and aplastic crisis, hemolytic anemias, and fetal death, as well as a rheumatic syndrome in adults. It is also reported to be responsible for anemias, fevers, pneumonitis, and aplastic crisis in AIDS patients. The human B19 parvovirus is most commonly implicated. Little is known about B19 due to its difficult in vitro propagation. Histologic evidence was shown in the bone marrow of a severely anemic rhesus monkey with advanced SIV immunodeficiency disease and suggested parvovirus infection in the rhesus as well. Bone marrow and other tissues from this animal were collected and cryopreserved. A pilot study was conducted to determine whether we could reisolate virus as well as reproduce the disease, and whether immunodeficient animal would more readily progress to disease, and if SIV is a cofactor of disease. We developed a molecular PCR assay for diagnosis of infection. Six animals were inoculated intravenously with the bone marrow preparation. 2of 3 naive animals not only developed progressive SIV immunodeficiency disease, but also severe anemia coincident with high reticulocytes and Parvovirus viremia the time of necropsy. The 3 previously SIV-infected animals, however, had only one animal progress to SIV disease, but none became anemic. A second study was then conducted with six additional SIV infected animals. Only two of six became infected and viremic. One animal progressed to disease, and Parvovirus was documented at necropsy, however, again no anemia was apparent. We are following the other animal for signs of SIV disease and/or anemia. This resistance to disease progression in the previously infected SIV animals was observed in both studies. It may be due to a lack of severe immunodeficiency from the original SIV. These animals were relatively stable, having all been infected with SIV for 1.5years or greater. In addition, they appear resistance to superinfection with the second SIV strain in the bone marrow inoculum, which had a more rapid disease course in the naive animals. FUNDING Base Grant, Venture Research. PUBLICATIONS None Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF IMMUNE COMPLEX IN SEVERE MALARIAL ANEMIA Principal Investigator & Institution: Stoute, Jose A.; Henry M. Jackson Fdn for the Adv Mil/Med Rockville, Md 20852 Timing: Fiscal Year 2002; Project Start 5-AUG-2002; Project End 0-JUN-2006 Summary: (provided by applicant): Severe anemia is one of the deadliest complications in children infected with Plasmodium falciparum in sub- Saharan Africa. This anemia cannot be accounted for solely on the basis of destruction of parasitized RBCs. Therefore, the long-term objective of this application is to identify the pathogenic mechanisms that lead to severe malarial anemia and that involve destruction of uninfected RBCs. Children with severe malarial anemia have acquired deficiencies of RBC complement regulatory proteins (CRPs) (CRl and CD55) and the expression of these proteins is age-dependent, being lowest among children with the highest risk of anemia. Other reported abnormalities in children with severe malarial anemia are the excessive production of immune complexes (ICs), pro-inflammatory cytokines and nitric oxide (NO). Preliminary data indicate that ICs contribute to the inflammatory response during malaria infection and that RBC CRl plays a crucial role in modulating the production of pro-inflammatory cytokines and NO in response to ICs. We postulate the following: 1) RBCs of children with severe malarial anemia are more susceptible to complement-mediated lysis than those of children with uncomplicated malaria due to deficiencies in RBC CR1 and CD55. 2) The level of pro-inflammatory cytokine and NO produced during malaria infection is modulated by the capacity of RBCs to bind and remove immune complexes from circulation. 3) There are no qualitative differences between ICs formed in children with severe malarial anemia and those formed in children with uncomplicated malaria. In the present application we propose to test these hypotheses by carrying out case-control and cross-sectional studies to determine if RBCs of children with severe malarial anemia have increased susceptibility to complementmediated lysis and decreased capacity to bind IC, and whether these parameters change as CRP expression changes with age. The studies proposed here will advance our understanding of the role of ICs and CRPs in the pathogenesis of severe malarial anemia, and of the nature of the ICs that form during malaria infection and their implications for the safety of future experimental malaria vaccines in children. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF IMMUNE RESPONSE IN SEVERE MALARIAL ANEMIA Principal Investigator & Institution: Udomsangpetch, Rachanee;; Mahidol University C/O Siriraj Hospital, Dhonburi Bangkok, Timing: Fiscal Year 2001; Project Start 5-JUL-2001; Project End 0-JUN-2002 Summary: The proposed research is designed to determine if excessive activity of the T helper lymphocyte type 1 (Th-1) immune response and decreased activity of the Th-2 immune response are involved in the pathogenesis of severe anemia in children and adults with Plasmodium falciparum malaria. Severe malarial anemia (hemoglobin A, 190G>A, and GAC deletion) associated with hereditary nonspherocytic hemolytic anemia. Author(s): Corrons JL, Garcia E, Tusell JJ, Varughese KI, West C, Beutler E. Source: Blood. 2003 July 1; 102(1): 353-6. Epub 2003 March 20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649162&dopt=Abstract
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Red cell carbohydrate metabolism in primary refractory anemias. Author(s): Palek J, Brabec V, Mircevova L, Volek V, Friedmann B. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1967 October; 18(1): 39-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6064691&dopt=Abstract
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Red cell distribution width in the diagnosis of iron deficiency anemia. Author(s): Viswanath D, Hegde R, Murthy V, Nagashree S, Shah R. Source: Indian J Pediatr. 2001 December; 68(12): 1117-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11838564&dopt=Abstract
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Red cell I antigen as immune complex receptor in drug-induced hemolytic anemias. Author(s): Duran-Suarez JR, Martin-Vega C, Argelagues E, Massuet L, Ribera A, Triginer J. Source: Vox Sanguinis. 1981 November-December; 41(5-6): 313-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7324446&dopt=Abstract
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Red cell membrane phosphatidylinositol kinase activity in hemolytic anemias and myeloproliferative diseases. Author(s): Boivin P, Galand C. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1989 June 30; 182(2): 165-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2550165&dopt=Abstract
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Red cell membrane protein phosphorylation in hemolytic anemias and muscular dystrophies. Author(s): Tsung PK, Palek J. Source: Muscle & Nerve. 1980 January-February; 3(1): 55-69. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6246419&dopt=Abstract
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Red cell membrane skeletal defects in hereditary and acquired hemolytic anemias. Author(s): Palek J, Lux SE. Source: Semin Hematol. 1983 July; 20(3): 189-224. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6353590&dopt=Abstract
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Reduced kidney function and anemia as risk factors for mortality in patients with left ventricular dysfunction. Author(s): Al-Ahmad A, Rand WM, Manjunath G, Konstam MA, Salem DN, Levey AS, Sarnak MJ. Source: Journal of the American College of Cardiology. 2001 October; 38(4): 955-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11583864&dopt=Abstract
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Reduced serum hydroxyl radical scavenging activity in erythropoietin therapy resistant renal anemia. Author(s): Hirayama A, Nagase S, Gotoh M, Ueda A, Ishizu T, Yoh K, Aoyagi K, Terao J, Koyama A. Source: Free Radical Research. 2002 November; 36(11): 1155-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592667&dopt=Abstract
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Reduced toxicity and prompt engraftment after minimal conditioning of a patient with Fanconi anemia undergoing hematopoietic stem cell transplantation from an HLA-matched unrelated donor. Author(s): Kurre P, Pulsipher M, Woolfrey A, Maris M, Sandmaier B, Kiem HP, Storb R. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 July; 25(7): 581-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847331&dopt=Abstract
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Reduction of cisplatin-induced anemia by the pineal indole 5-methoxytryptamine in metastatic lung cancer patients. Author(s): Lissoni P, Malugani F, Bukovec R, Bordin V, Perego M, Mengo S, Ardizzoia A, Tancini G. Source: Neuroendocrinol Lett. 2003 February-April; 24(1-2): 83-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743539&dopt=Abstract
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Re-evaluation of refractory anemia with excess blasts in transformation. Author(s): Ohyashiki K, Nishimaki J, Shoji N, Miyazawa K, Kimura Y, Ohyashiki JH. Source: Leukemia Research. 2001 November; 25(11): 933-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11597728&dopt=Abstract
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Refractory anemia with excess of blast cells: prognostic factors and effect of treatment with androgens or cytosine arabinoside. Results of a prospective trial in 58 patients. Cooperative Group for the Study of Aplastic and Refractory Anemias. Author(s): Najean Y, Pecking A. Source: Cancer. 1979 December; 44(6): 1976-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=389402&dopt=Abstract
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Refractory anemia with excess of blasts in transformation: a dying category? Author(s): Germing U, Gattermann N. Source: Leukemia Research. 2001 December; 25(12): 1095-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11684282&dopt=Abstract
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Refractory anemia with excess of blasts in transformation: analysis of reclassification according to the WHO proposals. Author(s): Strupp C, Gattermann N, Giagounidis A, Aul C, Hildebrandt B, Haas R, Germing U. Source: Leukemia Research. 2003 May; 27(5): 397-404. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12620291&dopt=Abstract
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Refractory anemia with ring sideroblasts associated with i(17q) and mutation of the TP53 gene. Author(s): Lazarevic V, Djordjevic V, Magic Z, Marisavljevic D, Colovic M. Source: Cancer Genetics and Cytogenetics. 2002 July 1; 136(1): 86-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12165459&dopt=Abstract
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Refractory anemia with ringed sideroblasts with a low IPSS score progressed rapidly with de novo appearance of multiple karyotypic abnormalities and into acute erythroleukemia (AML-M6A). Author(s): Iwase O, Iwama H, Okabe S, Ando K, Yaguchi M, Miyazawa K, Kimura Y, Kodama A, Fukutake K, Ohyashiki K. Source: Leukemia Research. 2000 July; 24(7): 597-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10867135&dopt=Abstract
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Refractory anemias, pre-leukemia and myelodysplasias. Author(s): Silver RT. Source: Revista Do Hospital Das Clinicas. 1985 November-December; 40(6): 266-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3836481&dopt=Abstract
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Refractory anemias. Author(s): Heller P, Fried W. Source: Disease-A-Month : Dm. 1967 April; : 3-38. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4859724&dopt=Abstract
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Refractory iron deficiency anemia as the primary clinical manifestation of celiac disease. Author(s): Mody RJ, Brown PI, Wechsler DS. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 February; 25(2): 169-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571473&dopt=Abstract
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Regular consumption of NaFeEDTA-fortified fish sauce improves iron status and reduces the prevalence of anemia in anemic Vietnamese women. Author(s): Thuy PV, Berger J, Davidsson L, Khan NC, Lam NT, Cook JD, Hurrell RF, Khoi HH. Source: The American Journal of Clinical Nutrition. 2003 August; 78(2): 284-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885710&dopt=Abstract
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Regulation of the Fanconi anemia pathway by monoubiquitination. Author(s): Gregory RC, Taniguchi T, D'Andrea AD. Source: Seminars in Cancer Biology. 2003 February; 13(1): 77-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507559&dopt=Abstract
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Relapse after allogeneic bone marrow transplantation for refractory anemia is increased by shielding lungs and liver during total body irradiation. Author(s): Anderson JE, Appelbaum FR, Schoch G, Barnett T, Chauncey TR, Flowers ME, Storb R. Source: Biology of Blood and Marrow Transplantation : Journal of the American Society for Blood and Marrow Transplantation. 2001; 7(3): 163-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11302550&dopt=Abstract
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Relationship between aplastic anemia and paroxysmal nocturnal hemoglobinuria. Author(s): Kinoshita T, Inoue N. Source: International Journal of Hematology. 2002 February; 75(2): 117-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11939256&dopt=Abstract
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Relationship between hepatocellular injury and transfusional iron overload prior to and during iron chelation with desferrioxamine: a study in adult patients with acquired anemias. Author(s): Jensen PD, Jensen FT, Christensen T, Nielsen JL, Ellegaard J. Source: Blood. 2003 January 1; 101(1): 91-6. Epub 2002 August 22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393528&dopt=Abstract
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Relationship of iron-deficiency anemia with esophagitis and hiatal hernia: hospital findings from a prospective, population-based study. Author(s): Ruhl CE, Everhart JE. Source: The American Journal of Gastroenterology. 2001 February; 96(2): 322-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11232670&dopt=Abstract
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Remission of severe aplastic anemia associated with hepatitis B virus infection after viral clearance: potential role of lamivudine. Author(s): Bozkaya H, Yurdaydin C, Toruner M, Arat M, Bozdayi AM, Erekul S, Cinar K, Koc H, Uzunalimoglu O. Source: Digestive Diseases and Sciences. 2002 August; 47(8): 1782-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12184530&dopt=Abstract
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Renal amyloidosis in a patient with homozygous sickle cell anemia and M694V/M694V mutation. Author(s): Akar H, Keven K, Nergizoglu G, Erturk S, Ates K, Erbay B, Akar N, Duman N, Karatan O. Source: Nephron. 2000 November; 86(3): 383-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11096315&dopt=Abstract
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Renal anemia and its hemodynamic response--findings invasively determined over a period of 20 years. Author(s): Schafer GE, Rehbein C, Stiegler T, Hampl H. Source: Clinical Nephrology. 2002 July; 58 Suppl 1: S52-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12227727&dopt=Abstract
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Renal cell carcinoma induced Coombs negative autoimmune hemolytic anemia and severe thrombocytopenia responsive to nephrectomy. Author(s): Kamra D, Boselli J, Sloane BB, Gladstone DE. Source: The Journal of Urology. 2002 March; 167(3): 1395. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11832746&dopt=Abstract
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Renal function in children with sickle cell anemia. Author(s): Bayazit AK, Noyan A, Aldudak B, Ozel A, Anarat A, Kilinc Y, Sasmaz, Gali E, Anarat R, Dikmen N. Source: Clinical Nephrology. 2002 February; 57(2): 127-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11863122&dopt=Abstract
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Renal lesions and clinical findings in thalassemia major and other chronic anemias with hemosiderosis. Author(s): Landing BH, Gonick HC, Nadorra RL, Hyman CB, Wells TR, VillarrealEngelhardt G, Mersch J, Agness CL. Source: Pediatr Pathol. 1989; 9(5): 479-500. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2813197&dopt=Abstract
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Report on the International Symposium on Vitamin-related anemias May 27-28, 1968 Skytop (Pennsylvania), U.S.A. Author(s): Weber F. Source: Int Z Vitaminforsch. 1968; 38(3): 438-44. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5708622&dopt=Abstract
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Resolution of chronic parvovirus b19-induced anemia, by use of highly active antiretroviral therapy, in a patient with acquired immunodeficiency syndrome. Author(s): Ware AJ, Moore T. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2001 April 1; 32(7): E122-3. Epub 2001 March 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11264051&dopt=Abstract
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Resolution of severe Donath-Landsteiner autoimmune hemolytic anemia temporally associated with institution of plasmapheresis. Author(s): Roy-Burman A, Glader BE. Source: Critical Care Medicine. 2002 April; 30(4): 931-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11940774&dopt=Abstract
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Response of Diamond-Blackfan anemia to metoclopramide: evidence for a role for prolactin in erythropoiesis. Author(s): Abkowitz JL, Schaison G, Boulad F, Brown DL, Buchanan GR, Johnson CA, Murray JC, Sabo KM. Source: Blood. 2002 October 15; 100(8): 2687-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12351372&dopt=Abstract
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Response to X-irradiation of Fanconi anemia homozygous and heterozygous cells assessed by the single-cell gel electrophoresis (comet) assay. Author(s): Djuzenova CS, Rothfuss A, Oppitz U, Speit G, Schindler D, Hoehn H, Flentje M. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2001 February; 81(3): 185-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11233966&dopt=Abstract
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Response to X-irradiation of Fanconi anemia homozygous and heterozygous cells assessed by the single-cell gel electrophoresis (comet) assay. Author(s): Djuzenova CS, Rothfuss A, Oppitz U, Spelt G, Schindler D, Hoehn H, Flentje M. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2001 February; 81(2): 185-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11232640&dopt=Abstract
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Results of allogeneic BMT in 16 patients with Fanconi's anemia. Author(s): Ayas M, Mustafa MM. Source: Bone Marrow Transplantation. 2000 June; 25(12): 1321-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10871742&dopt=Abstract
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Reticulocyte analysis in iron deficiency anemia and hemolytic anemia. Author(s): Butthep P, Wisedpanichkij R, Jindadamrongwech S, Kaewkethong P, Pattamakom S, Sila-Asna M, Bunyaratvej A. Source: J Med Assoc Thai. 2000 March; 83 Suppl 1: S114-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10865417&dopt=Abstract
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Reticulocyte cellular indices: a new approach in the diagnosis of anemias and monitoring of erythropoietic function. Author(s): Brugnara C. Source: Critical Reviews in Clinical Laboratory Sciences. 2000 April; 37(2): 93-130. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10811141&dopt=Abstract
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Reticulocyte size in nutritional anemias. Author(s): Clarkson DR, Moore EM. Source: Blood. 1976 November; 48(5): 669-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=974264&dopt=Abstract
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Reversal of iron deficiency anemia in a patient with gastric antral vascular ectasia treated with cyproheptadine. Author(s): Soykan I, Toruner M, Idilman R, Ozden A. Source: Journal of Clinical Gastroenterology. 2003 February; 36(2): 183-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12544207&dopt=Abstract
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Reversal of iron deficiency anemia-induced peripheral neuropathy by iron treatment in children with iron deficiency anemia. Author(s): Kabakus N, Ayar A, Yoldas TK, Ulvi H, Dogan Y, Yilmaz B, Kilic N. Source: Journal of Tropical Pediatrics. 2002 August; 48(4): 204-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12200980&dopt=Abstract
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Reverse mosaicism in Fanconi anemia: natural gene therapy via molecular selfcorrection. Author(s): Gross M, Hanenberg H, Lobitz S, Friedl R, Herterich S, Dietrich R, Gruhn B, Schindler D, Hoehn H. Source: Cytogenetic and Genome Research. 2002; 98(2-3): 126-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12697994&dopt=Abstract
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Reversible sideroblastic anemia associated with the tetracycline analogue COL-3. Author(s): Rudek MA, Horne M, Figg WD, Dahut W, Dyer V, Pluda JM, Reed E. Source: American Journal of Hematology. 2001 May; 67(1): 51-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11279658&dopt=Abstract
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Ribosomal proteins S3a, S13, S16, and S24 are not mutated in patients with DiamondBlackfan anemia. Author(s): Cmejla R, Blafkova J, Stopka T, Jelinek J, Petrtylova K, Pospisilova D. Source: Blood. 2001 January 15; 97(2): 579-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11202430&dopt=Abstract
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Risk factors for cytomegalovirus retinitis following bone marrow transplantation from unrelated donors in patients with severe aplastic anemia or myelodysplasia. Author(s): Kuriyama K, Todo S, Ikushima S, Fujii N, Yoshihara T, Tsunamoto K, Naya M, Hojo M, Hibi S, Morimoto A, Imashuku S. Source: International Journal of Hematology. 2001 December; 74(4): 455-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11794704&dopt=Abstract
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Risk factors for evolution of acquired aplastic anemia into myelodysplastic syndrome and acute myeloid leukemia after immunosuppressive therapy in children. Author(s): Kojima S, Ohara A, Tsuchida M, Kudoh T, Hanada R, Okimoto Y, Kaneko T, Takano T, Ikuta K, Tsukimoto I; Japan Childhood Aplastic Anemia Study Group. Source: Blood. 2002 August 1; 100(3): 786-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12130487&dopt=Abstract
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Risk factors for microalbuminuria in children with sickle cell anemia. Author(s): McBurney PG, Hanevold CD, Hernandez CM, Waller JL, McKie KM. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 August-September; 24(6): 473-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12218596&dopt=Abstract
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Rituximab chimeric anti-CD20 monoclonal antibody treatment for refractory hemolytic anemia in patients with lymphoproliferative disorders. Author(s): Trape G, Fianchi L, Lai M, Laurenti L, Piscitelli R, Leone G, Pagano L. Source: Haematologica. 2003 February; 88(2): 223-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604415&dopt=Abstract
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Rituximab for immune hemolytic anemia following T- and B-Cell-depleted hematopoietic stem cell transplantation. Author(s): Corti P, Bonanomi S, Vallinoto C, Balduzzi A, Uderzo C, Cazzaniga G, Gaipa G, Dassi M, Perseghin P, Rovelli A. Source: Acta Haematologica. 2003; 109(1): 43-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12486323&dopt=Abstract
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Rituximab for refractory childhood autoimmune hemolytic anemia. Author(s): Motto DG, Williams JA, Boxer LA. Source: Isr Med Assoc J. 2002 November; 4(11): 1006-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12489491&dopt=Abstract
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Rituximab for the treatment of refractory autoimmune hemolytic anemia in children. Author(s): Zecca M, Nobili B, Ramenghi U, Perrotta S, Amendola G, Rosito P, Jankovic M, Pierani P, De Stefano P, Bonora MR, Locatelli F. Source: Blood. 2003 May 15; 101(10): 3857-61. Epub 2003 January 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531800&dopt=Abstract
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Rituximab-based chemotherapy for steroid-refractory autoimmune hemolytic anemia of chronic lymphocytic leukemia. Author(s): Gupta N, Kavuru S, Patel D, Janson D, Driscoll N, Ahmed S, Rai KR. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 October; 16(10): 2092-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12357362&dopt=Abstract
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Roentgen appearance of anomalies associated with hypoplastic anemias of childhood: Fanconi's anemia and congenital hypoplastic anemia (erythrogenesis imperfecta). Author(s): Minagi H, Steinbach HL. Source: Am J Roentgenol Radium Ther Nucl Med. 1966 May; 97(1): 100-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5938027&dopt=Abstract
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Roentgenographic osseous manifestations of the anemias and the leukemias. Author(s): O'Hara AE. Source: Clinical Orthopaedics and Related Research. 1967 May-June; 52: 63-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5233390&dopt=Abstract
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Role of epistatic (modifier) genes in the modulation of the phenotypic diversity of sickle cell anemia. Author(s): Nagel RL, Steinberg MH. Source: Pediatric Pathology & Molecular Medicine. 2001 March-April; 20(2): 123-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673837&dopt=Abstract
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Role of ferritin supported in diagnosis of anemias of pregnancy. Author(s): Goodlin RC. Source: American Journal of Obstetrics and Gynecology. 1989 July; 161(1): 258-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2750816&dopt=Abstract
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Role of IL-10 for induction of anemia during inflammation. Author(s): Tilg H, Ulmer H, Kaser A, Weiss G. Source: Journal of Immunology (Baltimore, Md. : 1950). 2002 August 15; 169(4): 2204-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12165551&dopt=Abstract
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Role of uremic toxins in exacerbating anemia in renal failure. Author(s): Macdougall IC. Source: Kidney International. Supplement. 2001 February; 78: S67-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11168986&dopt=Abstract
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Rubella-associated aplastic anemia treated by syngeneic stem cell transplantations. Author(s): Kook H, Kim GM, Kim HJ, Kim CJ, Yoon WS, Hwang TJ. Source: American Journal of Hematology. 2000 August; 64(4): 303-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10911384&dopt=Abstract
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Runner's anemia. Author(s): Dang CV. Source: Jama : the Journal of the American Medical Association. 2001 August 8; 286(6): 714-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11495622&dopt=Abstract
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Ruptured Klebsiella pneumoniae liver abscess after high-dose cyclophosphamide for severe aplastic anemia. Author(s): Lee JJ, Kim HJ, Chung IJ, Kook H, Park MR, Kim CJ, Shin DH, Hwang TJ. Source: American Journal of Hematology. 2000 July; 64(3): 218-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10861821&dopt=Abstract
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Safety and immunogenicity of a conjugate vaccine against Haemophilus influenzae type b in splenectomized and nonsplenectomized patients with Cooley anemia. Author(s): Cimaz R, Mensi C, D'Angelo E, Fantola E, Milone V, Biasio LR, Carnelli V, Zanetti AR. Source: The Journal of Infectious Diseases. 2001 June 15; 183(12): 1819-21. Epub 2001 May 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11372038&dopt=Abstract
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Salmonella infection associated with a pet lizard in siblings with sickle cell anemia: an avoidable risk. Author(s): Rodgers GL, Long SS, Smergel E, Dampier C. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 January; 24(1): 75-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11902748&dopt=Abstract
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Sarcoidosis with cholangitis component in a patient with autoimmune hemolytic anemia. Author(s): Zaina A, Horn I, Manaster O, Braester A, Reshef R. Source: Isr Med Assoc J. 2000 September; 2(9): 712. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11062776&dopt=Abstract
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Schizocytosis in pernicious anemia mimicking thrombotic thrombocytopenic purpura. Author(s): Garderet L, Maury E, Lagrange M, Najman A, Offenstadt G, Guidet B. Source: The American Journal of Medicine. 2003 April 1; 114(5): 423-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714141&dopt=Abstract
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Scleroderma associated with anemia and thrombocytopenia that responded well to cyclosporin. Author(s): Kamada K, Kobayashi Y, Katada K, Takahashi Y, Chikayama S, Ikeda M, Kondo M. Source: Acta Haematologica. 2000; 104(2-3): 106-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11154984&dopt=Abstract
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Screening for anemia in children: AAP recommendations--a critique. Author(s): Kohli-Kumar M. Source: Pediatrics. 2001 September; 108(3): E56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11533374&dopt=Abstract
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Screening for iron deficiency anemia among children and adolescents. Author(s): Mahoney MC. Source: American Family Physician. 2000 August 1; 62(3): 671-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10950220&dopt=Abstract
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Screening for iron deficiency anemia by dietary history in a high-risk population. Author(s): Bogen DL, Duggan AK, Dover GJ, Wilson MH. Source: Pediatrics. 2000 June; 105(6): 1254-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10835066&dopt=Abstract
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Screening for paroxysmal nocturnal hemoglobinuria (PNH) clone in Egyptian children with aplastic anemia. Author(s): Rizk S, Ibrahim IY, Mansour IM, Kandil D. Source: Journal of Tropical Pediatrics. 2002 June; 48(3): 132-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12164595&dopt=Abstract
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Screening for stroke in sickle cell anemia: comparison of transcranial Doppler imaging and nonimaging US techniques. Author(s): Neish AS, Blews DE, Simms CA, Merritt RK, Spinks AJ. Source: Radiology. 2002 March; 222(3): 709-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11867789&dopt=Abstract
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Screening strategies for a highly polymorphic gene: DHPLC analysis of the Fanconi anemia group A gene. Author(s): Rischewski J, Schneppenheim R. Source: Journal of Biochemical and Biophysical Methods. 2001 January 30; 47(1-2): 53-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179761&dopt=Abstract
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Scurvy: an unusual cause of anemia. Author(s): Cohen SA, Paeglow RJ. Source: The Journal of the American Board of Family Practice / American Board of Family Practice. 2001 July-August; 14(4): 314-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11458974&dopt=Abstract
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Search for improved therapy of sickle cell anemia. Author(s): Nathan DG. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 December; 24(9): 700-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468906&dopt=Abstract
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Seasonal variation in risk of anemia among pregnant Nepali women. Author(s): Bondevik GT, Lie RT, Ulstein M, Kvale G. Source: International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics. 2000 June; 69(3): 215-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10854862&dopt=Abstract
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Second bone marrow transplantation for severe aplastic anemia: analysis of 34 cases. Author(s): de Medeiros CR, Bitencourt MA, Medeiros BC, Ioshizumi L, Pasquini R. Source: Bone Marrow Transplantation. 2001 November; 28(10): 941-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11753548&dopt=Abstract
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Seeing the good and bad in aplastic anemia: is autoimmunity in AA dysregulated or antineoplastic? Author(s): Nissen C, Schubert J. Source: The Hematology Journal : the Official Journal of the European Haematology Association / Eha. 2002; 3(4): 169-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12189561&dopt=Abstract
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Serologic diagnosis in the differentiation of autoimmune hemolytic anemias. Author(s): Gologan R, Berceanu S. Source: Med Interne. 1979 April-June; 17(2): 191-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=472642&dopt=Abstract
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Serous fluid cytology as a means of detecting hemophagocytosis in Epstein-Barr virus-induced autoimmune hemolytic anemia. Author(s): Zaharopoulos P. Source: Diagnostic Cytopathology. 2001 October; 25(4): 248-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11599110&dopt=Abstract
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Serum alpha-fetoprotein level in Fanconi's anemia: evaluation of 33 Turkish patients. Author(s): Aslan D, Gumruk F, Alikasifoglu M, Altay C. Source: American Journal of Hematology. 2002 December; 71(4): 275-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12447956&dopt=Abstract
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Serum chemistry templates for anemias: iron deficiency, blood loss, pernicious, and renal. Author(s): Casey AE, Casey JG, Downey E, Copeland H, Thomason S. Source: Ala J Med Sci. 1973 July; 10(3): 241-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4770156&dopt=Abstract
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Serum erythropoietin concentrations in patients with anemia--preliminary hemoglobin-related reference ranges. Author(s): Vogeser M, Schiel X. Source: Clin Lab. 2002; 48(11-12): 595-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12465743&dopt=Abstract
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Serum ferritin in refractory anemias. Author(s): Solomon LR, Hillman RS, Finch CA. Source: Acta Haematologica. 1981; 66(1): 1-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6794292&dopt=Abstract
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Serum free carnitine and total triglycerid levels in children with iron deficiency anemia. Author(s): Tanzer F, Hizel S, Cetinkaya O, Sekreter E. Source: Int J Vitam Nutr Res. 2001 January; 71(1): 66-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11276925&dopt=Abstract
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Serum iron and total iron binding capacity in anemias in children. Author(s): Tater ML, Singh RN, Gupta BD. Source: Indian Pediatrics. 1992 March; 29(3): 362-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1612683&dopt=Abstract
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Serum leptin levels in patients with sideropenic and pernicious anemia: the influence of anemia treatment. Author(s): Markova M, Haluzik M, Svobodova J, Rosicka M, Nedvidkova J, Haas T. Source: Physiological Research / Academia Scientiarum Bohemoslovaca. 2000; 49(6): 679-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11252534&dopt=Abstract
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Serum level of erythropoietin in anemias associated with chronic infection, malignancy, and primary hematopoietic disease. Author(s): Ward HP, Kurnick JE, Pisarczyk MJ. Source: The Journal of Clinical Investigation. 1971 February; 50(2): 332-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=5107467&dopt=Abstract
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Serum transferrin receptor (sTfR)--is it useful in diagnosis of iron deficiency anemia? Author(s): Lin SF. Source: Zhonghua Yi Xue Za Zhi (Taipei). 2002 February; 65(2): 61-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12014359&dopt=Abstract
278 Anemia
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Serum transferrin receptor and erythrocyte zinc protoporphyrin in patients with anemia. Author(s): Harthoorn-Lasthuizen EJ, van't Sant P, Lindemans J, Langenhuijsen MM. Source: Clinical Chemistry. 2000 May; 46(5): 719-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10794759&dopt=Abstract
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Serum transferrin receptor in the evaluation of the iron status in elderly hospitalized patients with anemia. Author(s): Joosten E, Van Loon R, Billen J, Blanckaert N, Fabri R, Pelemans W. Source: American Journal of Hematology. 2002 January; 69(1): 1-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11835323&dopt=Abstract
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Severe alloimmune hemolytic anemia after renal transplantation. Author(s): Odabas AR, Tutucu KN, Turkmen A, Keskin H, Sever MS. Source: Nephron. 2002; 92(3): 743-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12372972&dopt=Abstract
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Severe anemia after gastrointestinal hemorrhage in a Jehovah's Witness: new treatment strategies. Author(s): Gannon CJ, Napolitano LM. Source: Critical Care Medicine. 2002 August; 30(8): 1893-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12163811&dopt=Abstract
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Severe anemia and marrow plasmacytosis as presentation of Sjogren's syndrome. Author(s): Tanvetyanon T, Leighton JC. Source: American Journal of Hematology. 2002 March; 69(3): 233. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11891816&dopt=Abstract
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Severe anemia in young children after high and low malaria transmission seasons in the Kassena-Nankana district of northern Ghana. Author(s): Koram KA, Owusu-Agyei S, Utz G, Binka FN, Baird JK, Hoffman SL, Nkrumah FK. Source: Am J Trop Med Hyg. 2000 June; 62(6): 670-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11304052&dopt=Abstract
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Severe aplastic anemia and allogeneic hematopoietic stem cell transplantation. Author(s): Myer SA, Oliva J. Source: Aacn Clinical Issues. 2002 May; 13(2): 169-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011591&dopt=Abstract
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Severe aplastic anemia associated with chronic natural killer cell lymphocytosis. Author(s): Kaito K, Otsubo H, Ogasawara Y, Shimada T, Kasama K, Yahagi Y, Asai O, Usui N, Kobayashi M. Source: International Journal of Hematology. 2000 December; 72(4): 463-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11197212&dopt=Abstract
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Severe aplastic anemia associated with hepatitis and complicated by pulmonary aspergillosis: response to immune suppression and antifungal therapy. Author(s): Bond R, Walter A, Trigg ME. Source: Del Med J. 2002 August; 74(8): 339-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12194507&dopt=Abstract
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Severe aplastic anemia associated with thymic carcinoma and partial recovery of hematopoiesis after thymectomy. Author(s): Koizumi K, Nakao S, Haseyama Y, Kato H, Ohi M, Motohara T, Endo T, Sawada K, Koike T. Source: Annals of Hematology. 2003 June; 82(6): 367-70. Epub 2003 April 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12715207&dopt=Abstract
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Severe aplastic anemia with autoimmune thyroiditis showing no hematological response to intensive immunosuppressive therapy. Author(s): Tomonari A, Tojo A, Iseki T, Ooi J, Hase H, Shirafuji N, Tani K, Asano S. Source: Acta Haematologica. 2003; 109(2): 90-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12624493&dopt=Abstract
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Severe autoimmune hemolitic anemia as a potentially fatal complication of EBV infectious mononucleosis. Author(s): Brncic N, Sever-Prebilic M, Crnic-Martinovic M, Prebilic I. Source: International Journal of Hematology. 2001 October; 74(3): 352-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11721976&dopt=Abstract
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Severe autoimmune hemolytic anemia caused by a warm IgA autoantibody directed against the third loop of band 3 (RBC anion-exchange protein 1). Author(s): Janvier D, Sellami F, Missud F, Fenneteau O, Vilmer E, Cartron J, Rohrlich P. Source: Transfusion. 2002 December; 42(12): 1547-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473132&dopt=Abstract
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Severe autoimmune thrombocytopenia after allogeneic bone marrow transplantation for aplastic anemia. Author(s): Tomonari A, Tojo A, Lseki T, Ooi J, Nagayama H, Ogami K, Maekawa T, Shirafuji N, Tani K, Asano S. Source: International Journal of Hematology. 2001 August; 74(2): 228-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11594527&dopt=Abstract
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Severe Coombs'-negative autoimmune hemolytic anemia in a kidney transplant patient. Author(s): Shnaider A, Basok A, Rogachev BV, Zlotnik M, Tomer A. Source: American Journal of Nephrology. 2001 November-December; 21(6): 494-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11799268&dopt=Abstract
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Severe hemolytic anemia after repair of primum septal defect and cleft mitral valve. Author(s): Alehan D, Dogan R, Ozkutlu S, Elshershari H, Gumruk F. Source: Turk J Pediatr. 2001 October-December; 43(4): 329-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11765164&dopt=Abstract
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Severe hemolytic anemia and excessive leukocytosis masking mycoplasma pneumonia. Author(s): Daxbock F, Zedtwitz-Liebenstein K, Burgmann H, Graninger W. Source: Annals of Hematology. 2001 March; 80(3): 180-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11320906&dopt=Abstract
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Severe immune hemolytic anemia in disseminated tuberculosis with response to antituberculosis therapy. Author(s): Kuo PH, Yang PC, Kuo SS, Luh KT. Source: Chest. 2001 June; 119(6): 1961-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11399734&dopt=Abstract
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Severe iron deficiency anemia and asymptomatic nodular gastroduodenitis: an uncommon presentation of Helicobacter pylori infection in a child. Author(s): Nowicki MJ, Coyle WJ. Source: Clinical Pediatrics. 2001 February; 40(2): 111-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11261448&dopt=Abstract
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Severe iron deficiency anemia in 42 pediatric patients. Author(s): Sandoval C, Berger E, Ozkaynak MF, Tugal O, Jayabose S. Source: Pediatric Hematology and Oncology. 2002 April-May; 19(3): 157-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11936728&dopt=Abstract
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Severe iron deficiency anemia in a child with idiopathic pulmonary hemosiderosis: a case report. Author(s): Derbent M, Ozcay F, Saatci U, Ozbek N. Source: Turk J Pediatr. 2002 July-September; 44(3): 258-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12405442&dopt=Abstract
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Severe microangiopathic hemolytic anemia and thrombocytopenia in a child with Brucella infection. Author(s): Yaramis A, Kervancioglu M, Yildirim I, Soker M, Derman O, Tas MA. Source: Annals of Hematology. 2001 September; 80(9): 546-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11669306&dopt=Abstract
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Severe oesophagitis after allogeneic bone marrow transplantation for Fanconi's anemia. Author(s): Yakoub-Agha I, Damaj G, Garderet L, Bonnet J, Devergie A, Esperou H, Ribaud P, Socie G, Gluckman E. Source: Bone Marrow Transplantation. 2000 July; 26(2): 215-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10918434&dopt=Abstract
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Sharper focus on sickle cell anemia. Author(s): Thurmon TF. Source: J La State Med Soc. 2002 July-August; 154(4): 194-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12236403&dopt=Abstract
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Short and long-term results of the treatment of aplastic anemias with nandrolone decanoate. Author(s): Daiber A, Con I, Moenne S, Donoso A, Osorio G. Source: Medicina (B Aires). 1974 March; 34(2): 112-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4854276&dopt=Abstract
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Short period of administration of diethylstilbestrol in stuttering priapism in sickle cell anemia. Author(s): Gbadoe AD, Assimadi JK, Segbena YA. Source: American Journal of Hematology. 2002 April; 69(4): 297-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11921029&dopt=Abstract
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Short survival of phosphatidylserine-exposing red blood cells in murine sickle cell anemia. Author(s): de Jong K, Emerson RK, Butler J, Bastacky J, Mohandas N, Kuypers FA. Source: Blood. 2001 September 1; 98(5): 1577-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11520810&dopt=Abstract
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Sickle cell anemia and antisickling agents then and now. Author(s): Mehanna AS. Source: Current Medicinal Chemistry. 2001 February; 8(2): 79-88. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11172667&dopt=Abstract
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Sickle cell anemia and beta-globin gene cluster haplotypes in Colombia. Author(s): Cuellar-Ambrosi F, Mondragon MC, Figueroa M, Prehu C, Galacteros F, Ruiz-Linares A. Source: Hemoglobin. 2000 August; 24(3): 221-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10975441&dopt=Abstract
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Sickle cell anemia and dental caries: a literature review and pilot study. Author(s): Laurence B, Reid BC, Katz RV. Source: Spec Care Dentist. 2002 March-April; 22(2): 70-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12109598&dopt=Abstract
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Sickle cell anemia and hematological neoplasias. Author(s): Paydas S. Source: Leukemia & Lymphoma. 2002 July; 43(7): 1431-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12389625&dopt=Abstract
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Sickle cell anemia as an inflammatory disease. Author(s): Platt OS. Source: The Journal of Clinical Investigation. 2000 August; 106(3): 337-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10930436&dopt=Abstract
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Sickle cell anemia in the pediatric intensive care unit: novel approaches for managing life-threatening complications. Author(s): Jenkins TL. Source: Aacn Clinical Issues. 2002 May; 13(2): 154-68. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011590&dopt=Abstract
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Sickle cell anemia oral manifestations in a Venezuelan population. Author(s): Saint Clair de Velasquez Y, Rivera H. Source: Acta Odontol Latinoam. 1997; 10(2): 101-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11885236&dopt=Abstract
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Sickle cell anemia. Author(s): Lonergan GJ, Cline DB, Abbondanzo SL. Source: Radiographics : a Review Publication of the Radiological Society of North America, Inc. 2001 July-August; 21(4): 971-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11452073&dopt=Abstract
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Sickle cell anemia: the legacy of the patient (Walter Clement Noel), the interne (Ernest Irons), and the attending physician (James Herrick) and the facts of its discovery. Author(s): Haller JO, Berdon WE, Franke H. Source: Pediatric Radiology. 2001 December; 31(12): 889-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11727028&dopt=Abstract
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Sickle-cell anemia: report of a case in a newborn infant. Author(s): Quinn CT. Source: The Journal of Pediatrics. 2001 August; 139(2): 319. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11534499&dopt=Abstract
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Sideroblastic anemia. Author(s): Menon J, Mathews L. Source: Indian Pediatrics. 2001 August; 38(8): 926. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11521009&dopt=Abstract
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Sideroblastic anemias. Author(s): Lohse JR, Armitage JO, Foster MT. Source: Nebr Med J. 1976 October; 61(10): 389-93. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=972713&dopt=Abstract
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Sideroblastic anemias. An approach to diagnosis and management. Author(s): Sullivan AL, Weintraub LR. Source: The Medical Clinics of North America. 1973 March; 57(2): 335-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4570932&dopt=Abstract
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Sideroblastic anemias: variations on imprecision in diagnostic criteria, proposal for an extended classification of sideroblastic anemias. Author(s): Koc S, Harris JW. Source: American Journal of Hematology. 1998 January; 57(1): 1-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9423809&dopt=Abstract
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Signs and symptoms associated with the transfusion of WBC-reduced RBCs and nonWBC-reduced RBCs in patients with anemia and HIV infection: results from the Viral Activation Transfusion Study. Author(s): Lane TA, Gernsheimer T, Mohandas K, Assmann SF. Source: Transfusion. 2002 February; 42(2): 265-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11896345&dopt=Abstract
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Silent infarction as a risk factor for overt stroke in children with sickle cell anemia: a report from the Cooperative Study of Sickle Cell Disease. Author(s): Miller ST, Macklin EA, Pegelow CH, Kinney TR, Sleeper LA, Bello JA, DeWitt LD, Gallagher DM, Guarini L, Moser FG, Ohene-Frempong K, Sanchez N, Vichinsky EP, Wang WC, Wethers DL, Younkin DP, Zimmerman RA, DeBaun MR; Cooperative Study of Sickle Cell Disease. Source: The Journal of Pediatrics. 2001 September; 139(3): 385-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11562618&dopt=Abstract
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Silent infarcts in children with sickle cell anemia and abnormal cerebral artery velocity. Author(s): Pegelow CH, Wang W, Granger S, Hsu LL, Vichinsky E, Moser FG, Bello J, Zimmerman RA, Adams RJ, Brambilla D; STOP Trial. Source: Archives of Neurology. 2001 December; 58(12): 2017-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11735775&dopt=Abstract
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Single values of serum transferrin receptor and transferrin receptor ferritin index can be used to detect true and functional iron deficiency in rheumatoid arthritis patients with anemia. Author(s): Suominen P, Mottonen T, Rajamaki A, Irjala K. Source: Arthritis and Rheumatism. 2000 May; 43(5): 1016-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10817554&dopt=Abstract
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Skeletal changes in the anemias. Author(s): Moseley JE. Source: Semin Roentgenol. 1974 July; 9(3): 169-84. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4601847&dopt=Abstract
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Skin and nail changes in children with sickle cell anemia receiving hydroxyurea therapy. Author(s): O'branski EE, Ware RE, Prose NS, Kinney TR. Source: Journal of the American Academy of Dermatology. 2001 May; 44(5): 859-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11312437&dopt=Abstract
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Sleep disruption and objective sleepiness in children with beta-thalassemia and congenital dyserythropoietic anemia. Author(s): Tarasiuk A, Ali AH, Moser A, Freidman B, Tal A, Kapelushnik J. Source: Archives of Pediatrics & Adolescent Medicine. 2003 May; 157(5): 463-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742882&dopt=Abstract
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Soft tissue infection with Absidia corymbifera in a patient with idiopathic aplastic anemia. Author(s): Cloughley R, Kelehan J, Corbett-Feeney G, Murray M, Callaghan J, Regan P, Cormican M. Source: Journal of Clinical Microbiology. 2002 February; 40(2): 725-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11826008&dopt=Abstract
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Soluble transferrin receptor and immature reticulocytes are not useful for distinguishing iron-deficiency anemia from heterozygous beta-thalassemia. Author(s): de Lima GA, Grotto HZ. Source: Sao Paulo Medical Journal = Revista Paulista De Medicina. 2003 March 5; 121(2): 90-1. Epub 2003 July 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870058&dopt=Abstract
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Soluble transferrin receptor in iron-deficient patients with and without anemia. Author(s): Piedras J, Cinta-Severo Mdel C, Valdez K, Lupez-Karpovitch X. Source: Haematologica. 2003 March; 88(3): 348-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12651276&dopt=Abstract
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Soluble transferrin receptor level: a new marker of iron deficiency anemia, a common manifestation of gastric autoimmunity in type 1 diabetes. Author(s): De Block CE, Van Campenhout CM, De Leeuw IH, Keenoy BM, Martin M, Van Hoof V, Van Gaal LF. Source: Diabetes Care. 2000 September; 23(9): 1384-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10977038&dopt=Abstract
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Somatic mosaicism in Fanconi anemia: evidence of genotypic reversion in lymphohematopoietic stem cells. Author(s): Gregory JJ Jr, Wagner JE, Verlander PC, Levran O, Batish SD, Eide CR, Steffenhagen A, Hirsch B, Auerbach AD. Source: Proceedings of the National Academy of Sciences of the United States of America. 2001 February 27; 98(5): 2532-7. Epub 2001 Feb 13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11226273&dopt=Abstract
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Sorting out the common anemias. Author(s): Onega T. Source: Jaapa. 2000 September; 13(9): 30-2, 35-6, 39-44 Passim. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11521621&dopt=Abstract
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Special feature: pathological case of the month. Pernicious anemia and gastric atrophy in an adolescent female with multiorgan problems. Author(s): Dahshan A, Poulick J, Tolia V. Source: Archives of Pediatrics & Adolescent Medicine. 2001 May; 155(5): 609-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11343508&dopt=Abstract
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Specificity of the antiglobulin test in “auto-immune” hemolytic anemias. Author(s): Jeannet M. Source: Helv Med Acta. 1966 June; 33(2): 151-63. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4164324&dopt=Abstract
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Spectrin changes occur in erythrocytes from patients with Fanconi's anemia and their parents. Author(s): Straface E, Masella R, Principe DD, Franceschi C, Korkina LG, Zatterale A, Pagano G, Malorni W. Source: Biochemical and Biophysical Research Communications. 2000 July 14; 273(3): 899-901. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10891344&dopt=Abstract
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Spectrin oligomerization is cooperatively coupled to membrane assembly: a linkage targeted by many hereditary hemolytic anemias? Author(s): Giorgi M, Cianci CD, Gallagher PG, Morrow JS. Source: Experimental and Molecular Pathology. 2001 June; 70(3): 215-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11418000&dopt=Abstract
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Spectrum of sequence variation in the FANCG gene: an International Fanconi Anemia Registry (IFAR) study. Author(s): Auerbach AD, Greenbaum J, Pujara K, Batish SD, Bitencourt MA, Kokemohr I, Schneider H, Lobitzc S, Pasquini R, Giampietro PF, Hanenberg H, Levran O; International Fanconi Anemia Registry. Source: Human Mutation. 2003 February; 21(2): 158-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552564&dopt=Abstract
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S-phase-specific interaction of the Fanconi anemia protein, FANCD2, with BRCA1 and RAD51. Author(s): Taniguchi T, Garcia-Higuera I, Andreassen PR, Gregory RC, Grompe M, D'Andrea AD. Source: Blood. 2002 October 1; 100(7): 2414-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12239151&dopt=Abstract
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Splenic abscess, pleural effusion and severe anemia caused by Salmonella typhi. Author(s): Caksen H, Oner AF, Arslan S, Koseoglu B, Harman M, Atas B, Abuhandan M. Source: The Kobe Journal of Medical Sciences. 2000 October; 46(5): 201-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11417295&dopt=Abstract
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Splenic angiosarcoma and iron deficiency anemia in a 43-year-old man. Author(s): Thomas JP, Porcell A, Sagone AL. Source: Southern Medical Journal. 2001 June; 94(6): 640-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11440334&dopt=Abstract
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CHAPTER 2. NUTRITION AND ANEMIA Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and anemia.
Finding Nutrition Studies on Anemia 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 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 “anemia” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7 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 anemia: ·
Possible new developments in community control of iron-deficiency anemia. Author(s): Cornell University, Ithaca, NY. Source: Stephenson, L.S. Nutrition-reviews (USA). (February 1995). volume 53(2) page 23-30. china developing countries anaemia trace element deficiencies iron supplements who pregnancy weight gain human population children youth women 0029-6643 Summary: chine pays en developpement anemie carence en oligoelement fer complement alimentaire oms gestation gain de poids population humaine enfant jeunesse femme
Additional consumer oriented references include: ·
Anemia and iron nutrition in the aged. Source: Lynch, S.R. Nutrition-and-the-M.D (USA). (February 1985). volume 11(2) page 12. anaemia inflammation neoplasms iron diagnosis 0732-0167
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Clinical assessment of mild iron-deficiency anemia. Source: Nutrition-and-the-M.D (USA). (March 1987). volume 13(3) page 3-4. anaemia trace element deficiencies iron diagnosis forecasting 0732-0167
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Definition and prevalence of anemia in Bolivian women of childbearing age living at high altitudes: the effect of iron-folate supplementation. Author(s): Departement Sante, Institut Francais de Recherche Scientifique pour le Developpement en Cooperation (ORSTOM), Montpellier, France. Source: Berger, J Aguayo, V M San Miguel, J L LuJanuary, C Tellez, W Traissac, P NutrRevolume 1997 June; 55(6): 247-56 0029-6643
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Developmental and behavioral effects of iron deficiency anemia in infants. Author(s): University of Michigan. Source: Holst, M.C. Nutrition-today (USA). (Jan-February 1998). volume 33(1) page 2736. costa rica iron trace element deficiencies anaemia human behaviour nutritive value nutritional status infants forecasting children mental ability models psychological factors child care families brain neurophysiology 0029-666X
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Fatigue of anemia. Author(s): University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190, USA. Source: Eichner, E R Nutr-Revolume 2001 January; 59(1 Pt 2): S17-9 0029-6643
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Iron, anemia, and infection. Author(s): Hematology Unit, University of Chile, Santiago, Chile. Source: Walter, T Olivares, M Pizarro, F Munoz, C Nutr-Revolume 1997 April; 55(4): 111-24 0029-6643
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Iron-deficiency anemia in women. Source: Anonymous Harv-Womens-Health-Watch. 2002 November; 10(3): 3-5 1070-910X
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Iron-deficiency anemia increases risk of preterm delivery. Author(s): Department of Nutritional Sciences, University of Connecticut, Storrs 062694017. Source: Allen, L H Nutr-Revolume 1993 February; 51(2): 49-52 0029-6643
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Iron-deficiency anemia with hypoproteinemia in an infant. Source: Anonymous Nutr-Revolume 1989 February; 47(2): 48-50 0029-6643
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Long-term effects of iron deficiency anemia in infancy. Author(s): Western Reserve University School of Medicine, Cleveland Source: Lozoff, B. Nutrition-and-the-M.D (USA). (October 1992). volume 18(10) page 1-2. anaemia trace element deficiencies iron child care infants minerals 0732-0167
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Long-term follow-up of diabetes in two patients with thiamine-responsive megaloblastic anemia syndrome. Author(s): Department of Pediatrics, School of Medicine, University of Udine, Italy. Source: Valerio, G Franzese, A Poggi, V Tenore, A Diabetes-Care. 1998 January; 21(1): 38-41 0149-5992
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Plasma transferrin receptor helps to predict iron deficiency in the anemia of chronic disease. Author(s): Mineral Bioavailability Laboratory, USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA. Source: Fleming, D Wood, R J Nutr-Revolume 1995 June; 53(6): 167-9 0029-6643
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Should you worry about anemia? What to do if you're at risk. Source: Zupke, M.P. Environmental-nutrition (USA). (December 1993). volume 16(12) page 1, 6. anaemia trace element deficiencies iron risk nutrient intake 0893-4452
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Treatment of iron-deficiency anemia complicated by scurvy and folic acid deficiency. Author(s): Department of Medicine, Baystate Medical Center, Springfield, MA 01199. Source: Clark, N G Sheard, N F Kelleher, J F Nutr-Revolume 1992 May; 50(5): 134-7 0029-6643
The following information is typical of that found when using the “Full IBIDS Database” to search for “anemia” (or a synonym): ·
A rare association of primary biliary cirrhosis and pernicious anemia. Author(s): First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan. Source: Aoyama, H Sakugawa, H Nakasone, H Nakayoshi, T Kinjo, A Tamayose, M Higa, H Uema, E Chinen, T Tomiyama, R Uchima, N Kugai, Y Kinjo, F Saito, A Kinjo, M J-Gastroenterol. 2002; 37(7): 560-3 0944-1174
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A simple case of anemia: pathophysiology of a common symptom. Author(s): PharMerica in Greensboro, North Carolina, USA. Source: Cook, L S J-Intraven-Nurs. 2000 Sep-October; 23(5): 271-81 0896-5846
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Aggressive therapy of congestive heart failure and associated chronic renal failure with medications and correction of anemia stops or slows the progression of both diseases. Author(s): Department of Nephrology, Tel Aviv Medical Center, Israel.
[email protected] Source: Silverberg, D S Wexler, D Blum, M Sheps, D Schwartz, D Yachnin, T Baruch, R Tchebiner, J Zubkov, A Shaked, M Steinbruch, S Keren, G Iaina, A Perit-Dial-Int. 2001; 21 Suppl 3: S236-40 0896-8608
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Anemia management protocols and epoetin alfa administration: an algorithm approach. Case study of the anemic patient. Author(s): Winthrop University Hospital, Mineola, NY, USA. Source: Aiello, J Nephrol-Nurs-J. 2002 June; 29(3): 297-300 1526-744X
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Anemia of prematurity. Author(s): NICU, Stormont-Vail Regional Health Center, Topeka, Kansas 66604, USA.
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Source: Salsbury, D C Neonatal-Netw. 2001 August; 20(5): 13-20 0730-0832 ·
Antenatal vitamin A supplementation increases birth weight and decreases anemia among infants born to human immunodeficiency virus-infected women in Malawi. Author(s): Department of Epidemiology and Ophthalmology, Johns Hopkins University School of Hygiene and Public Health and School of Medicine, Baltimore, MD, USA. Source: Kumwenda, Newton Miotti, Paolo G Taha, Taha E Broadhead, Robin Biggar, Robert J Jackson, J Brooks Melikian, George Semba, Richard D Clin-Infect-Dis. 2002 September 1; 35(5): 618-24 1537-6591
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Assessment of the prevalence of iron deficiency anemia, by serum ferritin, in pregnant women of Southern Iran. Author(s): Hematology Research Center, Nemazee Hospital, Shiraz University of Medical Sciences, Iran. Source: Karimi, M Kadivar, R Yarmohammadi, H Med-Sci-Monit. 2002 July; 8(7): CR48892 1234-1010
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Diagnosing and treating anemia and iron deficiency in hemodialysis patients. Source: Foret, J P Nephrol-Nurs-J. 2002 June; 29(3): 292-6 1526-744X
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Effects of a vitamin E-bonded membrane and of glutathione on anemia and erythropoietin requirements in hemodialysis patients. Author(s): Nephrology and Dialysis Service, Manerbio Hospital, Brescia, Italy.
[email protected] Source: Usberti, M Gerardi, G Micheli, A Tira, P Bufano, G Gaggia, P Movilli, E Cancarini, G C De Marinis, S D'Avolio, G Broccoli, R Manganoni, A Albertin, A Di Lorenzo, D J-Nephrol. 2002 Sep-October; 15(5): 558-64 1120-3625
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Fulminant hepatic failure and autoimmune hemolytic anemia associated with Epstein-Barr virus infection. Author(s): Department of Paediatrics, Sisli Etfal Training and Research Hospital, Istanbul, Turkey.
[email protected] Source: Palanduz, A Yildirmak, Y Telhan, L Arapoglu, M Urganci, N Tufekci, S Kayaalp, N J-Infect. 2002 August; 45(2): 96-8 0163-4453
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Iron deficiency anemia increases nitric oxide production in healthy adolescents. Author(s): Department of Clinical Pathology, College of Medicine, Inha University, Inchon, Korea. Source: Choi, J W Pai, S H Kim, S K Ito, M Park, C S Cha, Y N Ann-Hematol. 2002 January; 81(1): 1-6 0939-5555
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Iron hydroxide polymaltose--cause of persistent iron deficiency anemia at delivery. Author(s): Nanavati Hospital, Hematology Dept, Seth GS Medical College & KEM Hospital, Mumbai. Source: Mehta, B C Indian-J-Med-Sci. 2001 November; 55(11): 616-20 0019-5359
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Iron status and the treatment of the anemia of prematurity. Author(s): Department of Pediatrics, Steele Memorial Children's Research Center, 1501 N. Campbell Ave., PO # 24-5073, The University of Arizona, Tucson, AZ 85724-5073, USA.
[email protected] Source: Kling, P J Winzerling, J J Clin-Perinatol. 2002 June; 29(2): 283-94 0095-5108
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Iron-deficiency anemia in women. Source: Anonymous Harv-Womens-Health-Watch. 2002 November; 10(3): 3-5 1070-910X
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Late post-transplant anemia in adult renal transplant recipients. An under-recognized problem? Author(s): Department of Pediatrics, Section of Pediatric Nephrology, Lucile Salter Packard Children's Hospital, Stanford University, Stanford, CA 94304, USA.
[email protected] Source: Yorgin, P D Scandling, J D Belson, A Sanchez, J Alexander, S R Andreoni, K A Am-J-Transplant. 2002 May; 2(5): 429-35 1600-6135
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Management of anemia in chronic kidney disease (predialysis) patients: nephrology nursing implications. Author(s): Case Western Reserve University School of Medicine, USA. Source: Wish, J B Weigel, K A Nephrol-Nurs-J. 2001 June; 28(3): 341-5 1526-744X
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Menatetrenone, a vitamin K2 analog, ameliorates cytopenia in patients with refractory anemia of myelodysplastic syndrome. Author(s): Third Department of Medicine, Kanazawa University School of Medicine, 131 Takaramachi, Kanazawa 920-8641, Japan.
[email protected] Source: Takami, A Asakura, H Nakao, S Ann-Hematol. 2002 January; 81(1): 16-9 09395555
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Mitochondria from cultured cells derived from normal and thiamine-responsive megaloblastic anemia individuals efficiently import thiamine diphosphate. Author(s): Department of Biological Sciences, Vanderbilt University, VU Station B 351634, Nashville TN 37235-1634, USA.
[email protected] Source: Song, Q Singleton, C K BMC-Biochem. 2002 April 25; 3(1): 8 1471-2091
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Myelodysplastic syndrome complicated by autoimmune hemolytic anemia: remission of refractory anemia following mycophenolate mofetil. Author(s): Division of Medical Oncology, Department of Medicine, Taipei Veterans General Hospital, #201, Sec. 2, Shi-Pai Road, Taiwan. Source: Lin, J T Wang, W S Yen, C C Chiou, T J Liu, J H Hsiao, L T Yang, M H Chao, T C Tai, C J Chen, P M Ann-Hematol. 2002 December; 81(12): 723-6 0939-5555
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Parenteral iron supplementation for the treatment of iron deficiency anemia in children. Author(s): Department of Pediatric Hematology and Oncology, II Pediatric Clinic, University of Bari, Piazza Giulio Cesare, 70124 Bari, Italy.
[email protected] Source: Surico, G Muggeo, P Muggeo, V Lucarelli, A Martucci, T Daniele, M Rigillo, N Ann-Hematol. 2002 Mar; 81(3): 154-7 0939-5555
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Possible effects of antioxidant status on increased platelet aggregation in childhood iron-deficiency anemia. Author(s): Department of Physiology, Ankara University School of Medicine, Turkey.
[email protected] Source: Tekin, D Yavuzer, S Tekin, M Akar, N Cin, S Pediatr-Int. 2001 February; 43(1): 74-7 1328-8067
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Prevalence of anemia during pregnancy: results of Valencia (Venezuela) anemia during pregnancy study. Author(s): Clinical Epidemiology Unit, Universidad de Carabobo, Ciudad Hospitalaria Dr. Enrique Tejera, Venezuela. Source: Marti Carvajal, A Pena Marti, G Comunian, G Munoz, S Arch-Latinoam-Nutr. 2002 Mar; 52(1): 5-11 0004-0622
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Sickle cell anemia in the pediatric intensive care unit: novel approaches for managing life-threatening complications. Author(s): Pediatric Critical Care, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892-1664, USA.
[email protected] Source: Jenkins, Tammara L AACN-Clin-Issues. 2002 May; 13(2): 154-68 1079-0713
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Superoxide dismutase and glutathione peroxidase in erythrocytes of patients with iron deficiency anemia: effects of different treatment modalities. Author(s): Department of Internal Medicine, Suleyman Demirel University School of Medicine, Isparta, Turkey.
[email protected] Source: Isler, Mehmet Delibas, Namik Guclu, Muhittin Gultekin, Fatih Sutcu, Recep Bahceci, Mehmet Kosar, Ali Croat-Med-J. 2002 February; 43(1): 16-9 0353-9504
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The role of hepcidin in iron sequestration during infections and in the pathogenesis of anemia of chronic disease. Author(s): Departments of Medicine and Pathology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
[email protected] Source: Ganz, T Isr-Med-Assoc-J. 2002 November; 4(11): 1043-5 1565-1088
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The role of histidine in the anemia of folate deficiency. Author(s): Department of Community and Preventive Medicine, New York Medical College, Valhalla, NY 10595, USA.
[email protected] Source: Cooperman, J M Lopez, R Exp-Biol-Med-(Maywood). 2002 December; 227(11): 998-1000 1535-3702
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Treatment of aplastic anemia by the kidney-tonifying and mediating method. Author(s): Department of Traditional Chinese Medicine, PLA 465 Hospital, Jilin Province, 132011. Source: Yu, Y Sun, W Cao, K Wang, X J-Tradit-Chin-Med. 2001 December; 21(4): 252-5 0254-6272
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Treatment of vitamin b(12)-deficiency anemia: oral versus parenteral therapy. Author(s): College of Pharmacy, The University of Oklahoma Health Sciences Center, Norman Regional Hospital, Norman, OK, USA.
[email protected] Source: Lane, L A Rojas Fernandez, C Ann-Pharmacother. 2002 Jul-August; 36(7-8): 1268-72 1060-0280
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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WebMDÒHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,,00.html
The following is a specific Web list relating to anemia; 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 (some Web sites are subscription based): ·
Vitamins Folic Acid Source: Healthnotes, Inc. www.healthnotes.com Folic Acid Source: Healthnotes, Inc. www.healthnotes.com Folic Acid Source: Integrative Medicine Communications; www.drkoop.com Folic acid Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,887,00.html
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Folic acid/vitamin B Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,936,00.html Pyridoxine Source: Integrative Medicine Communications; www.drkoop.com Pyridoxine Alternative names: Vitamin B6 (Pyridoxine) Source: Integrative Medicine Communications; www.drkoop.com Riboflavin Source: Integrative Medicine Communications; www.drkoop.com Riboflavin (vitamin B Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,895,00.html Vitamin A Source: Healthnotes, Inc. www.healthnotes.com Vitamin B Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10067,00.html Vitamin B12 Source: Healthnotes, Inc. www.healthnotes.com Vitamin B12 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin B12 (Cobalamin) Source: Integrative Medicine Communications; www.drkoop.com Vitamin B2 Source: Healthnotes, Inc. www.healthnotes.com Vitamin B2 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin B2 (Riboflavin) Source: Integrative Medicine Communications; www.drkoop.com Vitamin B6 Source: Healthnotes, Inc. www.healthnotes.com
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Vitamin B6 (Pyridoxine) Alternative names: Pyridoxine Source: Integrative Medicine Communications; www.drkoop.com Vitamin B6 (Pyridoxine) Source: Integrative Medicine Communications; www.drkoop.com Vitamin B9 (Folic Acid) Alternative names: Folate, Folic Acid Source: Integrative Medicine Communications; www.drkoop.com Vitamin C Source: Healthnotes, Inc. www.healthnotes.com Vitamin C Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,904,00.html Vitamin E Source: Healthnotes, Inc. www.healthnotes.com Vitamin E Alternative names: Alpha-Tocopherol, Beta-Tocopherol, D-Alpha-Tocopherol, Delta-Tocopherol, Gamma-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com ·
Minerals Alpha-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Aluminum, Calcium, and Magnesium-Containing Preparations Source: Integrative Medicine Communications; www.drkoop.com Betaine Hydrochloride Source: Healthnotes, Inc. www.healthnotes.com Betaine Hydrochloride Source: Prima Communications, Inc.www.personalhealthzone.com Beta-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Biotin Source: Healthnotes, Inc. www.healthnotes.com Chromium Source: Healthnotes, Inc. www.healthnotes.com
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Copper Source: Healthnotes, Inc. www.healthnotes.com Copper Source: Integrative Medicine Communications; www.drkoop.com Copper Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,886,00.html D-Alpha-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Delta-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Folate Source: Integrative Medicine Communications; www.drkoop.com Folate Source: Prima Communications, Inc.www.personalhealthzone.com Gabapentin Source: Healthnotes, Inc. www.healthnotes.com Gamma-Tocopherol Source: Integrative Medicine Communications; www.drkoop.com Iodine Source: Healthnotes, Inc. www.healthnotes.com Iron Source: Healthnotes, Inc. www.healthnotes.com Iron Alternative names: Ferrous Sulfate Source: Integrative Medicine Communications; www.drkoop.com Iron Source: Prima Communications, Inc.www.personalhealthzone.com L-Carnitine Source: Healthnotes, Inc. www.healthnotes.com Magnesium Source: Healthnotes, Inc. www.healthnotes.com Potassium-Sparing Diuretics Source: Integrative Medicine Communications; www.drkoop.com
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Zinc Source: Healthnotes, Inc. www.healthnotes.com Zinc Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Prima Communications, Inc.www.personalhealthzone.com Zinc/copper Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,938,00.html ·
Food and Diet Coffee Source: Healthnotes, Inc. www.healthnotes.com Ferrous Sulfate Source: Integrative Medicine Communications; www.drkoop.com Garlic Alternative names: Allium sativum Source: Healthnotes, Inc. www.healthnotes.com Tea Source: Healthnotes, Inc. www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND ANEMIA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to anemia. At the conclusion of this chapter, we will provide additional sources.
The Combined Health Information Database The Combined Health Information Database (CHID) is a bibliographic database produced by health-related agencies of the U.S. federal government (mostly from the National Institutes of Health) that can offer concise information for a targeted search. The CHID database is updated four times a year at the end of January, April, July, and October. Check the titles, summaries, and availability of CAM-related information by using the “Simple Search” option at the following Web site: http://chid.nih.gov/simple/simple.html. In the drop box at the top, select “Complementary and Alternative Medicine.” Then type “anemia” (or synonyms) in the second search box. We recommend that you select 100 “documents per page” and to check the “whole records” options. The following was extracted using this technique: ·
Foods that Fight Pain: Revolutionary New Strategies for Maximum Pain Relief Source: New York, NY: Harmony Books. 1999. 347 p. Contact: Available from Harmony Books. 231 Broad Street, Nevada City, CA 95959. (530) 265-9564. PRICE: $14.00. ISBN: 0609804367. Summary: This book is intended to help people fight pain by using common foods, traditional supplements, and herbs. It explains which foods contribute to pain and how to avoid them, which foods are pain-safe but high in nutrition, and which foods can actively soothe pain by improving blood circulation, relieving inflammation, and balancing hormones. An introduction describes how food can fight pain at any of the stages of the pain process: the initial injury, the inflammatory response, the pain message traveling through the nerves, and the brain's perception of pain. Part 1 discusses conditions related to poor circulation, such as backaches and chest pain. Part 2 addresses conditions caused by food sensitivities and inflammation, including
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migraines, other headaches, joint ailments, stomach aches and digestive problems, and fibromyalgia. Part 3 discusses hormone-related conditions such as menstrual pain, breast pain, and cancer pain. Part 4 discusses metabolic and immune problems, including carpal tunnel syndrome, diabetes, herpes and shingles, sickle cell anemia, kidney stones, and urinary infections. Part 5 discusses the roles of exercise, rest, and sleep in pain relief; describes several stress-reducing exercises; and explains why the body rebels against certain foods. The book includes menus and recipes, a glossary of ingredients, a list of resources, a list of suggested readings, and an index.
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 anemia 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 “anemia” (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 anemia: ·
A randomized, active-control, pilot trial of front-loaded dosing regimens of darbepoetin-alfa for the treatment of patients with anemia during chemotherapy for malignant disease. Author(s): Glaspy JA, Jadeja JS, Justice G, Fleishman A, Rossi G, Colowick AB. Source: Cancer. 2003 March 1; 97(5): 1312-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12599240&dopt=Abstract
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Acquired aplastic anemia in children: incidence, prognosis and treatment options. Author(s): Locasciulli A. Source: Paediatric Drugs. 2002; 4(11): 761-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390048&dopt=Abstract
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Aged garlic extract therapy for sickle cell anemia patients. Author(s): Takasu J, Uykimpang R, Sunga M, Amagase H, Niihara Y. Source: Bmc Blood Disorders [electronic Resource]. 2002 June 19; 2(1): 3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12086586&dopt=Abstract
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Anemia of cancer in intermediate-grade non-Hodgkin's lymphoma. Author(s): Morrow TJ, Volpe S, Gupta S, Tannous RE, Fridman M. Source: Southern Medical Journal. 2002 August; 95(8): 889-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12190227&dopt=Abstract
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Anemia prophylaxis in adolescent school girls by weekly or daily iron-folate supplementation. Author(s): Agarwal KN, Gomber S, Bisht H, Som M.
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Source: Indian Pediatrics. 2003 April; 40(4): 296-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736400&dopt=Abstract ·
Anemia, Myopathy, and Pansteatitis in Vitamin E-deficient Captive Marmosets (Callithrix spp.). Author(s): Juan-Salles C, Prats N, Resendes A, Domingo M, Hilton D, Ruiz JM, Garner MM, Valls X, Marco AJ. Source: Veterinary Pathology. 2003 September; 40(5): 540-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949411&dopt=Abstract
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Antenatal vitamin A supplementation increases birth weight and decreases anemia among infants born to human immunodeficiency virus-infected women in Malawi. Author(s): Kumwenda N, Miotti PG, Taha TE, Broadhead R, Biggar RJ, Jackson JB, Melikian G, Semba RD. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2002 September 1; 35(5): 618-24. Epub 2002 August 02. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12173139&dopt=Abstract
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Blood pressure, hematologic and erythrocyte fragility changes in children suffering from sickle cell anemia following ascorbic acid supplementation. Author(s): Jaja SI, Ikotun AR, Gbenebitse S, Temiye EO. Source: Journal of Tropical Pediatrics. 2002 December; 48(6): 366-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12521281&dopt=Abstract
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Cardiac abnormalities in children with sickle cell anemia. Author(s): Batra AS, Acherman RJ, Wong WY, Wood JC, Chan LS, Ramicone E, Ebrahimi M, Wong PC. Source: American Journal of Hematology. 2002 August; 70(4): 306-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12210812&dopt=Abstract
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Carnitine as adjuvant therapy in the management of renal anemia. Author(s): Cianciaruso B, Torraca S, De Blasio A, Fiorillo M, Marino R. Source: Contrib Nephrol. 2002; (137): 426-30. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12101988&dopt=Abstract
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Cerebral blood flow and vasodilatory capacity in anemia secondary to chronic renal failure. Author(s): Kuwabara Y, Sasaki M, Hirakata H, Koga H, Nakagawa M, Chen T, Kaneko K, Masuda K, Fujishima M. Source: Kidney International. 2002 February; 61(2): 564-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11849397&dopt=Abstract
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Clinical and laboratory manifestations of congenital dyserythropoietic anemia type I in young adults. Author(s): Shalev H, Kapleushnik Y, Haeskelzon L, Degani O, Kransnov T, Sphilberg O, Moser A, Yaniv I, Tamary H. Source: European Journal of Haematology. 2002 March; 68(3): 170-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12068798&dopt=Abstract
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Coenzyme Q10 in plasma and erythrocytes: comparison of antioxidant levels in healthy probands after oral supplementation and in patients suffering from sickle cell anemia. Author(s): Niklowitz P, Menke T, Wiesel T, Mayatepek E, Zschocke J, Okun JG, Andler W. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2002 December; 326(1-2): 155-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12417107&dopt=Abstract
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Combatting anemia in adolescent girls: a report from India. Author(s): Kanani S. Source: Mothers Child. 1994; 13(1): 1-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12287929&dopt=Abstract
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Comparative effects of deferiprone and deferoxamine on survival and cardiac disease in patients with thalassemia major: a retrospective analysis. Author(s): Piga A, Gaglioti C, Fogliacco E, Tricta F. Source: Haematologica. 2003 May; 88(5): 489-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745268&dopt=Abstract
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Considerations for optimal iron use for anemia due to chronic kidney disease. Author(s): Hudson JQ, Comstock TJ. Source: Clinical Therapeutics. 2001 October; 23(10): 1637-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11726002&dopt=Abstract
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Cultural feeding practices and child-raising philosophy contribute to iron-deficiency anemia in refugee Hmong children. Author(s): Culhane-Pera KA, Naftali ED, Jacobson C, Xiong ZB. Source: Ethn Dis. 2002 Spring; 12(2): 199-205. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12019928&dopt=Abstract
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Current issues for the prevention and treatment of iron deficiency anemia. Author(s): Zlotkin S. Source: Indian Pediatrics. 2002 February; 39(2): 125-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11867841&dopt=Abstract
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Does a clinical pathway improve the quality of care for sickle cell anemia? Author(s): Co JP, Johnson KB, Duggan AK, Casella JF, Wilson M. Source: Jt Comm J Qual Saf. 2003 April; 29(4): 181-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12698808&dopt=Abstract
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Double-blind randomized control trial of the effect of recombinant human erythropoietin on chemotherapy-induced anemia in patients with non-small cell lung cancer. Author(s): Kunikane H, Watanabe K, Fukuoka M, Saijo N, Furuse K, Ikegami H, Ariyoshi Y, Kishimoto S. Source: International Journal of Clinical Oncology / Japan Society of Clinical Oncology. 2001 December; 6(6): 296-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11828949&dopt=Abstract
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Effect of dietary habits on prevalence of anemia in pregnant women of Delhi. Author(s): Sharma JB, Soni D, Murthy NS, Malhotra M. Source: The Journal of Obstetrics and Gynaecology Research. 2003 April; 29(2): 73-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12755525&dopt=Abstract
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Epstein-Barr virus associated diffuse large B-cell lymphoma complicated by autoimmune hemolytic anemia and pure red cell aplasia. Author(s): Katayama H, Takeuchi M, Yoshino T, Munemasa M, Tada A, Soda R, Takahashi K. Source: Leukemia & Lymphoma. 2001 July; 42(3): 539-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11699422&dopt=Abstract
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Eradication of iron deficiency anemia through food fortification: the role of the private sector. Author(s): Mehansho H. Source: The Journal of Nutrition. 2002 April; 132(4 Suppl): 831S-3S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11925491&dopt=Abstract
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Folate supplementation in sickle cell anemia. Author(s): Hoffer LJ. Source: The New England Journal of Medicine. 2003 August 21; 349(8): 813; Author Reply 813. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930937&dopt=Abstract
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Health care resource utilization and the impact of anemia management in patients with chronic kidney disease. Author(s): London R, Solis A, Goldberg GA, Wade S, Ryu S.
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Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2002 September; 40(3): 539-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12200806&dopt=Abstract ·
Hepatosplenic gammadelta T-cell lymphoma presenting with immune-mediated thrombocytopenia and hemolytic anemia (Evans' syndrome). Author(s): Motta G, Vianello F, Menin C, De Nicolo A, Agata S, Altavilla G, Pietrogrande F, Girolami A. Source: American Journal of Hematology. 2002 April; 69(4): 272-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11921021&dopt=Abstract
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Impact of daily versus weekly hematinic supplementation on anemia in pregnant women. Author(s): Gomber S, Agarwal KN, Mahajan C, Agarwal N. Source: Indian Pediatrics. 2002 April; 39(4): 339-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976463&dopt=Abstract
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Impact of permethrin-treated bed nets on malaria, anemia, and growth in infants in an area of intense perennial malaria transmission in western Kenya. Author(s): ter Kuile FO, Terlouw DJ, Kariuki SK, Phillips-Howard PA, Mirel LB, Hawley WA, Friedman JF, Shi YP, Kolczak MS, Lal AA, Vulule JM, Nahlen BL. Source: Am J Trop Med Hyg. 2003 April; 68(4 Suppl): 68-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749488&dopt=Abstract
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Ingestion of water-soluble soybean fiber prevents gastrectomy-induced iron malabsorption, anemia and impairment of voluntary running exercise performance in rats. Author(s): Shiga K, Hara H, Okano G, Aoyama Y. Source: The Journal of Nutrition. 2003 April; 133(4): 1120-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672929&dopt=Abstract
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Iron-deficiency anemia in young working women can be reduced by increasing the consumption of cereal-based fermented foods or gooseberry juice at the workplace. Author(s): Gopaldas T. Source: Food Nutr Bull. 2002 March; 23(1): 94-105. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11975375&dopt=Abstract
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Is weekly iron and folic acid supplementation as effective as daily supplementation for decreasing incidence of anemia in adolescent girls? Author(s): Perrin E, Rothman R, Coyne-Beasley T, Ford C, Bordley WC. Source: Archives of Pediatrics & Adolescent Medicine. 2002 February; 156(2): 128-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11814372&dopt=Abstract
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Late complications following treatment for severe aplastic anemia (SAA) with highdose cyclophosphamide (Cy): follow-up of a randomized trial. Author(s): Tisdale JF, Maciejewski JP, Nunez O, Rosenfeld SJ, Young NS. Source: Blood. 2002 December 15; 100(13): 4668-70. Epub 2002 June 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393567&dopt=Abstract
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Parenteral iron supplementation for the treatment of iron deficiency anemia in children. Author(s): Surico G, Muggeo P, Muggeo V, Lucarelli A, Martucci T, Daniele M, Rigillo N. Source: Annals of Hematology. 2002 March; 81(3): 154-7. Epub 2002 February 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11904741&dopt=Abstract
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Pathological response to preoperative chemoradiation worsens with anemia in nonsmall cell lung cancer patients. Author(s): Robnett TJ, Machtay M, Hahn SM, Shrager JB, Friedberg JS, Kaiser LR. Source: Cancer Journal (Sudbury, Mass.). 2002 May-June; 8(3): 263-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12074326&dopt=Abstract
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Permethrin-treated bed nets in the prevention of malaria and anemia in adolescent schoolgirls in western Kenya. Author(s): Leenstra T, Phillips-Howard PA, Kariuki SK, Hawley WA, Alaii JA, Rosen DH, Oloo AJ, Nahlen BL, Kager PA, ter Kuile FO. Source: Am J Trop Med Hyg. 2003 April; 68(4 Suppl): 86-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749490&dopt=Abstract
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Pernicious anemia with neuropsychiatric dysfunction in a patient with sickle cell anemia treated with folate supplementation. Author(s): Dhar M, Bellevue R, Carmel R. Source: The New England Journal of Medicine. 2003 May 29; 348(22): 2204-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12773647&dopt=Abstract
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Persistence and emergence of anemia in children during participation in the Special Supplemental Nutrition Program for Women, Infants, and Children. Author(s): Kahn JL, Binns HJ, Chen T, Tanz RR, Listernick R. Source: Archives of Pediatrics & Adolescent Medicine. 2002 October; 156(10): 1028-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12361450&dopt=Abstract
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Prevention and control of iron deficiency anemia amongst young children. Author(s): Kapil U. Source: Indian Pediatrics. 2003 April; 40(4): 293-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736399&dopt=Abstract
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Pulmonary dysfunction in transfusion-dependent patients with thalassemia major. Author(s): Carnelli V, D'Angelo E, Pecchiari M, Ligorio M, D'Angelo E. Source: American Journal of Respiratory and Critical Care Medicine. 2003 July 15; 168(2): 180-4. Epub 2003 May 08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738605&dopt=Abstract
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Randomized, controlled trial of daily iron supplementation and intermittent sulfadoxine-pyrimethamine for the treatment of mild childhood anemia in western Kenya. Author(s): Desai MR, Mei JV, Kariuki SK, Wannemuehler KA, Phillips-Howard PA, Nahlen BL, Kager PA, Vulule JM, ter Kuile FO. Source: The Journal of Infectious Diseases. 2003 February 15; 187(4): 658-66. Epub 2003 Feb 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12599083&dopt=Abstract
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Recurrent transient ischemic attacks in a 15-year-old boy with beta-thalassemia minor and thrombophilia. Contribution of perfusion SPECT to clinical diagnosis. Author(s): Engelborghs S, Pickut BA, De Deyn PP. Source: Acta Neurol Belg. 2003 June; 103(2): 99-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892004&dopt=Abstract
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Regular consumption of NaFeEDTA-fortified fish sauce improves iron status and reduces the prevalence of anemia in anemic Vietnamese women. Author(s): Thuy PV, Berger J, Davidsson L, Khan NC, Lam NT, Cook JD, Hurrell RF, Khoi HH. Source: The American Journal of Clinical Nutrition. 2003 August; 78(2): 284-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885710&dopt=Abstract
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Relationship between hepatocellular injury and transfusional iron overload prior to and during iron chelation with desferrioxamine: a study in adult patients with acquired anemias. Author(s): Jensen PD, Jensen FT, Christensen T, Nielsen JL, Ellegaard J. Source: Blood. 2003 January 1; 101(1): 91-6. Epub 2002 August 22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393528&dopt=Abstract
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Reversal of cardiac complications in thalassemia major by long-term intermittent daily intensive iron chelation. Author(s): Miskin H, Yaniv I, Berant M, Hershko C, Tamary H. Source: European Journal of Haematology. 2003 June; 70(6): 398-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756023&dopt=Abstract
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Safety monitoring of cardiac and hepatic systems in beta-thalassemia patients with chelating treatment in Taiwan. Author(s): Peng CT, Chow KC, Chen JH, Chiang YP, Lin TY, Tsai CH.
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Source: European Journal of Haematology. 2003 June; 70(6): 392-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12756022&dopt=Abstract ·
Salmonella infection associated with a pet lizard in siblings with sickle cell anemia: an avoidable risk. Author(s): Rodgers GL, Long SS, Smergel E, Dampier C. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 January; 24(1): 75-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11902748&dopt=Abstract
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Transfusion-dependent congenital dyserythropoietic anemia type I successfully treated with allogeneic stem cell transplantation. Author(s): Ayas M, al-Jefri A, Baothman A, al-Mahr M, Mustafa MM, Khalil S, Karaoui M, Solh H. Source: Bone Marrow Transplantation. 2002 April; 29(8): 681-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12180113&dopt=Abstract
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Treating severe anemia in a trauma patient who is a Jehovah's witness. Author(s): Gilcreast DM, Avella P, Camarillo E, Mullane G. Source: Critical Care Nurse. 2001 April; 21(2): 69-72, 75-8, 80-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11858442&dopt=Abstract
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Treatment of aplastic anemia by the kidney-tonifying and mediating method. Author(s): Yu Y, Sun W, Cao K, Wang X. Source: J Tradit Chin Med. 2001 December; 21(4): 252-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12014121&dopt=Abstract
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Women's perceptions of iron deficiency and anemia prevention and control in eight developing countries. Author(s): Galloway R, Dusch E, Elder L, Achadi E, Grajeda R, Hurtado E, Favin M, Kanani S, Marsaban J, Meda N, Moore KM, Morison L, Raina N, Rajaratnam J, Rodriquez J, Stephen C. Source: Social Science & Medicine (1982). 2002 August; 55(4): 529-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12188461&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.comÒ: 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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WebMDÒHealth: 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/
The following is a specific Web list relating to anemia; 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 (some Web sites are subscription based): ·
General Overview Anemia Source: Integrative Medicine Communications; www.drkoop.com Anemia Source: Integrative Medicine Communications; www.drkoop.com Athletic Performance Source: Healthnotes, Inc. www.healthnotes.com Hemophilia Source: Integrative Medicine Communications; www.drkoop.com Histoplasmosis Source: Integrative Medicine Communications; www.drkoop.com Hypercholesterolemia Source: Integrative Medicine Communications; www.drkoop.com Immune Function Source: Healthnotes, Inc. www.healthnotes.com Iron-Deficiency Anemia Source: Healthnotes, Inc. www.healthnotes.com Leukemia Source: Integrative Medicine Communications; www.drkoop.com
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Loiasis Source: Integrative Medicine Communications; www.drkoop.com Lymphatic Filariasis Source: Integrative Medicine Communications; www.drkoop.com Meningitis Source: Integrative Medicine Communications; www.drkoop.com Menorrhagia Source: Healthnotes, Inc. www.healthnotes.com Myelofibrosis Source: Integrative Medicine Communications; www.drkoop.com Myeloproliferative Disorders Source: Integrative Medicine Communications; www.drkoop.com Night Blindness Source: Healthnotes, Inc. www.healthnotes.com Parasitic Infection, Histoplasmosis Source: Integrative Medicine Communications; www.drkoop.com Parasitic Infection, Roundworms Source: Integrative Medicine Communications; www.drkoop.com Phenylketonuria Source: Healthnotes, Inc. www.healthnotes.com Pinworm Source: Integrative Medicine Communications; www.drkoop.com Polycythemia Vera Source: Integrative Medicine Communications; www.drkoop.com Pregnancy and Postpartum Support Source: Healthnotes, Inc. www.healthnotes.com Prostate Cancer Source: Healthnotes, Inc. www.healthnotes.com Prostate Cancer Source: Integrative Medicine Communications; www.drkoop.com Restless Legs Syndrome Source: Healthnotes, Inc. www.healthnotes.com River Blindness Source: Integrative Medicine Communications; www.drkoop.com
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Roundworms Source: Integrative Medicine Communications; www.drkoop.com Rubella Source: Integrative Medicine Communications; www.drkoop.com Shock Source: Integrative Medicine Communications; www.drkoop.com Sickle Cell Anemia Source: Healthnotes, Inc. www.healthnotes.com Sickle cell anemia Source: Integrative Medicine Communications; www.drkoop.com Skin Disorders, Erythema Source: Integrative Medicine Communications; www.drkoop.com Stomach Inflammation Source: Integrative Medicine Communications; www.drkoop.com Threadworm Source: Integrative Medicine Communications; www.drkoop.com Thrombocytosis Source: Integrative Medicine Communications; www.drkoop.com Trichinosis Source: Integrative Medicine Communications; www.drkoop.com Ulcerative Colitis Source: Integrative Medicine Communications; www.drkoop.com Visceral Larva Migrans Source: Integrative Medicine Communications; www.drkoop.com Vitamin B12 Deficiency Source: Healthnotes, Inc. www.healthnotes.com Vitiligo Source: Healthnotes, Inc. www.healthnotes.com Whipworm Source: Integrative Medicine Communications; www.drkoop.com
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Alternative Therapy Apple diet Alternative names: apple-cleansing regimen apple-diet cleansing routine apple-diet regimen apple-diet therapy Source: The Canoe version of A Dictionary of Alternative-Medicine Methods, by Priorities for Health editor Jack Raso, M.S., R.D. Hyperlink: http://www.canoe.ca/AltmedDictionary/a.html Chelation therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,679,00.html Colon therapy Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,682,00.html Macrobiotics Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,714,00.html
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Chinese Medicine Anxixiang Alternative names: Benzoin; Anxixiang (An Xi Xiang); Benzoinum Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Baishao Alternative names: White Peony Root; Radix Paeoniae Alba Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Colla Carapacis et Plastri Testudinis Alternative names: Glue of Tortoise Shell Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Hyperlink: http://www.newcenturynutrition.com/cgilocal/patent_herbs_db/db.cgi?db=default&Chinese=Colla%20carapacis%20et%20Pl astri%20Testudinis&mh=10&sb=---&view_records=View+Records Colla Corii Asini Alternative names: Donkey-hide Glue; %Colla Corii Asini%% Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Hyperlink: http://www.newcenturynutrition.com/cgilocal/patent_herbs_db/db.cgi?db=default&Chinese=Colla%20Corii%20Asini&mh= 10&sb=---&view_records=View+Records
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Danggui Alternative names: Chinese Angelica; Radix Angelicae Sinensis Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Dihuang Alternative names: Digitalis Leaf; Yangdihuangye; Folium Digitalis Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Dingkun Dan Alternative names: Dingkun Pills; Dingkun Dan (Ding Kun Dan) Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Hyperlink: http://www.newcenturynutrition.com/cgilocal/patent_herbs_db/db.cgi?db=default&Chinese=Dingkun%20Dan&mh=10&sb =---&view_records=View+Records Gouqizi Alternative names: Barbary Wolfberry Fruit; Fructus Lycii Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Heshouwu Alternative names: Fleeceflower Root; Radix Polygoni Multiflori Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Hongqi Alternative names: Manyinflorescenced Sweetvetch Root; Radix Hedysari Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Huangqi Alternative names: Milkvetch; Radix Astragali Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Jixueteng Alternative names: Suberect Spatholobus Stem; Caulis Spatholobi Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Longyanrou Alternative names: Longan Aril; Longyanrou (Long Yan Rou); Arillus Longan Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/
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Shengxue Wan Alternative names: Shengxue Pills; Shengxue Wan (Sheng Xue Wan) Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China Hyperlink: http://www.newcenturynutrition.com/cgilocal/patent_herbs_db/db.cgi?db=default&Chinese=Shengxue%20Wan&mh=10&s b=---&view_records=View+Records Shudihuang Alternative names: Prepared Rehmannia Root; Radix Rehmanniae Preparata Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ Zhiheshouwu Alternative names: Prepared FLeeceflower Root; Radix Polygoni Multiflori Preparata Source: Chinese Materia Medica Hyperlink: http://www.newcenturynutrition.com/ ·
Herbs and Supplements 5-Aminosalicylic Acid Derivatives Source: Integrative Medicine Communications; www.drkoop.com Alfalfa Alternative names: Medicago sativa Source: Healthnotes, Inc. www.healthnotes.com Aminoglycosides Source: Integrative Medicine Communications; www.drkoop.com Angelica sinensis Source: Integrative Medicine Communications; www.drkoop.com Antibiotic Combination: Sulfa Drugs Source: Integrative Medicine Communications; www.drkoop.com Anticonvulsants Source: Healthnotes, Inc. www.healthnotes.com Antituberculosis Agents Source: Integrative Medicine Communications; www.drkoop.com Aristolochia Alternative names: Snakeroot, Guaco; Aristolochia sp Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/
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Arnica Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,753,00.html Aspirin Source: Healthnotes, Inc. www.healthnotes.com Astragalus Alternative names: Astragalus membranaceus, Astragalus membranaceus var. mongholicus, Huang-qi, Milk-Vetch Root Source: Integrative Medicine Communications; www.drkoop.com Astragalus membranaceus Source: Integrative Medicine Communications; www.drkoop.com Astragalus mongholicus Alternative names: Astragalus membranaceus, Astragalus membranaceus var. mongholicus, Huang-qi, Milk-Vetch Root Source: Integrative Medicine Communications; www.drkoop.com AZT Source: Healthnotes, Inc. www.healthnotes.com Barbiturates Source: Integrative Medicine Communications; www.drkoop.com Beta-Carotene Source: Healthnotes, Inc. www.healthnotes.com Biguanides Source: Integrative Medicine Communications; www.drkoop.com Bile Acid Sequestrants Source: Integrative Medicine Communications; www.drkoop.com Bisphosphonate Derivatives Source: Integrative Medicine Communications; www.drkoop.com Blood-building formula Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10101,00.html Blue-green Algae Source: Integrative Medicine Communications; www.drkoop.com Carbamazepine Alternative names: Atretol, Carbatrol, Epitol, Tegretol, Tegretol XR Source: Prima Communications, Inc.www.personalhealthzone.com
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Carotenoids Source: Healthnotes, Inc. www.healthnotes.com Cephalosporins Source: Integrative Medicine Communications; www.drkoop.com Chinese Angelica Source: Integrative Medicine Communications; www.drkoop.com Chitosan Source: Healthnotes, Inc. www.healthnotes.com Chlorophyll Source: Healthnotes, Inc. www.healthnotes.com Cobalamin Source: Integrative Medicine Communications; www.drkoop.com Dandelion Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10021,00.html Danggui Alternative names: Angelica sinensis, Chinese Angelica, Dang Gui, Danngui, Dong Qua, Tang Kuei, Tan Kue Bai zhi(Note: Dong quai should not be confused with Angelica root or Angelica seed.) Source: Integrative Medicine Communications; www.drkoop.com Dong Quai Alternative names: Angelica sinensis Source: Healthnotes, Inc. www.healthnotes.com Dong Quai Alternative names: Angelica sinensis, Chinese Angelica, Dang Gui, Danngui, Dong Qua, Tang Kuei, Tan Kue Bai zhi(Note: Dong quai should not be confused with Angelica root or Angelica seed.) Source: Integrative Medicine Communications; www.drkoop.com Dong Quai Source: Prima Communications, Inc.www.personalhealthzone.com Electrolytes Source: Integrative Medicine Communications; www.drkoop.com Flavonoids Source: Healthnotes, Inc. www.healthnotes.com Histamine H2 Antagonists Source: Integrative Medicine Communications; www.drkoop.com
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Huang-qi Source: Integrative Medicine Communications; www.drkoop.com Hydantoin Derivatives Source: Integrative Medicine Communications; www.drkoop.com Inhalant, Systemic, and Topical Corticosteroids Source: Integrative Medicine Communications; www.drkoop.com Juniperus Alternative names: Juniper; Juniperus sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Lepidium meyenii1 Alternative names: Maca; Lepidium meyenii Walp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/ Liver Extracts Source: Healthnotes, Inc. www.healthnotes.com Loop Diuretics Source: Integrative Medicine Communications; www.drkoop.com Macrolides Source: Integrative Medicine Communications; www.drkoop.com Milk-Vetch Root Source: Integrative Medicine Communications; www.drkoop.com Miscellaneous Source: Integrative Medicine Communications; www.drkoop.com Miscellaneous Preparations Source: Integrative Medicine Communications; www.drkoop.com Monophasic, Biphasic, and Triphasic Preparations Source: Integrative Medicine Communications; www.drkoop.com Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Source: Integrative Medicine Communications; www.drkoop.com Omeprazole Source: Healthnotes, Inc. www.healthnotes.com Pau d'arco Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,811,00.html
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Penicillin Derivatives Source: Integrative Medicine Communications; www.drkoop.com Phenobarbital Alternative names: Bellatal, Solfoton Source: Prima Communications, Inc.www.personalhealthzone.com Primidone Alternative names: Mysoline Source: Prima Communications, Inc.www.personalhealthzone.com Proton Pump Inhibitors (Gastric Acid Secretion Inhibitors) Source: Integrative Medicine Communications; www.drkoop.com Quinolones Source: Integrative Medicine Communications; www.drkoop.com Reverse Transcriptase Inhibitors Source: Integrative Medicine Communications; www.drkoop.com Salicylates Source: Integrative Medicine Communications; www.drkoop.com Spirulina Alternative names: Blue-green Algae Source: Integrative Medicine Communications; www.drkoop.com St. John's Wort Source: Prima Communications, Inc.www.personalhealthzone.com Tang Kuei Source: Integrative Medicine Communications; www.drkoop.com Tetracycline Derivatives Source: Integrative Medicine Communications; www.drkoop.com Theophylline Derivatives Source: Integrative Medicine Communications; www.drkoop.com Thyroid Hormones Source: Healthnotes, Inc. www.healthnotes.com Triamterene Source: Healthnotes, Inc. www.healthnotes.com Trimethoprim Source: Healthnotes, Inc. www.healthnotes.com Trimethoprim/Sulfamethoxazole Source: Healthnotes, Inc. www.healthnotes.com
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Uricosuric Agents Source: Integrative Medicine Communications; www.drkoop.com Valproic Acid Source: Healthnotes, Inc. www.healthnotes.com Valproic Acid Derivatives Source: Integrative Medicine Communications; www.drkoop.com Vasodilators Source: Integrative Medicine Communications; www.drkoop.com Zanthoxylum Alternative names: Prickly Ash; Zanthoxylum sp. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Hyperlink: http://www.herbmed.org/
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 ANEMIA Overview In this chapter, we will give you a bibliography on recent dissertations relating to anemia. 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 “anemia” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on anemia, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Anemia 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 anemia. 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: ·
An Investigation of the Effects of Counseling on Adolescents with Diagnosed Sickle Cell Anemia by Huntley, Ola Mae, Edd from University of San Francisco, 1983, 141 pages http://wwwlib.umi.com/dissertations/fullcit/8404364
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Characterization of Zebrafish Mutant Merlot As a Non-mammalian Vertebrate Model for Congenital Anemia due to Protein 4.1 Deficiency by Shafizadeh, Ebrahim; Phd from Medical College of Georgia, 2002, 131 pages http://wwwlib.umi.com/dissertations/fullcit/3055176
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Cytotoxic T Lymphocyte Responses to Marek's Disease Herpesvirus-encoded Glycoproteins and Their Impairment by Chicken Infectious Anemia Virus by Grimsrud, Carrie Justine; Phd from Cornell University, 2002, 221 pages http://wwwlib.umi.com/dissertations/fullcit/3050395
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Defective Dna Double-strand Break Repair Activity in Fanconi Anemia Fibroblasts by Donahue, Sarah Louise; Phd from University of Minnesota, 2003, 157 pages http://wwwlib.umi.com/dissertations/fullcit/3076318
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Diet, Parasitism, and Anemia in the Prehistoric Southwest by Reinhard, Karl Jan, Phd from Texas A&m University, 1988, 215 pages http://wwwlib.umi.com/dissertations/fullcit/8913432
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Differential Perceptions of Sickle Cell Anemia Patients by Battle, Stanley Fred, Phd from University of Pittsburgh, 1980, 189 pages http://wwwlib.umi.com/dissertations/fullcit/8018278
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Drawing Blood: Medical Conceptions of Disease in 20th Century America, from Chlorosis to Sickle Cell Anemia (twentieth Century, Blood Diseases) by Wailoo, Keith, Phd from University of Pennsylvania, 1992, 425 pages http://wwwlib.umi.com/dissertations/fullcit/9308675
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Factors That Influence Iron Deficiency Anemia among Infants Who Attend the Women, Infants and Children (wic) Program by Chowa, Lydia Siphiwe; Drph from Loma Linda University, 2002, 131 pages http://wwwlib.umi.com/dissertations/fullcit/3056875
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Genetic and Phenotypic Variation of the Equine Infectious Anemia Virus Surface Unit Envelope Glycoprotein during Disease Progression by Sponseller, Brett Alan; Phd from Iowa State University, 2003, 138 pages http://wwwlib.umi.com/dissertations/fullcit/3085946
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Identification of the Areas of Knowledge and Behavioral Skills for Sickle Cell Anemia Patient Education Program Development by Graumlich, Sally Elizabeth, Edd from University of Cincinnati, 1989, 347 pages http://wwwlib.umi.com/dissertations/fullcit/9003236
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Impact of Sickle Cell Anemia on Attitudes and Relationships among Particular Family Members. by Sellers, Frank, Jr., Phd from University of Pittsburgh, 1974, 128 pages http://wwwlib.umi.com/dissertations/fullcit/7419522
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Iron-deficiency Anemia among Village Women of the Middle Hills of Nepal by Malville, Nancy Jean, Phd from University of Colorado at Boulder, 1987, 252 pages http://wwwlib.umi.com/dissertations/fullcit/8716268
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Law, Medicine and Public Policy: the Sickle Cell Anemia Control Act of 1972. a Case Study by Schmidt, Robert Milton, Phd from Emory University, 1982, 269 pages http://wwwlib.umi.com/dissertations/fullcit/8214059
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Life, Ethics, and Sickle Cell Anemia: a Single Gene Disorder in a Contingent World (senegal) by Fullwiley, Duana Clarice; Phd from Univ. of Calif., Berkeley with the Univ. of Calif., San Francisco, 2002, 388 pages http://wwwlib.umi.com/dissertations/fullcit/3082612
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Maximal Oxygen Uptake of Male Sickle Cell Anemia Trait Subjects. by Robinson, Joe Richard, Edd from Arizona State University, 1975, 150 pages http://wwwlib.umi.com/dissertations/fullcit/7516258
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Neuropsychological Functioning in Children with Sickle Cell Anemia by Swift, Andrea Veruki, Phd from University of Georgia, 1987, 110 pages http://wwwlib.umi.com/dissertations/fullcit/8712695
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Porotic Hyperostosis As an Indicator of Anemia: an Overview of Correlation and Cause by Hill, Mary Cassandra; Phd from University of Massachusetts Amherst, 2001, 202 pages http://wwwlib.umi.com/dissertations/fullcit/3000310
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Primaquine-induced Hemolytic Anemia: Formation and Mechanism of Action of the Hemotoxic Metabolite 6-methoxy-8-hydroxylamoniquinoline (maq-noh) by Bolchoz, Laura Jane Campbell; Phd from Medical University of South Carolina, 2002, 146 pages http://wwwlib.umi.com/dissertations/fullcit/3050229
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Relationships of Zinc, Copper, Cholesterol and Erythrocyte Oxidant Stress in Sickle Cell Anemia by Bereza, Ulana Lydia, Phd from The University of Michigan, 1985, 207 pages http://wwwlib.umi.com/dissertations/fullcit/8520868
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Respiratory Function in Children with Sickle Cell Anemia. by Borden, Michael Douglas, Phd from Temple University, 1977, 149 pages http://wwwlib.umi.com/dissertations/fullcit/7713543
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Sociomedical Investigation of Sickle Cell Anemia: Screening and Coping. by Oke, Ezekiel Adewale, Phd from University of Kentucky, 1977, 173 pages http://wwwlib.umi.com/dissertations/fullcit/7815760
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Studies on Patients with Fanconi's Anemia by Finkelberg, Rosanna; Phd from University of Toronto (canada), 1977 http://wwwlib.umi.com/dissertations/fullcit/NK35204
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The Concept of Genetic Disease and Theories of Medical Progress. (volumes I and Ii) (sickle Cell Anemia) by Juengst, Eric Thomas, Phd from Georgetown University, 1985, 459 pages http://wwwlib.umi.com/dissertations/fullcit/8613937
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The Etiology of Iron Deficiency Anemia during Pregnancy among Rural Mothers in Malaysia by Arshad, Fatimah; Phd from The University of British Columbia (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NL20582
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The Expectations for the Future of Children with Hematologic Disorders and Their Mothers (sickle Cell Anemia, Itp) by Schiller, Marilyn, Phd from New York University, 1989, 182 pages http://wwwlib.umi.com/dissertations/fullcit/9004322
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The Impact of Health Adjustment and Perceived Social Support on the Career Exploration of Adolescents Living with Sickle Cell Anemia by Lochard, Claudine Marie Madeleine; Phd from State University of New York at Albany, 2002, 141 pages http://wwwlib.umi.com/dissertations/fullcit/3068762
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The Psychoeducational Effects of Sickle Cell Anemia: Analysis of School Success/nonsuccess in a Group of Children with Sickle Cell Anemia by Allen, Patrick Lawrence, Edd from University of Cincinnati, 1983, 172 pages http://wwwlib.umi.com/dissertations/fullcit/8323183
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The Role of Reactive Oxygen and Nitrogen Species in the Development of Fanconi Anemia, an Inherited Bone Marrow Failure Disorder by Hadjur, Suzana; Phd from The University of British Columbia (canada), 2002, 147 pages http://wwwlib.umi.com/dissertations/fullcit/NQ75021
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The Role of Rev-sr Protein Interactions in the Regulation of Equine Infectious Anemia Virus Replication by Park, Gregory Saang; Phd from Iowa State University, 2003, 141 pages http://wwwlib.umi.com/dissertations/fullcit/3085936
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The Signifying Disease: Difference, Discrimination and the Discourse of Sickle Cell Anemia by Tapper, Melbourne Ximines, Phd from The University of Connecticut, 1990, 388 pages http://wwwlib.umi.com/dissertations/fullcit/9102040
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The Social Support Needs of Parents of Children with Sickle Cell Anemia (natural, Helping Networks, System) by Lester, Bernadette Maria Fitts, Dsw from The University of Alabama, 1985, 137 pages http://wwwlib.umi.com/dissertations/fullcit/8519400
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Vitamin a and Anemia in Zimbabwean Infants by Miller, Melissa A. Farmer; Phd from The Johns Hopkins University, 2002, 233 pages http://wwwlib.umi.com/dissertations/fullcit/3046517
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 ANEMIA Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning anemia.
Recent Trials on Anemia The following is a list of recent trials dedicated to anemia.8 Further information on a trial is available at the Web site indicated. ·
A Monoclonal Antibody Conditioning Regimen for Allogeneic Stem Cell Transplant in Patients with Fanconi Anemia. Condition(s): Fanconi's Anemia Study Status: This study is currently recruiting patients. Sponsor(s): Baylor College of Medicine; Texas Children's Hospital; The Methodist Hospital Purpose - Excerpt: Patients eligible for this study have an aggressive blood disease, Fanconi anemia (FA) that requires an allogeneic (meaning the cells come from a donor) stem cell transplant using a family member or nearly identical matched donor. Stem cells are cells in the bone marrow and blood that can form a whole new blood system. Usually, these patients are given high doses of chemotherapy before receiving a stem cell transplant in order to keep the immune system from rejecting the donor stem cells, and to kill any diseased cells that remain in the body. However, some patients, due to complications with their condition, may have a high risk of acquiring possibly lifethreatening treatment-related side effects such as graft versus host disease (GVHD). GVHD occurs when the new stem cells (graft) recognize that the body tissues of the patient (host) are different from those of the donor. When this happens, cells in the graft may attack the host organs, primarily the skin, the liver and the intestines. Even with the strongest available treatments, graft rejection can occur or some diseased cells may survive and cause relapse. Instead of the high dose chemotherapy usually given before a transplant, this research study uses a new pre-treatment combination of two drugs,
8
These are listed at www.ClinicalTrials.gov.
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Anti-CD45 and CAMPATH-1H. Anti-CD45 and CAMPATH-1H are antibodies against certain types of blood cells, including FA cells. CAMPATH-1H is particularly important because it stays active in the body for a long time after infusion, which means it may work longer at preventing GVHD symptoms. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00058565 ·
A Study to Determine whether Therapy with Daclizumab Will Benefit Patients with Bone Marrow Failure Condition(s): Aplastic Anemia; Pure Red Cell Aplasia; Thrombocytopenic Purpura Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Participants in this study are suffering from rare and serious blood disorders. In aplastic anemia, the bone marrow stops producing red blood cells, platelets, and white blood cells. In pure red cell aplasia, the bone marrow stops producing red cells, and in amegakaryocytic thrombocytopenic purpura, the bone marrow stops producing platelets. Current treatment approaches for these disorders include bone marrow transplant and/or immunosuppression. However, bone marrow transplant is not always possible, and immunosuppression has serious side effects. This study will investigate whether daclizumab can be used to treat these disorders. Daclizumab is a genetically engineered human antibody that blocks the interleukin-2 receptor on immune cells. It has been used successfully in many transplant patients to reduce the rate of organ rejection. Participants will undergo a complete history and physical examination. A bone marrow aspiration and biopsy will be performed to confirm the type of bone marrow failure. About 5 tablespoons of blood will be drawn for baseline tests and research purposes. Daclizumab will be administered every 2 weeks by vein in a 30-minute infusion. The first dose will be given at NIH and the next four may be given at NIH or by the participant's primary hematologist. The treatment will last 8 weeks. Participants must also see their referring physician or NIH physicians every 2 weeks for blood counts. In the fourth and eighth weeks of the study and at the 3month follow-up visit, 2 tablespoons of blood will be drawn at NIH. At the 1-month follow-up visit to NIH, 5 tablespoons of blood will be drawn and another bone marrow aspiration and biopsy performed. Risks from bone marrow aspiration and biopsy and blood draws include discomfort. Daclizumab is usually well-tolerated; however, it may weaken immunity against certain bacteria and viruses. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001962
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Anemia in Patients with a Non-Myeloid Malignancy Condition(s): Anemia; Neoplasms Study Status: This study is currently recruiting patients. Sponsor(s): Amgen
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Purpose - Excerpt: Chemotherapy can often cause anemia in patients with cancer. anemia is a low number of red blood cells. The symptoms of anemia may include fatigue, dizziness, headache, chest pain, and shortness of breath. Erythropoietin is a hormone made by the kidneys that signals the bone marrow to produce more red blood cells. Recombinant human erythropoeitin has been produced in the laboratory and has the same effect as the hormone produced by the body. Use of recombinant human erythropoeitin allows the body to produce more red blood cells, possibly eliminating or decreasing your symptoms and the need for a red blood cell transfusion. Recombinant human erythropoeitin is FDA approved to treat anemia in cancer patients receiving chemotherapy. This clinical study is investigating the effectiveness of darbepoetin alfa for the treatment of anemia in patients with non-myeloid malignanices who are receiving multicycle chemotherapy. Darbepoetin alfa is a recombinant erythropoeitic protein that stimulates the production of red blood cells. This medication has not been approved to treat cancer patients with anemia, however it has been approved by the FDA to treat chronic renal failure patients with anemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00038064 ·
Bone marrow transplant from donor using less toxic conditioning for patient with high risk hemoglobinopathies Condition(s): Sickle Cell Anemia; Hemoglobinopathy; Thalassemia Study Status: This study is currently recruiting patients. Sponsor(s): Baylor College of Medicine; Texas Children's Hospital; The Methodist Hospital Purpose - Excerpt: The major goal of this study is to determine the risks and benefits of stem cell transplants in combination with a newer, less toxic conditioning chemotherapy treatment in patients with severe sickle cell disease (SCD) or sickle hemoglobin variants (hemoglobin SC or hemoglobin SB0/+), or homozygous b0/+ thalassemia or severe B0/+ thalassemia variants. Participation in this project will be for one year, with follow up evaluations done every 6 months thereafter for 10 years or until participants are 18 years old. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00040417
·
Bone Marrow transplant from related donor for patients with high risk hemoglobinopathies Condition(s): Sickle Cell Anemia; Hemoglobinopathy; Thalassemia Study Status: This study is currently recruiting patients. Sponsor(s): Baylor College of Medicine; The Methodist Hospital; Texas Children's Hospital
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Purpose - Excerpt: The major goal of this study is to determine the risks and benefits of bone marrow transplants in patients with severe thalassemia or sickle cell disease. Participation in this project will be for two years. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00040469 ·
Collection of Biological Samples from Patients with Hepatitis-Associated Aplastic Anemia Condition(s): Aplastic Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will collect samples of blood, stool, bone marrow, or other tissues from patients with hepatitis-associated aplastic anemia to investigate a possible association between exposure to viruses and the development of aplastic anemia in these patients. Cells from the samples obtained may be grown in the laboratory for future studies. Patients' samples may be used to: - Study abnormalities that occur in hepatitis-associated aplastic anemia; - Test for various viruses; - Test immune function; Measure factors related to the patients' disease or diseases they may be at risk for; Evaluate the effectiveness of current therapies, refine treatment approaches, and identify potential new therapies; - Identify possible measures for disease prevention; - Identify possible genetic factors associated with hepatitis-associated aplastic anemia. Patients 2 years of age and older with severe aplastic anemia that developed within 6 months of an episode of hepatitis may be eligible for this study. Participants will complete questionnaires and provide tissue samples as described below. Questionnaires All patients (or another respondent for the patient) will fill out a questionnaire including demographic information (age, gender, race, ethnic group, education level, state of residence), current symptoms, medications, medical history, and history of possible exposures to toxins or viruses. A second questionnaire, which includes questions related to mental health, sexual behavior, alcohol and drug use, is optional for participants age 21 and older. These questionnaires are designed to uncover features of hepatitisassociated aplastic anemia and possibly reveal a common cause of the disease. Sample Collections - Blood- will be collected at the time of the patient's initial evaluation or upon enrollment into the study and possibly periodically during the study. Blood will be drawn through a needle in an arm vein. - Bone marrow- may be collected as part of the patient's standard medical care or specifically for research purposes of this study. For this procedure, the skin over the hipbone and the outer surface of the bone itself are numbed with an injection of a local anesthesia. Then, a larger needle is inserted into the hipbone and marrow is drawn into a syringe. Marrow cells are suctioned two to six times during the 15-minute procedure. - Stool- will be provided by the patient. Livertissue may be biopsied as part of the patient's general medical care or for NIH patients, as part of their enrollment in a treatment protocol. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00050115
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Combination Therapy of Severe Aplastic Anemia Condition(s): Aplastic Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will test the safety and effectiveness of a combination of three drugs in treating severe aplastic anemia and preventing its recurrence. Two drugs used in this trial-ATG and cyclosporine-are standard combination therapy for aplastic anemia. This study will try to improve this therapy in three ways: 1) by altering the drug regimen to allow the drugs to work better; 2) by reducing the risk of kidney damage; and 3) by adding a third drug-mycophenolate mofetil-to try to prevent disease relapse. Patients with severe aplastic anemia who do not have a suitable bone marrow donor or who decline bone marrow transplantation may participate in this study. Patients will have a skin test for ATG allergy, chest X-ray, blood test, and bone marrow aspiration before treatment begins. ATG will then be started, infused through a vein continuously for 4 days. Ten days after ATG is stopped, cyclosporine treatment will begin, taken twice a day by mouth in either liquid or capsule form and will continue for 6 months. Also, in the first 2 weeks of treatment, patients will be given a full dose of corticosteroid (prednisone) to prevent serum sickness that could develop as a side effect of ATG therapy. The dosage will be decreased after that. Mycophenolate will be started at the same time as ATG, in two daily doses by mouth, and will continue for 18 months. Patients will be hospitalized at the beginning of the study. During this time, blood will be drawn at 3-week intervals and a bone marrow examination will be repeated 3 months after treatment has begun. Additional tests, including X-rays may be required. After hospital discharge, patients will be followed on an outpatient basis at 3-month intervals. The patients' own physician will perform blood tests weekly and kidney and liver function tests every 2 weeks during cyclosporine therapy. Transfusions may be required initially. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001964
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Darbepoetin Alfa Compared With Epoetin alfa in Treating Anemia in Patients Receiving Chemotherapy for Cancer Condition(s): Fatigue; Anemia; unspecified adult solid tumor, protocol specific Study Status: This study is currently recruiting patients. Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Darbepoetin alfa and epoetin alfa may stimulate red blood cell production to treat patients who have anemia and are receiving chemotherapy. It is not yet known whether darbepoetin alfa is more effective than epoetin alfa in treating anemia. PURPOSE: Randomized phase III trial to compare the effectiveness of darbepoetin alfa with that of epoetin alfa in treating anemia in patients who are receiving chemotherapy for cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00046982 ·
Epoetin beta in Treating Anemia in Patients With Cervical Cancer Condition(s): Anemia; Cervical Cancer Study Status: This study is currently recruiting patients. Sponsor(s): AGO Ovarian Cancer Study Group Purpose - Excerpt: RATIONALE: Epoetin beta may stimulate red blood cell production to prevent or control anemia in patients treated with chemotherapy and radiation therapy. PURPOSE: Randomized phase IV trial to determine the effectiveness of epoetin beta in treating anemia in patients who are receiving cisplatin and radiation therapy for stage IIB, stage III, or stage IVA cervical cancer. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00046969
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Evaluation of Hydroxyurea Plus L-arginine or Sildenafil to Treat Sickle Cell Anemia Condition(s): Sickle Cell Anemia Study Status: This study is currently recruiting patients. Sponsor(s): Warren G Magnuson Clinical Center (CC) Purpose - Excerpt: Patients with sickle cell disease have abnormal hemoglobin (the protein in red blood cells that carries oxygen to the body). This abnormality causes red blood cells to take on a sickle shape, producing disease symptoms. Fetal hemoglobin, a type of hemoglobin present in fetuses and babies, can prevent red cells from sickling. The drug hydroxyurea increases fetal hemoglobin production in patients with sickle cell disease by making a molecule called nitric oxide. The drugs L-arginine and Sildenafil (Viagra) increase the amount or the effect of nitric oxide. This study will evaluate: - The safety of giving L-arginine or Sildenafil together with hydroxyurea in patients with sickle cell disease; - The effectiveness of L-arginine plus hydroxyurea or Sildenafil plus hydroxyurea in increasing fetal hemoglobin in patients with sickle cell disease; and The effectiveness of L-arginine plus hydroxyurea or Sildenafil and hydroxyurea in lowering blood pressure in the lungs of patients with sickle cell disease. (Pulmonary blood pressure is elevated in about one-third of patients with sickle cell disease, and this condition increases the risk of dying from the disease.) Patients with hemoglobin S-only, S-beta-thalassemia, or other sickle cell disease genotype may be eligible for this study. Before starting treatment, patients will have a complete medical history and physical examination. All patients will take hydroxyurea once a day every day by mouth for at least 2 months. They will be admitted to the NIH Clinical Center to take their first dose of hydroxyurea, and will have blood drawn through a catheter (plastic tube placed in a vein) every hour for 6 hours for tests to determine nitric oxide levels. After discharge, they will return to the clinic once every 2 weeks to check for treatment side effects and for blood tests to monitor hemoglobin and fetal hemoglobin levels. After fetal hemoglobin levels have been stable for 2 months, patients will be admitted to the Clinical Center for their first dose of L-arginine (for men) or Sildenafil (for women). Again, blood samples will be collected through a catheter once an hour for 6 hours. If there are no complications, patients will be discharged and will continue taking hydroxyurea once a day and L-arginine or Sildenafil three times a day for at least 3
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months until fetal hemoglobin levels have been stable for at least 2 months. Patients will return to the clinic for blood tests every week for 2 weeks and then every 2 weeks to monitor hemoglobin and fetal hemoglobin levels and to check for treatment side effects. Patients will have eye examinations before and during treatment. Some patients with sickle cell disease develop abnormalities in the blood vessels of the eye. Also, Sildenafil can cause temporary changes in color vision. Rarely, more serious eye problems can occur, such as bleeding from the eye blood vessels or damage to the retina-a layer of tissue that lines the back of the eye. Patients will also have an echocardiogram (ultrasound of the heart) before beginning treatment, after hydroxyurea treatment, and after 1 and 3 months of combined treatment with hydroxyurea and L-arginine or Sildenafil to help measure blood pressure in the lungs. Patients who develop complications from L-arginine or Sildenafil may continue in the study on hydroxyurea alone. Patients whose fetal hemoglobin levels increase with the combination therapy of hydroxyurea and L-arginine or Sildenafil may continue to take them. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00056433 ·
Heart Failure and Anemia Condition(s): Heart Failure; Anemia Study Status: This study is currently recruiting patients. Sponsor(s): Amgen Purpose - Excerpt: This study evaluates the safety and efficacy of darbepoetin alfa to treat anemia in subjects with heart failure of NYHA class 2 to 4. The study assesses the effect of the treatment on exercise capacity and heart failure symptoms. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049985
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Immunosuppression and Stem Cell Transplantation for Relapsed Aplastic Anemia Condition(s): Aplastic Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will examine 1) whether it is possible to collect enough stem cells (cells produced by the bone marrow that mature into white and red blood cells and platelets) from patients with aplastic anemia to use for future treatment, and 2) whether patients who have been treated successfully and relapse will benefit from autologous stem cell transfusion (transfusion of their own stem cells). Patients 12 years of age or older with aplastic anemia who have been successfully treated with immunosuppressive drugs and are now in remission may be eligible for this study. Participants will undergo a complete history and physical examination, bone marrow biopsy (removal of a small sample of bone marrow from the hip bone) and blood tests, plus procedures to collect stem cells, as follows: -G-CSF (Filgrastim) administration - G-
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CSF will be given by injection under the skin daily for up to 10 days. This drug causes stem cells to move from the marrow into the blood where they can be collected more easily. - Apheresis - Stem cells will be collected through apheresis, usually starting the 5th to 6th day of Filgrastin injections. For this procedure, whole blood is collected through a needle in an arm vein. The blood circulates through a cell separator machine where the white cells and stem cells are removed. The red cells, platelets and plasma are returned to the body through a second needle in the other arm. The procedure takes about 5 hours. Up to five procedures, done on consecutive days, may be required to collect enough cells for transplantation. If enough cells are collected, they will be purified (treated to remove the white blood cells) using an experimental device. Removing the lymphocytes may reduce the chance of relapse of aplastic anemia following the stem cell transplant. The stem cells will be frozen for later use, if needed. Follow-up - Participants are followed at NIH at 6-month intervals. Patients who relapse will return to the NIH for standard treatment with cyclosporin A and, if needed, antithymocyte globulin. Patients whose cell counts remain very low and do not improve with this treatment will undergo stem cell transplantation with the stem cells previously collected. The procedure involves the following: - Cyclophosphamide administration Cyclophosphamide will be given through a vein over a 1-hour period each day for 2 days to eliminate the failed bone marrow and white cells causing the disease. - Stem cell infusion - The stem cells will be thawed and given through a vein over 30 to 60 minutes. G-CSF will also be given to boost white cell counts. - Patients will receive antibiotics to help prevent infection, beginning 5 days before cyclophosphamide. - Blood counts will be taken daily. Red cells and platelets will be transfused to maintain safe levels. - After discharge from the hospital, follow-up visits will be scheduled for 1, 3, 6, 12, 24, 36, and 60 months after treatment for examinations and tests to evaluate the response to treatment. Four to 6 tablespoons of blood will be collected at each visit. Bone marrow aspirates and biopsies will be done at the 3-month and 12-month visits. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011830 ·
Improving Immunosuppressive Treatment for Patients with Severe Aplastic Anemia Condition(s): Aplastic Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Immunosuppressive treatment (administering drugs that suppress the immune system) is often successful for people with severe aplastic anemia (SAA). However, SAA patients tend to be highly susceptible to relapse, even after successful immunosuppressive treatment. Research suggests that SAA is an autoimmune disease and thus may require longer immunosuppressive treatment with different drugs. The purpose of this study is to compare two immunosuppressive regimens with the goal of decreasing relapse in SAA patients. Study participants will be placed in one of two study groups. One group will receive a combined drug treatment of antithymocyte globulin (ATG), cyclosporine (CsA) and sirolimus for six months. The other group will receive a combined treatment of ATG and CsA for 6 months, followed by a slow taper of CsA over the next 18 months. Upon admission to NIH, patients will undergo several days of preliminary testing and receive the medications; they will be hospitalized
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during this period (7-10 days). Study participants will have blood drawn periodically during treatment. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061360 ·
Improving the Results of Bone Marrow Transplantation for Patients with Severe Congenital Anemias Condition(s): Congenital Hemolytic Anemia; Diamond-Blackfan Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: People with severe congenital anemias, such as sickle cell anemia, thalassemia, and Diamond Blackfan anemia, have been cured with bone marrow transplantation (BMT). The procedure, however, is limited to children younger than the age of 16 because the risks are lower for children than for adults. The purpose of this study is to explore the use of a BMT regimen that, instead of chemotherapy, uses a low dose of radiation, combined with two immunosuppressive drugs. This type BMT procedure is described as nonmyeloablative, meaning that it does not destroy the patient's bone marrow. It is hoped that this type of BMT will be safe for patients normally excluded from the procedure because of their age and other reasons. To participate in this study, patients must be between the ages of 18 and 65 and have a sibling who is a well-matched stem-cell donor. Beyond the standard BMT protocol, study participants will undergo additional procedures. The donor will receive G-CSF by injection for five days; then his or her stem cells will be collected and frozen one month prior to BMT. Approximately one month later, the patient will be given two immunesuppressing drugs, Campath 1-H and Sirolimus, as well as a single low dose of total body irradiation and then the cells from the donor will be infused. Prior to their participation in this study, patients will undergo the following evaluations: a physical exam, blood work, breathing tests, heart-function tests, chest and sinus x-rays, and bone-marrow sampling. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061568
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Inhaled Nitric Oxide and Transfusion Therapy for Patients with Sickle Cell Anemia and Secondary Pulmonary Hypertension Condition(s): Sickle Cell Anemia; Pulmonary Hypertension Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will test whether inhaling nitric oxide gas mixed with room air can improve pulmonary hypertension (high blood pressure in the lungs) in patients with sickle cell anemia. It is estimated that 20 to 30 percent of patients with sickle cell anemia have moderate to severe pulmonary hypertension, a disease
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complication associated with higher rates of illness and death. Patients with sickle cell disease 18 years of age or older may be eligible to participate in one or more parts of this three-stage study. Candidates will be screened with a medical history, physical examination, electrocardiogram, echocardiogram and blood tests. Those enrolled will undergo the following tests and procedures: Stage 1: Patients will be tested to determine the cause of pulmonary hypertension. They will have an echocardiogram (ultrasound study of the heart); a test for asthma, with measurement of arterial blood oxygen levels; oxygen breathing study with measurement of arterial blood oxygen levels; chest X-ray; computed tomography (CT) scans of the lung with and without contrast material; magnetic resonance imaging (MRI) of the heart; 6-minute walk to measure the distance covered in that time at a comfortable pace; night-hawks oxygen measurement while sleeping; blood tests for HIV, hepatitis virus, lupus and arthritis and pregnancy; pulmonary ventilation/perfusion scan with evaluation of shunt fraction to the brain and kidney; and exercise studies will be performed to determine oxygen and carbon dioxide consumption and production and to measure the anaerobic threshold. Stage 2: Patients who proceed with stage 2 will have a detailed MRI evaluation of the heart and will be admitted to the Clinical Center intensive care unit for the following procedure: A small intravenous (IV) catheter (plastic tube) is placed in the patient arm and a longer tube, called a central line, in a deeper neck or leg vein. A long thin tube is then inserted through the vein into the heart and the lung artery to measure all blood pressures in the heart and lungs directly. Following baseline measurements the following medications will be delivered for two hours each, separated by a 30 minute wash-out period. The patients is then given oxygen to breathe for 2 hours, followed by infusion of prostacyclin, a blood pressure-lowering drug, for 2 hours; and finally inhaled nitric oxide for 2 hours. A small blood sample (3 tablespoons) of blood is drawn during the nitric oxide administration. Stage 3: Patients who participate in this stage of the study will remain in the ICU with the catheters in place for an additional 24 hours. During this time, they will breathe nitric oxide. Lung pressures will be measured every 4 hours and blood will be drawn prior to the initiation of NO breathing and at 4 and 8 weeks for neutrophil and monocyte mRNA expression chip profiling. Patients will remain in the hospital for observation one more day. At home, they will continue to breathe nitric oxide continuously for 2 months, using a tank of gas that delivers the nitric oxide through tubes placed in the nose. They will be followed at the clinic weekly for blood tests and an echocardiogram. They will do a 6-minute walk every 2 weeks. Patients who improve with nitric oxide therapy will have the option of continuing treatment. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00023296 ·
L-glutamine Therapy for Sickle Cell Anemia Condition(s): Anemia, Sickle Cell; Thalassemia Study Status: This study is currently recruiting patients. Sponsor(s): FDA Office of Orphan Products Development Purpose - Excerpt: This is a study to determine the efficacy of L-glutamine as therapy for sickle cell anemia and sickle O-thalassemia. Phase(s): Phase II; Phase III Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029887 ·
Medical Treatment for Diamond Blackfan Anemia Condition(s): Fanconi's Anemia; Hematologic Disease Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Diamond Blackfan anemia (DBA) is a condition in which the bone marrow is underdeveloped. DBA is considered a congenital disease, meaning patients are born with it. In DBA there is a lack of cells that give rise to red blood cells. The other elements produced in the bone marrow, such as white blood cells and platelets, are normal. Standard treatments used for this disorder such as steroids and bone marrow transplants are associated with failure, relapse, side-effects, increased morbidity, and even death. Two drugs, antithymocyte globulin (ATG) and cyclosporin have been used to treat DBA, but have only provided occasional responses. No study has ever combined these two drugs for the treatment of DBA. This study is designed to explore the combined use of ATG and cyclosporine as a rational approach to the treatment of DBA. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001749
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Mobilization of Stem Cells with G-CSF for Collection from Patients with DiamondBlackfan Anemia Condition(s): Diamond Blackfan Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will provide information needed to develop more effective treatments for patients with Diamond-Blackfan anemia (DBA). Current treatments include steroids, such as prednisone, and blood transfusions. These treatments have potential long-term risk and side effects, including osteoporosis and impaired growth from steroids or iron overload from transfusions. In addition, as patients reach adulthood, they can develop acute leukemia or bone marrow failure. The only cure for DBA is bone marrow transplant, a procedure that itself carries serious risks and is an option for only about 25 percent of patients. DBA is caused by a mutation (error) in a gene that codes for producing red blood cells from stem cells (blood-forming cells produced by the bone marrow). In 5 to 10 years, gene transfer therapy may prove to be an effective treatment for DBA. Before this treatment can be considered, however, more information is needed about DBA patients and how their stem cells function. This study will examine: 1) whether stem cells of patients with DBA respond to G-CSF the same way those of healthy people do. (G-CSF is a drug that causes stem cells to move from the bone marrow to the blood stream, where they can be collected more easily and in larger numbers by a procedure called leukapheresis, described below. If G-CSF does not work well in DBA patients, other collection strategies will have to be explored); and 2) whether the genetic error in DBA can be corrected by gene transfer into patients' stem cells. Patients with Diamond-Blackfan anemia 4 years of age and older who weigh at
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least 27 pounds and who are dependent on red blood cell transfusions may be eligible for this study. Candidates will have a medical history taken and a physical examination and will be seen by the Clinical Center's Department of Medicine Transfusion for leukapheresis evaluation. They will have a bone marrow aspiration and biopsy to confirm the diagnosis of DBA. For these tests, the hip area is anesthetized and a needle is used to draw bone marrow from the hipbone. If needed, the procedure will be done under sedation. Patients will be given G-CSF by injection under the skin for up to 6 days. Blood and stem cell counts will be measured from a teaspoon of blood drawn each morning. On the morning of the fifth dose, the patient will undergo leukapheresis for collection of stem cells. For this procedure, a large catheter (with a diameter no larger than that of a straw) is placed in an arm vein to allow blood to flow into a cell separator machine. Most children and some adults do not have veins large and strong enough for this tubing, so a large intravenous line called a "central line" is placed into a large vein in the neck or groin. This is done under sedation and with a local anesthetic. While the patient lies on a bed or recliner, whole blood is collected through a catheter in one arm or the central line, the stem cells are separated out by spinning, then the red cells, platelets and plasma are returned through a second catheter in the other arm or a second opening in the central line. The procedure takes about 3 to 5 hours, during which the patient can watch television or videos and have family members at the bedside for company. When the procedure is completed, the patient's participation in the protocol ends. Some of the stem cells collected by leukapheresis will be used for research and some will be frozen and stored for possible future transplantation into the patient, if required. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011505 ·
Phase I Study of Amifostine in Patients With Bone Marrow Failure Related to Fanconi's Anemia Condition(s): Fanconi's Anemia Study Status: This study is currently recruiting patients. Sponsor(s): Dana-Farber/Harvard Cancer Center Purpose - Excerpt: Objectives: I. Evaluate the toxicity of amifostine in patients with bone marrow failure related to Fanconi's anemia. II. Determine the efficacy of this treatment regimen in this patient population. III. Evaluate the effect of this treatment regimen on bone marrow progenitor cell proliferation and peripheral blood mononuclear cell apoptosis in these patients. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006127
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Phase I/II Randomized Study of Hydroxyurea With or Without Clotrimazole in Patients With Sickle Cell Anemia Condition(s): Sickle Cell Anemia
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Study Status: This study is currently recruiting patients. Sponsor(s): FDA Office of Orphan Products Development; University of North Carolina Purpose - Excerpt: Objectives: I. Compare the efficacy of hydroxyurea with or without clotrimazole in terms of limiting the severity of anemia and the rate of hemolysis in patients with sickle cell anemia. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004492 ·
Phase I/II Study of Nonmyeloablative Allogeneic Bone Marrow Transplantation in Patients With High Risk Hemoglobinopathy Condition(s): Graft Versus Host Disease; Sickle Cell Anemia; Thalassemia Study Status: This study is currently recruiting patients. Sponsor(s): Fairview University Medical Center Purpose - Excerpt: Objectives: I. Demonstrate the absence of grade 3 or 4 regimen related toxicity in patients with high risk hemoglobinopathy treated with busulfan, fludarabine, anti-thymocyte globulin, and radiotherapy followed by allogeneic hematopoietic stem cell transplantation. II. Determine the incidence of chimerism at 100 days, 6 months, and 1 year following this treatment regimen in this patient population. III. Determine the incidence of grade 2-4 and 3-4 acute graft vs host disease (GVHD) at 100 days following this treatment regimen in this patient population. IV. Determine the incidence of chronic GVHD at 6 months and 1 year following this treatment regimen in this patient population. V. Compare the quality of life at 1 year with the pretransplant assessment in these patients treated with this regimen. VI. Determine the survival at 100 days and 1 year in these patients. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005897
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Phase II Study of Arginine Butyrate With or Without Epoetin alfa in Patients With Thalassemia Intermedia Condition(s): beta-Thalassemia Study Status: This study is currently recruiting patients. Sponsor(s): Boston University School of Medicine Purpose - Excerpt: Objectives: I. Determine whether arginine butyrate with or without epoetin alfa can stimulate gammaglobin chain production to a degree that decreases anemia and results in hematologic improvement in patients with thalassemia intermedia. II. Determine whether a proportional increase in gammaglobin synthesis and mRNA and an improvement in nonalfa and alfaglobin chain imbalance by at least 10% over baseline correlate with improved hematologic response in these patients when treated with this regimen. III. Determine whether a decrease in hemolysis, as assayed by a decrease in LDH, compared to baseline levels correlates with improved hematologic response in these patients when treated with this regimen. IV. Determine whether any
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particular genotypes are more responsive than others to this therapy in these patients. V. Determine whether baseline epoetin alfa levels, gender, and/or baseline reticulocyte counts (or percent circulating nucleated erythroblasts) correlate with improved hematologic response in these patients when treated with this regimen. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006136 ·
Phase II Study of Azacitidine and Phenylbutyrate in Patients With Thalassemia Major Condition(s): Thalassemia Major Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Objectives: I. Determine the safety and efficacy of azacitidine and phenylbutyrate in treatment of patients with thalassemia major. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00007072
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Rabbit Antithymocyte Globulin Versus Campath-1H for Treating Severe Aplastic Anemia Condition(s): Aplastic Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will compare two new treatments for people with severe aplastic anemia, a potentially fatal disease in which patients do not produce normal numbers of blood cells. Because they have too few red cells, patients may tire easily, have chest pains, and be short of breath even at rest. Too few white cells leave patients vulnerable to serious infections and possibly death. Too few platelets cause abnormal bleeding and easy bruising. Bleeding in the brain (stroke) can be fatal. Standard treatment with horse antithymocyte globulin (h-ATG), cyclosporine (CsA), and corticosteroids is effective, but patients often relapse. The treatments to be evaluated in this study are: 1) rabbit ATG (r-ATG) plus CsA plus corticosteroids; and 2) Campath1H. r-ATG is made by injecting rabbits with white blood cells. The rabbit's immune system makes antibodies to destroy the foreign white cells. The antibodies are collected and purified to make r-ATG. CsA is commonly used to prevent rejection of donated tissue after bone marrow or organ transplantation and, in combination with h-ATG, for treating aplastic anemia. Corticosteroids suppress the immune system and are given to prevent or reduce the symptoms of serum sickness, which can develop in response to the rabbit proteins in the r-ATG. Campath-1H is a laboratory-made antibody currently used to treat chronic lymphocytic leukemia. It destroys white blood cells called lymphocytes that, in aplastic anemia, are responsible for destruction of bone marrow stem cells. Patients 15 years of age and older with severe aplastic anemia may be eligible
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for this study. Candidates will be screened with a medical history, physical examination, blood tests, and bone marrow biopsy. Participants are randomly assigned to one of two treatment groups: 1) r-ATG, CsA, and steroids, or 2) Campath-1H. For both treatments, it is suggested that a central venous line (large plastic tube) be placed in a large vein in the neck or chest. This tube can stay in the body and be used the entire treatment period to deliver the study drug and other medications, transfuse blood, and withdraw blood samples. Group 1 patients receive r-ATG by vein for 5 days, CsA by mouth as a liquid or capsule for 6 months, and a full dose of steroids by mouth for at least 2 weeks. After 2 weeks, when the risk of serum sickness-a reaction to the r-ATG-declines, the steroid dose is decreased. Group 2 patients receive Campath-1H by vein for 10 days. Because this drug suppresses the immune system, patients also take medicines to prevent herpes virus infection and Pneumocystis carinii-a type of pneumonia-and to treat cytomegalovirus infection, if it develops. All patients are hospitalized for the initial testing and treatment (about 2 weeks) when the risk of infection and seizures is highest. In addition to drug treatment, patients undergo the following procedures: - Blood tests: Throughout the hospital admission, blood samples are drawn daily to check drug side effects and the response to treatment. Samples are drawn less frequently for later tests. Bone marrow examination: A bone marrow sample is collected before beginning treatment, at 6 months, and then yearly. For this test, the area above the hip bone is numbed with a local anesthetic and a small sample of bone and marrow is withdrawn through a needle. - Chest x-ray may be done upon admission. - Other blood tests and xrays may be required to evaluate and treat symptoms that may develop. - Follow-up: Blood tests are done weekly by the patient's private doctor, and patients return to NIH for examinations at 3-month intervals. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065260 ·
Radiation Therapy and Cisplatin With or Without Epoetin Alfa in Treating Patients With Cervical Cancer and Anemia Condition(s): Anemia; Cervical Cancer; Drug Toxicity; Quality of Life; radiation toxicity Study Status: This study is currently recruiting patients. Sponsor(s): Gynecologic Oncology Group; National Cancer Institute (NCI); National Cancer Institute of Canada Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage tumor cells. Epoetin alfa may stimulate red blood cell production to treat anemia in patients who have received chemotherapy and/or radiation therapy for cervical cancer. PURPOSE: Randomized phase III trial to study the effectiveness of epoetin alfa in treating anemia in patients who have cervical cancer. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00017004
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Safety & Efficacy of ICL670 vs. deferoxamine in Beta-thalassemia patients with iron overload due to blood transfusions Condition(s): beta-Thalassemia Study Status: This study is currently recruiting patients. Sponsor(s): Novartis Pharmaceuticals Purpose - Excerpt: The purpose of this study is to deterimine if the new orally active iron chelator, ICL670, is as effective and as safe as deferoxamine in preventing accumulation of iron in the body while a patient is undergoing repeated blood transfusions. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061750
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Secondary Pulmonary Hypertension in Adults with Sickle Cell Anemia Condition(s): Pulmonary Hypertension; Sickle Cell Anemia Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The purpose of this study is to determine how often people with sickle cell anemia develop pulmonary hypertension-a serious disease in which blood pressure in the artery to the lungs is elevated. Men and women 18 years of age and older with sickle cell anemia may be eligible for this study. Participants will undergo an evaluation at Howard University's Comprehensive Sickle Cell Center in Washington, D.C. or at the National Institutes of Health in Bethesda, Maryland. It will include the following: -medical history -physical examination -blood collection (no more than 50 ml., or about 1/3 cup) to confirm the diagnosis of sickle cell anemia, sickle cell trait or beta-thalassemia (Some blood will be stored for future research testing on sickle cell anemia.) -echocardiogram (ultrasound test of the heart) to check the pumping action of the heart and the rate at which blood travels through the tricuspid valve. Following this evaluation, a study nurse will contact participants twice a month for 2 months and then once every 3 months for the next 3 years for a telephone interview. The interview will include questions about general health and recent health-related events, such as hospitalizations or emergency room visits. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011648
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Stem Cell Transplantation after Reduced-Dose Chemotherapy for Patients with Sickle Cell Disease or Thalassemia Condition(s): Hemoglobinopathies; Anemia, Sickle Cell; Hemoglobin SC Disease; Thalassemia; Thalassemia Major Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Allergy and Infectious Diseases (NIAID)
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Purpose - Excerpt: The purpose of this study is to find out if using a lower dose of chemotherapy before stem cell transplantation can cure patients of sickle cell anemia or thalassemia while causing fewer severe side effects than conventional high dose chemotherapy with transplantation. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00034528 ·
Study of Allogeneic Bone Marrow Transplantation Following Cyclophosphamide and Radiotherapy in Patients With Fanconi's Anemia Condition(s): Fanconi's Anemia Study Status: This study is currently recruiting patients. Sponsor(s): Fairview University Medical Center Purpose - Excerpt: Objectives: I. Determine the effectiveness of moderate dose cyclophosphamide and total lymphoid radiotherapy in terms of improving the survival and reducing the morbidity following allogeneic bone marrow transplantation in patients with Fanconi's aplastic anemia. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005891
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Study of Allogeneic Bone Marrow Transplantation Following Cyclophosphamide and Radiotherapy in Patients With Myelodysplastic Syndrome and Acute Leukemia Related to Fanconi's Anemia Condition(s): Fanconi's Anemia; Myelodysplastic Nonlymphocytic, Acute; Leukemia, Lymphocytic, Acute
Syndromes;
Leukemia,
Study Status: This study is currently recruiting patients. Sponsor(s): Fairview University Medical Center Purpose - Excerpt: Objectives: I. Determine the effectiveness of moderate dose cyclophosphamide and radiotherapy in terms of improving survival and reducing the morbidity following allogeneic bone marrow transplantation in patients with myelodysplastic syndrome and acute leukemia related to Fanconi's anemia. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005892 ·
Study of Allogeneic Bone Marrow Transplantation Using Matched, Related Donors in Patients With Nonmalignant Hematologic Disorders Condition(s): Neutropenia; Sickle Cell Anemia; Thalassemia Major; Red-Cell Aplasia, Pure Study Status: This study is currently recruiting patients. Sponsor(s): Fairview University Medical Center
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Purpose - Excerpt: Objectives: I. Determine the efficacy of bone marrow transplantation using matched related donors in patients with nonmalignant hematologic disorders. II. Determine the quality of life, absence of adverse effects (e.g., graft versus host disease and B cell lymphoproliferative disease), and completeness of recovery of their underlying condition in these patients with this treatment regimen. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005893 ·
Thalassemia (Cooley's Anemia) Clinical Research Network Condition(s): Anemia (Cooley's); beta-Thalassemia; Blood Disease; Thalassemia; Osteoporosis Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To accelerate research in the management of thalassemia, standardize existing treatments, and evaluate new ones in a network of clinical centers. The emphasis will be on clinical trials that help identify optimal therapy. Therapeutic trials may involve investigational drugs, drugs already approved but not currently used, and drugs currently used. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000623
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Thalidomide and Epoetin alfa in Treating Anemia in Patients With Myelodysplastic Syndrome Condition(s): de novo myelodysplastic syndromes; secondary myelodysplastic syndromes; previously treated myelodysplastic syndromes; Anemia Study Status: This study is currently recruiting patients. Sponsor(s): Fallon Clinic Purpose - Excerpt: RATIONALE: Thalidomide may stop or slow the growth of cancer cells. Epoetin alfa may stimulate red blood cell production. Combining thalidomide with epoetin alfa may improve anemia, decrease the need for blood transfusions, and improve the quality of life in patients with myelodysplastic syndrome. PURPOSE: Phase II trial to study the effectiveness of combining thalidomide with epoetin alfa in treating anemia in patients who have myelodysplastic syndrome. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00053001
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Thalidomide in Treating Anemia in Patients With Myelodysplastic Syndrome Condition(s): Refractory Anemia; refractory anemia with ringed sideroblasts; refractory anemia with excess blasts; de novo myelodysplastic syndromes; Chronic Myelomonocytic Leukemia; previously treated myelodysplastic syndromes Study Status: This study is currently recruiting patients. Sponsor(s): Roswell Park Cancer Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Thalidomide may be an effective treatment for anemia caused by myelodysplastic syndrome. PURPOSE: Randomized phase II trial to study the effectiveness of thalidomide in treating anemia in patients who have myelodysplastic syndrome. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00030550
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Umbilical Cord Blood Transplantation in Treating Patients With Severe Aplastic Anemia, Malignant Thymoma, or Myelodysplasia Condition(s): Refractory Anemia; refractory anemia with ringed sideroblasts; de novo myelodysplastic syndromes; previously treated myelodysplastic syndromes; secondary myelodysplastic syndromes Study Status: This study is currently recruiting patients. Sponsor(s): Ireland Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Umbilical cord blood transplantation may allow doctors to give higher doses of chemotherapy or radiation therapy and kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of umbilical cord blood transplantation in treating patients who have severe aplastic anemia, malignant thymoma, or myelodysplasia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003336
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Comparing Therapies for the Treatment of Severe Aplastic Anemia Condition(s): Aplastic Anemia; Hematologic Disease Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Severe Aplastic anemia (SAA) is a rare and very serious blood disorder in which the bone marrow stops producing the cells which make up blood; red blood cells, white blood cells, and platelets. Researchers believe this is caused by an autoimmune reaction, a condition in which the natural defense system of the body begins attacking itself. In SAA the immune system begins attacking the bone marrow. Red blood cells are responsible for carrying oxygen to all of the organ systems in the body, and low numbers (anemia) can cause difficulty breathing and fatigue. Platelets are responsible for normal blood clotting and low numbers can result in easy bruising and
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bleeding which can be deadly. White blood cells are responsible for fighting infections, and low numbers of these can lead to frequent infections, the most common cause of death in patients with aplastic anemia. SAA can be treated by bone marrow transplant (BMT) or by drugs designed to slow down the immune system (immunosuppressants). BMT can be successful, but it requires a donor with matched bone marrow, making this therapy available only to a few patients. BMT with unmatched bone marrow can fail and cause dangerous side effects. Presently, the two drugs used to treat SAA by slowing down the immune system (immunosuppression) are antithymocyte globulin (ATG) and cyclosporin A (CSA). When used in combination these two drugs can improve most patients' condition. However, one third of the patients who respond to this therapy experience a relapse of SAA. In addition, some patients treated with ATG/CSA can later develop other disorders of the blood. Recently, researchers have found that another immunosuppressive drug called cyclophosphamide, has been successful at treating patients with SAA. In addition, patients treated with cyclophosphamide do not experience relapses or develop other disorders of the blood. In this study researchers would like to compare the combinations of antithymocyte globulin (ATG) and cyclosporin A (CSA) to cyclophosphamide and cyclosporin A (CSA) for the treatment of SAA. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001626 ·
Darbepoetin alfa in Treating Anemia in Patients With Cancer Who Are Receiving Chemotherapy Condition(s): Anemia; unspecified adult solid tumor, protocol specific Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Jonsson Comprehensive Cancer Center Purpose - Excerpt: RATIONALE: Darbepoetin alfa may stimulate red blood cell production and may be effective in treating anemia in patients who are receiving chemotherapy. PURPOSE: Randomized phase II trial to determine the effectiveness of darbepoetin alfa in treating anemia in patients who are receiving chemotherapy for cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00039247
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Gene Therapy for the Treatment of Fanconi's Anemia Type C Condition(s): Fanconi's Anemia; Pancytopenia Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Fanconi's anemia is an inherited disorder that can produce bone marrow failure. In addition, some patients with Fanconi's anemia have physical defects usually involving the skeleton and kidneys. The major problem for most patients is
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aplastic anemia, the blood counts for red blood cells, white blood cells, and platelets are low because the bone marrow fails to produce these cells. Some patients with Fanconi's anemia can develop leukemia or cancers of other organs. Many laboratory studies have suggested that Fanconi's anemia is caused by an inherited defect in the ability of cells to repair DNA. Recently, the gene for one of the four types of Fanconi's anemia, type C, has been identified. It is known that this gene is defective in patients with Fanconi's anemia type C. Researchers have conducted laboratory studies that suggest Fanconi's anemia type C may be treatable with gene therapy. Gene therapy works by placing a normal gene into the cells of patients with abnormal genes responsible for Fanconi's anemia type C. After the normal gene is in place, new normal cells can develop and grow. Drugs can be given to these patients kill the remaining abnormal cells. The new cells containing normal genes and will not be harmed by these drugs. The purpose of this study is to test whether researchers can safely place the normal Fanconi's anemia type C gene into cells of patients with the disease. The gene will be placed into special cells in the bone marrow called stem cells. These stem cells are responsible for producing new red blood cells, white blood cells, and platelets. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001399 ·
Hydroxyurea for the Treatment of Patients with Sickle Cell Anemia Condition(s): Sickle Cell Anemia Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: A total of fifty severely affected patients with homozygous sickle cell disease or other sickling disorders (e.g. B negative or B positive Thalassemia/Sickle) who are greater than 18 years of age will be eligiblity for treatment. Such patients must be able to tolerate an extensive period without blood transfusion and have relatively well preserved renal and hepatic function (creatinine less than 1.5 mg/dl and normal liver function test with exception of a mild elevation in transaminase). Evidence of severe sickle cell anemia will include recurrent pain crisis, chronic bone oain, evidence of aseptic necrosis with symptoms, and intractable leg ulcer, etc. On admission to the study, each patient will receive a complete history and physical examination. These data and standard laboratory evaluation, including a test for pregnancy if appropriate, will be adequate to ascertain whether any of the criteria for exclusion are present. Each patient must accept responsibility for for using an effective means of contraception. Patients who are found to be HIV positive will be excluded from the study. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001197
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Phase I Pilot Study of CD34 Enriched, Fanconi's Anemia Complementation Group C Gene Transduced Autologous Peripheral Blood Stem Cell Transplantation in Patients With Fanconi's Anemia Condition(s): Fanconi's Anemia Study Status: This study is no longer recruiting patients. Sponsor(s): University of Minnesota Cancer Center Purpose - Excerpt: Objectives: I. Determine the safety of transferring the Fanconi anemia complementation group C (FACC) gene to hematopoietic progenitors by retroviral mediated gene transfer in patients with Fanconi's anemia, complementation group C. II. Determine the extent of engraftment following this treatment regimen without prior ablation of recipient marrow in these patients. III. Determine the ability of this treatment regimen to correct the cell phenotype and improve hematopoietic function in these patients. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005896
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5-Azacytidine and Phenylbutyrate to Treat Severe Thalassemia Condition(s): Beta Thalassemia Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This study will evaluate the safety and effectiveness of 5-azacytidine and phenylbutyrate for treating thalassemia major. Patients with this disease have abnormal production of hemoglobin (the oxygen-carrying protein in red blood cells), which leads to red blood cell destruction. As a result, patients require frequent red cell transfusions over many years. Because of these transfusions, however, excess iron is deposited in various body organs-such as the heart, liver, thyroid gland and, in men, the testes-impairing their function. Fetal hemoglobin-a type of hemoglobin that is produced during fetal and infant life-can substitute for adult hemoglobin and increase the levels of red cells in the body. After infancy, however, this type of hemoglobin is no longer produced in large quantities. 5-azacytidine can increase fetal hemoglobin levels, but this drug can damage DNA, which in turn can increase the risk of cancer. This study will try to lessen the harmful effects of 5-azacytidine by using only one or two doses of it, followed by long-term therapy with phenylbutyrate, a drug that may be as effective as 5-azacytidine with less harmful side effects. Patients 18 years of age and older with severe thalassemia major may be eligible for this study. Before beginning treatment, candidates will have a medical history and physical examination, blood tests, chest Xray, electrocardiogram (EKG), bone marrow biopsy (removal of a small sample of bone marrow from the hip for microscopic examination) and whole-body magnetic resonance imaging (MRI). For the biopsy, the area of the hip is anesthetized and a special needle is inserted to draw bone marrow from the hipbone. For the MRI scan, a strong magnetic field is used to produce images that will identify sites where the body is making red blood cells. During this procedure, the patient lies on a table in a narrow cylinder containing a magnetic field. Earplugs are placed in the ears to muffle the loud thumping sounds the machine makes when the magnetic fields are being switched. An intravenous (IV) catheter (flexible tube inserted into a vein) is placed in a large vein of
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the patient's neck, chest or arm for infusion of 5-azacytidine at a constant rate over 4 days. Patients who do not respond to this first dose of 5-azacytidine will be given the drug again after about 50 days. If they do not respond to the second dose, alternate treatments will have to be considered. Patients who respond to 5-azacytidine will begin taking phenylbutyrate on the 14th day after 5-azacytidine was started. They will take about 10 large pills 3 times a day, continuing for as long as the treatment is beneficial. All patients will be hospitalized for at least 6 days starting with the beginning of 5azacytidine therapy. Those who are well enough may then be discharged and continue treatment as an outpatient. Patients will be monitored with blood tests daily for 2 weeks and then will be seen weekly for about another 5 weeks. Bone marrow biopsies will be repeated 6 days after treatment begins and again at 2 weeks and 7 weeks. MRI will be repeated 7 weeks after treatment begins. After 7 weeks, patients will be seen at 3-month intervals. Bone marrow biopsies will be done every 6 months for the first 3 years after treatment. Patients will have red cell transfusions as needed and chelation therapy to remove excess iron. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005934 ·
A study of the efficacy and safety of ICA-17043 (with or without hydroxyurea) in patients with sickle cell anemia. Condition(s): Sickle Cell Disease; Sickle Cell Anemia Study Status: This study is completed. Sponsor(s): Icagen Purpose - Excerpt: ICA-17043 is being developed for the chronic treatment of patients with sickle cell disease (SCD) in both adults and children. ICA-17043 is a potent and specific inhibitor of a channel in human red blood cells (RBCs) that blocks RBC dehydration. ICA-17043 is expected to inhibit RBC dehydration and thus should prevent or delay the sickling process. By reducing sickled cells, an improvement in anemia, a reduction in painful crises, and ultimately, less end-organ disease is anticipated. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00040677
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Diagnostic Pilot Study of Dual Energy Absorptiometry in the Detection of Osteopenia or Osteoporosis in Patients With Thalassemia Major Condition(s): Osteoporosis; Thalassemia Major; Osteopenia Study Status: This study is completed. Sponsor(s): National Center for Research Resources (NCRR); Children's Hospital of Philadelphia Purpose - Excerpt: Objectives: I. Determine the frequency and severity of osteopenia and osteoporosis in patients with thalassemia major who undergo dual energy x-ray
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absorptiometry, and correlate these findings with other relevant endocrinologic measurements. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006138 ·
Effects of Nitric Oxide and Nitroglycerin in Patients with Sickle Cell Anemia Condition(s): Chest Pain; Sickle Cell Anemia Study Status: This study is completed. Sponsor(s): Warren G Magnuson Clinical Center (CC) Purpose - Excerpt: Sickle cell anemia is the most common genetic disease affecting African-Americans. About 1 in every 1000 African-Americans has the disease and 1 in every 12 carry the genes that could be passed on to their children. People with sickle cell anemia have abnormal hemoglobin, the molecules responsible for carrying oxygen in the blood. The abnormal hemoglobin can cause damage to the red blood cells. The damaged red blood cell may then stick in the blood vessels and cause pain and injury to organs. Some of the complications caused by the sticking of blood cells are called acute pain crisis and acute chest syndrome (ACS). Nitric oxide (NO) is a gas that has been proposed as a possible therapy for the ACS complication of sickle cell anemia. Studies have shown that NO may favorably affect sickle cell hemoglobin molecules, thereby improving blood flow through small vessels. This study is designed to evaluate the effects of NO, when taken in combination with a drug called nitroglycerin on patients with sickle cell anemia and normal volunteers. The effects of these two drugs only last while the patient is receiving them. Researchers hope the information learned from this study will help to develop new therapies for sickle cell anemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001716
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Epoetin alfa With or Without Dexamethasone in Treating Fatigue and Anemia in Patients With Hormone-Refractory Prostate Cancer Condition(s): recurrent prostate cancer; Anemia; Fatigue Study Status: This study is not yet open for patient recruitment. Sponsor(s): Eastern Cooperative Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Epoetin alfa may stimulate red blood cell production and may help improve cancer-related anemia and fatigue. Steroid therapy with dexamethasone may increase the effectiveness of epoetin alfa. It is not yet known if epoetin alfa is more effective with or without dexamethasone in treating anemia-related fatigue in patients with prostate cancer. PURPOSE: Randomized phase III trial to compare the effectiveness of epoetin alfa with or without dexamethasone in treating anemia-related fatigue in patients who have prostate cancer that is refractory to treatment with hormone therapy. Phase(s): Phase III Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00060398 ·
Hydroxyurea to Treat Beta-Thalassemia (Cooley's Anemia) Condition(s): Beta Thalassemia; Hemoglobinopathy Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This 12-month study will evaluate the safety and effectiveness of hydroxyurea in treating beta-thalassemia, a type of anemia caused by defective hemoglobin (the oxygen-carrying pigment in blood). Hemoglobin is composed of two protein chains-alpha globin chains and beta globin chains; patients with betathalassemia do not make beta globin. Patients often require frequent red blood cell transfusions. This leads to iron overload, which, in turn, requires iron chelation therapy (removal of iron from the blood). Some drugs, including hydroxyurea, can stimulate production of a third type of protein chain called gamma chains. In the womb, the fetus makes this type of protein instead of beta globin. It is not until after birth, when the fetus no longer produces gamma globin that the beta globin deficiency becomes apparent. Gamma chain synthesis improves hemoglobin and red blood cell production, correcting the anemia. This study will determine if and at what dose hydroxyurea treatment reduces patients' need for red blood cell transfusions and whether certain factors might predict which patients are likely benefit from this treatment. Patients 15 years and older with moderately severe beta-thalassemia may be eligible for this study. Participants will take hydroxyurea daily at a dose calculated according to the patient's body size. Blood will be drawn weekly to measure blood cell and platelet counts. The drug dosage may be increased after 12 weeks of treatment and again after 24 weeks if the white cell and platelet counts remain stable. Patients who respond dramatically to treatment may continue to receive hydroxyurea for up to 3 years. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001958
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Mycophenolate Mofetil and Cyclosporine to Treat Relapsing Aplastic Anemia Condition(s): Aplastic Anemia Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This study will examine the safety and effectiveness of a new drug combination for treating patients with severe aplastic anemia. Patients with aplastic anemia produce too few blood cells, causing fatigue, easy bruising and bleeding, and susceptibility to infections. In many cases, the very low blood counts result from an autoimmune process-that is, the patient's own immune system suppresses production of blood cells by the bone marrow. Although immune-suppressing drugs, such as cyclosporine, can restore normal cell counts, many patients have disease relapses. These patients require long-term therapy with cyclosporine, which can cause harmful side effects. This study will examine whether a lower dose of cyclosporine given together with mycophenolate mofetil (MMF) can maintain blood counts as effectively as full-dose
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cyclosporine treatment, and whether MMF alone can reduce the chances of future relapses. Patients 4 years of age and older with severe aplastic anemia who have relapsed after immune suppressing therapy may be eligible for this study. Participants will be randomly assigned to receive either standard cyclosporine therapy or experimental therapy with cyclosporine and MMF. Patients receiving standard cyclosporine therapy will receive a full dose of the drug for at least 3 months. Those taking both cyclosporine and MMF will take MMF plus half-dose cyclosporine for 3 months and continue MMF for an additional 6 months. Both drugs are taken twice a day by mouth. All patients will have about 120 milliliters (4 ounces) of blood drawn at the beginning of the study to evaluate immune system activity and bone marrow function, and to look for genetic material of certain viruses. Bone marrow aspirations and biopsies will be done at the beginning of the study, and at 6 and 12 months. For these tests, the area of the hip is anesthetized and a special needle is used to draw bone marrow from the hipbone. The patient's local doctor will be asked to do blood tests for chemistries, liver function and cyclosporine levels weekly for the first month and then every other week. Patients will return to NIH for evaluations 3, 6 and 12 months after treatment and then once a year. About 100 ml (7 tablespoons) of blood will be drawn at each visit. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005935 ·
Stem Cell Factor Medication for Aplastic Anemia Condition(s): Aplastic Anemia; Pancytopenia Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: This trial, sponsored by Amgen, Inc., which produces the recombinant methionyl human stem cell factor (r-metHuSCF), also involves two other institutions. The primary objective is determination of the safety of administering multiple doses of r-metHuSCF in the setting of acquired aplastic anemia and evaluation of the effect of r-metHuSCF on peripheral blood counts. Potential effects of r-metHuSCF on frequency of need for red cell or platelet transfusions and on bone marrow morphology/cellularity will also be evaluated. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001398
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Stem Cell Transplantation (SCT) for Genetic Diseases Condition(s): Thrombocytopenia; Metachromatic Leukodystrophy; Fanconi's Anemia; Thalassemia Major; Pure Red-Cell Aplasia; Inborn Errors of Metabolism Study Status: This study is completed. Sponsor(s): National Center for Research Resources (NCRR); University of California, Los Angeles
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Purpose - Excerpt: Objectives: I. Ascertain whether stem cell transplantation (SCT) is an effective method by which missing or dysfunctional enzymes can be replaced in patients with various inborn errors of metabolism. II. Determine whether clinical manifestations of the specific disease may be arrested or reversed by this treatment. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004378 ·
Study of ICL670 in iron overload from beta-thalassemia unable to be treated with deferoxamine or chronic anemias Condition(s): beta-Thalassemia; Myelodysplastic Syndromes; Fanconi Syndrome; Anemia, Diamond-Blackfan; Anemia, Aplastic Study Status: This study is completed. Sponsor(s): Novartis Pharmaceuticals Purpose - Excerpt: The purpose of this study is to determine the effects of the oral iron chelator ICL670 on liver iron content after one year of treatment in patients with iron overload from repeated blood transfusions. Beta-thalassemia patients unable to be treated with deferoxamine or patients with rare chronic anemias such as Myelodysplastic Syndrome, Fanconi's Syndrome, Blackfan-Diamond Syndrome, and Pure Red Blood Cell anemia are eligible for this study. Liver iron content will be measured by liver biopsy at the beginning of the study and after one year of treatment. However, those patients living in the San Francisco/Oakland area may have a SQUID in place of the liver biopsy if the biopsy is not medically possible for them. The SQUID is a non-invasive magnetic means to measure liver iron content. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061763
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 “anemia” (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:
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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 ANEMIA 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 “anemia” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on anemia, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Anemia By performing a patent search focusing on anemia, 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
9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on anemia: ·
6-aryl pyrimidines for treating aplastic anemia Inventor(s): Fast; Patricia E. (Kalamazoo, MI), Stringfellow; Dale A. (Kalamazoo, MI) Assignee(s): The Upjohn Company (Kalamazoo, MI) Patent Number: 4,619,933 Date filed: August 25, 1983 Abstract: A method for treating aplastic anemia by systemic administration of a 6-aryl pyrimidine compound or a pharmaceutically acceptable salt thereof in association with a pharmaceutical carrier to a human or animal having aplastic anemia. Excerpt(s): The preparation and use of 2-amino-5-halo-6-alkyl-4-pyrimidinols as antiviral agents is known (U.S. Pat. No. 3,956,302 and Nichols, Weed and Underwood, Antimicrobial Agents and Chemotherapy 9,433, 1976). Preparation of 2-amino-5-bromo6-phenyl-4-pyrimidinol (V, where X.sub.3 is Br and X.sub.1 is phenyl) has been reported (Brown and Stevens, JCS Perkin I, 1023, 1975) but no utility has been described for this material. Snell, Elias and Freeman in GB No. 1,223,686 (1967) disclose a variety of 5,6disubstituted 2-amino-4-pyrimidinols, such as 2-dimethylamino-5-bromo-6-methyl-4pyrimidinol. Various 5-unsubstituted 2-amino-6-arylpyrimidinols are known (e.g., Shirahawa, Yakuyaku Fasshi 50, 1562, 1960 (CA 55, 10651b); Kulkarui et al., J. Sci. and Ind. Res. Indil, 19C, 6, 1960; and U.S. Pat. No. 2,776,283. Diuretics and cardioregulatory properties are described for various 2-amino and 2-substituted amino-5-aminomethyl and 5-aryl-6-aryl-4-pyrimidinols, U.S. Pat. No. 2,704,285, U.S. Pat. No. 2,723,777 and U.S. Pat. No. 2,776,283. ... The 2-amino-6-aryl-5-substituted pyrimidinols of this invention have been shown to exhibit antiviral activity, an improved therapeutic ratio and fewer side effects and are useful in preventing and treating viral infections. The antiviral activity of many of the compounds is associated with increased production of interferon. Other compounds exhibit antiviral activity but do not induce interferon production. ... The 2-amino-6-aryl-5-substituted pyrimidinols of this invention exhibit immunoregulatory activity of the following types: increased antibody formation, increase in natural killer cells, activation of macrophages, increase in hematopoietic stem cells and decrease in generation of allospecific killer cells. Web site: http://www.delphion.com/details?pn=US04619933__
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An improved method of treating sickle cell anemia Inventor(s): Duncan; Alexander (Dunwoody, GA), Hunter; Robert L. (Tucker, GA) Assignee(s): Emory University (Atlanta, GA) Patent Number: 4,837,014 Date filed: January 13, 1989 Abstract: In accordance with the present invention, a method is provided that is effective in treating sickle cell anemia. The method comprises a method of treating a person with sickle cell disease comprising the step of injecting into the person with sickle cell disease a solution with an effective concentration of a surface active copolymer of the following formula:HO(C.sub.2 H.sub.4 O).sub.b (C.sub.3 H.sub.6 O).sub.a (C.sub.2 H.sub.4 O).sub.b Hwherein a is an integer such that the hydrophobe
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represented by (C.sub.3 H.sub.6 O) has a molecular weight of approximately 950 to 4000 and b is an integer such that the hydrophile portion represented by (C.sub.2 H.sub.4 O) constitutes approximately 50% to 90% by weight of the compound. Excerpt(s): The present invention relates to a composition and method for lysing fibrin clots, dissolving thrombi, and reestablishing and maintaining perfusion of ischemic tissue. More particularly, the present invention relates to a composition comprising certain ethylene oxide-propylene oxide condensation products, which are surface-active copolymers, in combination with fibrinolytic enzymes. ... The term "fibrinolytic enzyme" means any enzyme that is capable of cleaving fibrin. Enzymes that are capable of cleaving fibrin include, but are not limited to, streptokinase, urokinase, tissue plasminogen activator (t-PA) produced from cell cultures, tissue plasminogen activator produced by recombinant DNA technology (rt-PA) and tissue plasminogen activator produced by prourokinase (k-PA). The terms "isotonic solution" or "isoosmotic solution" are defined a solutions having the same or similar osmotic pressure as blood. The terms clot, fibrin clot and thrombus are used interchangeably. ... Each year about 550,000 Americans die from heart attacks. Even more--close to 700,000--have heart attacks and live. While a heart attack victim may survive, part of his or her heart will almost certainly die. The death of heart muscle, called myocardial infarction, is due to coronary artery thrombosis in 70-90% of the cases. When a thrombosis, or blood clot, occludes one of the arteries of the heart, it compromises the flow of blood to the surrounding muscle This deprives the muscle of oxygen and other nutrients. In the past, nothing could be done to reverse this process. The high technology devices in intensive care units mostly supported patients so they could live while a portion of their heart died. Web site: http://www.delphion.com/details?pn=US04837014__ ·
Assay for equine infectious anemia virus Inventor(s): Peterson; Darrell (Chesterfield, VA), Hu; Peisheng (Richmond, VA) Assignee(s): Virginia Commonwealth University (Richmond, VA) Patent Number: 5,427,907 Date filed: February 23, 1990 Abstract: The present invention is directed toward the use of a synthetic peptide as the antigen in an immunoassay for the detection of antibodies against the equine infectious anemia virus in the serum of horses. The synthetic peptide corresponds to the amino acid sequence of an antigenic portion of the GP-45 envelope protein of the equine infectious anemia virus. The immunoassay may be a direct second antibody immunoassay, a one or two step sandwich immunoassay, or a competitive immunoassay. Excerpt(s): The present invention relates to a synthetic peptide and its use in an immunoassay for the detection of Equine Infectious Anemia (EIA) viral infection. ... Equine Infectious Anemia is a viral disease, commonly known as swamp fever, which primarily affects horses and ponies. There is no known cure for the disease. Diagnosis and isolation is the only way to control the disease. ... The accepted way to diagnose the presence of EIA has been to detect the presence of antibodies specific for the disease in the serum of affected animals using the Coggins or agar gel diffusion test described in U.S. Pat. No. 3,929,982 and U.S. Pat. No. 3,932,601. In the Coggins test, a prepared antigen is placed alongside the serum to be tested in an agar or gel medium. If EIA
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antibodies are present in the test serum, they will diffuse toward the antigen forming a precipitin line in the agar medium where they eventually meet. Web site: http://www.delphion.com/details?pn=US05427907__ ·
Automated method and apparatus for classification of cells with application to the diagnosis of anemia Inventor(s): Bacus; James W. (Hinsdale, IL) Assignee(s): Rush-Presbyterian-St. Luke's Medical Center (Chicago, IL) Patent Number: 4,199,748 Date filed: February 3, 1978 Abstract: A method and apparatus are disclosed for measuring characteristics of cells, such as red blood cells, and for analyzing parameters of the cell characteristics to define a patient's blood. These parameters may be compared for resemblance to predetermined reference characteristic values for a blood cell pathological condition such as a specific kind of anemia or for a normal blood. A report may be generated showing such resemblance to an anemia or to a normal blood. A report may be generated showing parameters of a multivariate dispersion of distribution for a subpopulation of biconcave cells, an indication of skewness of the distribution of the cells with regard to shape variations in central pallor size; the proportion of abnormal kinds of cells found, and closeness of blood to several specific anemias. To expedite the system, a plurality of microprocessors are employed with one microprocessor controlling the imaging means and the summing of measured characteristics while one or more additional microprocessors are measureing characteristics and analyzing the digitized image signals. An improved method of measuring central pallor size is provided. Excerpt(s): This invention relates to an apparatus for automatically analyzing blood, and through the accumulation of measured properties from individual cells, of thereby classifying the blood specimen according to its close resemblance to the normal or to various pathological conditions. More particularly it is concerned with automatically classifying red blood cells and by accumulating measurements relative to each cell generating characteristic values, which by automated means identify the given blood specimen as typical of either normal or of the pathological condition of a specific type of red cell disorder or anemic condition. ... According to present medical practice, the diagnosis of a particular one of more than a dozen major types of anemia uses three broad categories of information; (1) mean descriptors of cell number, size and hemoglobin content, (2) subjective microscopic visual evaluation of the stained blood cells by a trained hemotologist, and (3) specific biochemical or other tests to pinpoint the precise cause of the anemia. ... With conventional equipment, the most common of the first category of red cell sample descriptors are; (1) the red cell count, or the number of red cells per unit volume of blood, (2) the hemoglobin content, or amount of hemoglobin per unit volume of blood, (3) the packed cell volume, or the percentage of blood occupied by red cells, (4) a mean cell size parameter, usually taken as the mean cell volume, which is derived by dividing the packed cell volume by the red cell count, (5) a mean cell hemoglobin parameter, which is derived by dividing the total blood hemoglobin content by the red cell count, and (6) the mean cell hemoglobin concentration, which is derived by dividing the total cell hemoglobin by the packed cell volume. Web site: http://www.delphion.com/details?pn=US04199748__
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cDNA for fanconi anemia complementation group A Inventor(s): Lo Ten Foe; Jerome R. (An Almere, NL), Joenje; Hans (Lelystad, NL) Assignee(s): Fanconi Anemia Research Fund, Inc. (Eugene, OR) Patent Number: 5,952,190 Date filed: October 4, 1996 Abstract: A cDNA molecule corresponding to the gene for human Fanconi anemia of complementation group A is disclosed. Also disclosed is the theoretical amino acid sequence of the FA-A protein. Methods of using these biological materials in the diagnosis and treatment of Fanconi anemia are presented. Excerpt(s): The present invention relates to the cloning and sequencing of the human cDNA molecule corresponding to the gene for Fanconi Anemia of complementation group A (FA-A). The present invention also relates to methods of screening for and detection of FA-A carriers, FA-A disease diagnosis, prenatal FA-A screening and diagnosis, and gene therapy utilizing recombinant DNA technologies. ... Fanconi Anemia (FA) is a rare and usually fatal human disorder characterized by progressive bone marrow failure, increased risk of malignancy and multiple congenital abnormalities mostly associated with developmental hypoplasia. It affects approximately one in 300,000 individuals (Swift, 1971). ... The disorder may be associated with a variety of overt congenital somatic anomalies, such as hypoplasia or other malformations of the kidney, cutaneous hyperpigmentation, and bony abnormalities, particularly hypoplastic or absent thumbs and radii (Glanz and Fraser, 1982). However, these clinical manifestations of FA are extremely variable, both in type and severity, and so diagnosis of the disease on this basis alone is difficult and unreliable. Web site: http://www.delphion.com/details?pn=US05952190__
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Compositions and methods for therapy and prevention of cancer, AIDS, and anemia Inventor(s): Samid; Dvorit (Rockville, MD) Assignee(s): The United States of America as represented by the Department of Health (Washington, DC) Patent Number: 5,877,213 Date filed: June 7, 1995 Abstract: Compositions and methods of treating anemia, cancer, AIDS, or severs .beta.chain hemoglobinopathies by administering a therapeutically effective amount of phenylacetate or pharmaceutically acceptable derivatives thereof or derivatives thereof alone or in combination or in conjunction with other therapeutic agents. Pharmacologically-acceptable salts alone or in combinations and methods of preventing AIDS and malignant conditions, and inducing cell differentiation are also aspects of this invention. Excerpt(s): This invention relates to methods of using phenylacetic acid and its pharmaceutically acceptable derivatives as antitumor, and antiviral agents, and treatment of severe beta-chain hemoglobinopathies. ... Some of the most dreadful epidemics, inherited diseases and cancerous infections in the history of mankind are
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afflicting the world's people at a rapid and discomforting rate. These maladies are being caused in many instances by the increasing cases of cancer, of viral infections, such as human immunodeficiency viruses (HIV) or HTLV and of severe beta-chain hemoglobinopathies. When one pauses to reflect upon the devastating pain, suffering and ultimately death experienced by persons afflicted, these moments of reflection underscore the tremendous importance which must be accorded medical research. In response to the need to alleviate suffering and add comfort to human life, the scientific community throught the world is searching for effective treatments to prevent or ameliorate diseases. ... In order to present the enormous scope of this unitary invention in a comprehensive form while preserving the essential need for clarity in presentment, this invention focusing on phenylacetate and its derivatives will be described in the following three (3) subsections, designated herein as A. Phenylacetate In Cancer prevention and maintenance therapy; B. Phenylacetate and its derivatives in the Treatment and Prevention of AIDS; and C. Induction of fetal hemoglobin synthesis in .beta.-chain hemoglobinopathies by phenylacetate and its derivatives. Web site: http://www.delphion.com/details?pn=US05877213__ ·
Compositions and methods for therapy and prevention of pathologies including cancer, AIDS and anemia Inventor(s): Samid; Dvorit (Rockville, MD) Assignee(s): The United States of America as represented by the Secretary of the (Washington, DC) Patent Number: 5,635,532 Date filed: October 12, 1993 Abstract: Compositions and methods of treating anemia, cancer, AIDS, or severe .beta.chain hemoglobinopathies by administering a therapeutically effective amount of phenylacetate or pharmaceutically acceptable derivatives thereof or derivatives thereof alone or in combination or in conjunction with other therapeutic agents. Pharmacologically-acceptable salts alone or in combinations and methods of preventing AIDS and malignant conditions, and inducing cell differentiation are also aspects of this invention. Excerpt(s): This invention relates to methods of using phenylacetic acid and its pharmaceutically acceptable derivatives to treat and prevent pathologies and to modulate cellular activities. In particular, this invention relates to A) phenylacetate and its derivatives in cancer prevention and maintenance therapy, B) phenylacetate and its derivatives in the treatment and prevention of AIDS, C) induction of fetal hemoglobin synthesis in .beta.-chain hemoglobinopathy by phenylacetate and its derivatives, D) use of phenylacetic acid and its derivatives in wound healing, E) use of phenylacetic acid and its derivatives in treatment of diseases associated with interleukin-6, F) use of phenylacetic acid and its derivatives in the treatment of AIDS-associated CNS dysfunction, G) use of phenylacetic acid and its derivatives to enhance immunosurveillance, H) methods of monitoring the dosage level of phenylacetic acid and its derivatives in a patient and/or the patient response to these drugs, I) the activation of the PPAR by phenylacetic acid and its derivatives, J) use of phenylacetic acid and its derivatives in treatment of cancers having a multiple-drug resistant phenotype, and K) phenylacetic acid and its derivatives, correlation between potency and lipophilicity. ... Phenylacetic acid (PAA) is a protein decomposition product found throughout the phylogenetic spectrum, ranging from bacteria to man. Highly conserved
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in evolution, PAA may play a fundamental role in growth control and differentiation. In plants, PAA serves as a growth hormone (auxin) promoting cell proliferation and enlargement at low doses (10.sup.-5 -10.sup.-7 M), while inhibiting growth at higher concentrations. The effect on animal and human cells is less well characterized. In humans, PAA is known to conjugate glutamine with subsequent renal excretion of phenylacetylglutamine (PAG). The latter, leading to waste nitrogen excretion, has been the basis for using PAA or preferably its salt sodium phenylacetate (NaPA, also referenced herein as that active anionic meoity, phenylacetate or "PA") in the treatment of hyperammonemia associated with inborn errors of ureagenesis. Clinical experience indicates that acute or long-term treatment with high NaPA doses is well tolerated, essentially free of adverse effects, and effective in removing excess glutamine. [Brusilow, S. W., Horwich, A. L. Urea cycle enzymes. Metabolic Basis of inherited Diseases, Vol. 6:629-633 (1989)]. These characteristics should be of value in treatments of cancer and prevention of cancer, treatments which inhibit virus replication and treatments of severe beta-chain hemoglobinopathies. ... Glutamine is the major nitrogen source for nucleic acid and protein synthesis, and a substrate for energy in rapidly dividing normal and tumor cells. Compared with normal tissues, most tumors, due to decreased synthesis of glutamine along with accelerated utilization and catabolism, operate at limiting levels of glutamine availability, and consequently are sensitive to further glutamine depletion. Considering the imbalance in glutamine metabolism in tumor cells and the ability of PAA to remove glutamine, PAA has been proposed as a potential antitumor agent; however, no data has previously been provided to substantiate this proposal. [Neish, W. J. P. "Phenylacetic Acid as a Potential Therapeutic Agent for the Treatment of Human Cancer", Experentia, Vol. 27, pp. 860-861 (1971)]. Web site: http://www.delphion.com/details?pn=US05635532__ ·
Compositions and methods for therapy and prevention of pathologies including cancer, AIDS, and anemia Inventor(s): Samid; Dvorit (Rockville, VA) Assignee(s): The United States of America as represented by the Department of Health (Washington, DC) Patent Number: 5,710,178 Date filed: June 6, 1995 Abstract: Compositions and methods of treating anemia, cancer, AIDS, or severe .beta.chain hemoglobinopathies by administering a therapeutically effective amount of phenylacetate or pharmaceutically acceptable derivatives thereof or derivatives thereof alone or in combination or in conjunction with other therapeutic agents. Pharmacologically-acceptable salts alone or in combinations and methods of preventing AIDS and malignant conditions, and inducing cell differentiation are also aspects of this invention. Excerpt(s): This invention relates to methods of using phenylacetic acid and its pharmaceutically acceptable derivatives to treat and prevent pathologies and to modulate cellular activities. In particular, this invention relates to A) phenylacetate and its derivatives in cancer prevention and maintenance therapy, B) phenylacetate and its derivatives in the treatment and prevention of AIDS, C) induction of fetal hemoglobin synthesis in .beta.-chain hemoglobinopathy by phenylacetate and its derivatives, D) use of phenylacetic acid and its derivatives in wound healing, E) use of phenylacetic acid and its derivatives in treatment of diseases associated with interleukin-6, F) use of
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phenylacetic acid and its derivatives in the treatment of AIDS-associated CNS dysfunction, G) use of phenylacetic acid and its derivatives to enhance immunosurveillance, H) methods of monitoring the dosage level of phenylacetic acid and its derivatives in a patient and/or the patient response to these drugs, I) the activation of the PPAR by phenylacetic acid and its derivatives, J) use of phenylacetic acid and its derivatives in treatment of cancers having a multiple-drug resistant phenotype, and K) phenylacetic acid and its derivatives, correlation between potency and lipophilicity. ... Phenylacetic acid (PAA) is a protein decomposition product found throughout the phylogenetic spectrum, ranging from bacteria to man. Highly conserved in evolution, PAA may play a fundamental role in growth control and differentiation. In plants, PAA serves as a growth hormone (auxin) promoting cell proliferation and enlargement at low doses (10.sup.-5 -10.sup.-7 M), while inhibiting growth at higher concentrations. The effect on animal and human cells is less well characterized. In humans, PAA is known to conjugate glutamine with subsequent renal excretion of phenylacetylglutamine (PAG). The latter, leading to waste nitrogen excretion, has been the basis for using PAA or preferably its salt sodium phenylacetate (NaPA, also referenced herein as that active anionic meoity, phenylacetate or "PA") in the treatment of hyperammonemia associated with inborn errors of ureagenesis. Clinical experience indicates that acute or long-term treatment with high NaPA doses is well tolerated, essentially free of adverse effects, and effective in removing excess glutamine. ›Brusilow, S. W., Horwich, A. L. Urea cycle enzymes. Metabolic Basis of Inherited Diseases, Vol. 6:629-633 (1989)!. These characteristics should be of value in treatments of cancer and prevention of cancer, treatments which inhibit virus replication and treatments of severe beta-chain hemoglobinopathies. ... Glutamine is the major nitrogen source for nucleic acid and protein synthesis, and a substrate for energy in rapidly dividing normal and tumor cells. Compared with normal tissues, most tumors, due to decreased synthesis of glutamine along with accelerated utilization and catabolism, operate at limiting levels of glutamine availability, and consequently are sensitive to further glutamine depletion. Considering the imbalance in glutamine metabolism in tumor cells and the ability of PAA to remove glutamine, PAA has been proposed as a potential antitumor agent; however, no data has previously been provided to substantiate this proposal. ›Neish, W. J. P. "Phenylacetic Acid as a Potential Therapeutic Agent for the Treatment of Human Cancer", Experentia, Vol. 27, 860-861 (1971)!. Web site: http://www.delphion.com/details?pn=US05710178__ ·
Cytokine related to hemolytic anemia and method of use Inventor(s): Larochelle; Andre (Toronto, CA), de Medicis; Eveline (Sherbrooke, CA) Assignee(s): Universite de Sherbrooke (Quebec, CA) Patent Number: 6,114,306 Date filed: April 15, 1997 Abstract: Pyruvate kinase deficiency is a blood disease characterized by hemolytic anemia. PCR analysis of cDNA leukocytic extracts of patients with hereditary pyruvate kinase deficiency anemia revealed two overexpressed markers when compared to extracts from healthy individuals. These two markers, proposed as human markers A and B and associated with hereditary hemolytic anemia, have been cloned (HUMDNAMA and HUMDNAMB, Gen Bank Association numbers M64700 and M64701). Our attention has focused on human DNA marker B, a 451 bp open-reading frame. The marker has been cloned in the bacteria vector pGEX-2TK and the expressed
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protein, called HMF (hemolytic anemia related factor), has been tested for biological activity. It has been observed that the HMF-glutathione transferase fusion protein, added to freshly prepared leukocytes cultures, has an immediate cytotoxic effect and a delayed lymphoblastic effect. The lymphoblastic effect is greatly enhanced when erythrocytes are added to the leucocytes. The sequence of HUMDNAMB is 48% homologous to bovine interferon A-alpha, and 63% in the region 303-416 bp. The matrix analysis of the amino acid sequence of HMF reveals also a structural similarly with interferon. Structural properties and biological activities of HMF support a its role as a cytokine. Excerpt(s): Polymerase chain reaction (PCR) is not restricted to DNA templates. RNA may also be amplified by PCR, because Taq polymerase possesses weak reverse transcriptase activity [1]. Since nonspecific PCR has been successfully exploited as a fingerprinting method and as a tool for polymorphism detection in genomic DNA [2,3], we have made use of nonspecific PCR to investigate alterations in gene expression in congenital hemolytic anemia. ... The cellular integrity of the red blood cells depends on proteins that belong to four distinct functional systems: responsible for the repair of oxidative damage (pentose phosphate shunt-glutathione pathway), the system responsible for the transport of oxygen (hemoglobins), the system responsible for the cellular exchanges (membrane and cytoskeleton), and energy generation (glycolytic pathway). In each of these systems, mutations have been found that are responsible for hereditary hemolytic disorders. Among others, hereditary non-spherocytic anemia may be caused by deficiency of pyruvate kinase in the glycolytic pathway [4]. Hemolytic anemia occurs whenever the steady-state normal number of red cells is diminished, due to decreased stability. Since the bone marrow has the capability to increase its production of erythrocytes [5], hemolytic anemia is characterized by both increased hemolysis and increased erythropoiesis. Hence, the higher turnover rate of red blood cells is indicated by reticulocytosis and elevated bilirubinemia. ... Using nonspecific PCR, we have obtained evidence that the expression of several genes is activated in blood cells four from patients with hereditary hemolytic anemia. Three are diagnosed with pyruvate kinase deficiency and one is of unknown cause. Two markers have been already identified and have been proposed to be human markers associated with hereditary hemolytic anemia [18]. We present here the genetic expression studies of marker B. This marker shows homology with bovine interferon .alpha.-A gene. Since interferon has a role as a differentiation factor in the erythroid cell lineage and is used as a therapeutic agent to treat hairy cell leukemia, marker B may be another related interleukin which may be used to develop pharmaceutical agents to be advantageously used in the treatment of hemolytic anemia caused inter alia by pyruvate kinase deficiency. This disease does not respond well to the well-known hematopoiesis growth factor, erythropoietin [21]. Marker A is, on the other hand, homologous to plateletderived growth factor receptor (PDGFr). We still do not know if marker A is part of a DNA sequence encoding a receptor which responds to marker B or if marker A responds to another growth factor, like PDGF. Web site: http://www.delphion.com/details?pn=US06114306__
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Fanconi Anemia Type C gene Inventor(s): Strathdee; Craig A. (Nepean, CA), Wevrick; Rachel (Menlo Park, CA), Buchwald; Manuel (Toronto, CA), Mathew; Christopher George Porter (London, GB2) Assignee(s): The United Medical And Dental Schools of Guy's and St. Thomas's Hospitals (London, GB2), HSC Research & Development Limited Partnership (Toronto, CA) Patent Number: 5,681,942 Date filed: May 15, 1995 Abstract: Fanconi Anemia is a human genetic disease, the precise cause of which is, to date, unknown. This invention provides an isolated human cDNA molecule which is able to specifically complement, in one type of Fanconi Anemia, (type C) the characteristic defect exhibited by cells derived from patients with Fanconi Anemia. The genomic gene from which this cDNA is derived is also provided as is the sequence of the protein encoded by this gene. Mutations in this gene are proposed to underlie Fanconi Anemia Type C. Diagnostic and therapeutic applications which derive from this work are described. The murine homolog of the human cDNA is also provided. Excerpt(s): The present invention relates generally to a gene associated with the human Fanconi Anemia (FA) disease process, and, more particularly, to the identification, isolation and cloning of this gene. The present invention also identifies the murine homolog of the human cDNA sequence corresponding to this gene. The present invention also relates to methods of screening for and detection of FA carriers, FA diagnosis, prenatal FA screening and diagnosis, and gene therapy utilizing recombinant DNA technologies. ... Fanconi Anemia (FA) is a rare and usually fatal human disorder of DNA repair characterized by progressive bone marrow failure, increased risk of malignancy and multiple congenital abnormalities mostly associated with developmental hypoplasia. It affects approximately one in 300,000 individuals (Swift, 1971). ... The disorder may be associated with a variety of overt congenital somatic anomalies, such as hypoplasia or other malformations of the kidney, cutaneous hyperpigmentation, and bony abnormalities, particularly hypoplastic or absent thumbs and radii (Glanz and Fraser, 1982). However, these clinical manifestations of FA are extremely variable, both in type and severity, and so diagnosis of the disease on this basis alone is difficult and unreliable. Web site: http://www.delphion.com/details?pn=US05681942__
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Fluorescence polarization--based diagnostic assay for equine infectious anemia virus Inventor(s): Jolley; Michael E. (34469 N. Circle Dr., Round Lake, IL 60073), Tencza; Sarah B. (401 Olympia Rd., Pittsburgh, PA 15211), Montelaro; Ronald C. (127 Greenbriar Dr., Wexford, PA 15090), Nasir; Mohammad S. (1012 Highgate La., Grayslake, IL 60030) Assignee(s): none reported Patent Number: 6,350,574 Date filed: September 21, 1999 Abstract: A fluorescence polarization assay for Equine Infectious Anemia Virus utilizes a short peptide reagent probe derived from a conserved immunodominant region of gp45. The probe is N-terminally labeled, preferably with 6-carboxyfluorescein, and purified by HPLC, which reacts in a homogenous assay with anti-EIAV antibodies
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contained in the serum of field infected horses and ponies. The assay has a sensitivity of about 90 percent with a specificity approaching 100 percent. Excerpt(s): This invention is related to the field of veterinary diagnostics and, more particularly, to a homogeneous fluorescence polarization-based assay to detect specific antibodies contained in the blood of horses and ponies infected with the lentivirus, aetiologic for Equine Infectious Anemia (EIA). ... Equine Infectious Anemia Virus (EIAV) is a lentivirus genetically related to human immunodeficiency virus type 1 (HIV1) that infects horses, ponies, and other equids (for a recent review see Montelaro, et al., "Equine Retroviruses, in J. A. Levy, Ed., The Retroviridae, Vol. 2, p. 257 (Plenum Press: 1993 N.Y.). It causes a chronic disease characterized by a period of cyclic fevers and viremia, followed by clinical quiescence. The animals generally survive this disease but remain infected, becoming lifelong inapparent carriers; they appear to be healthy but in fact still may have virus in their blood There are thousands of EIAV-positive horses in the US; most of them reside in the "hot zone", a group of 18 states along the Gulf coast and Mississippi valley (see Cordes, "Equine Infectious Anemia", USDA 91-55-032 (1996)). The disease is most prevalent there due to the humid environment that favors growth of horse flies, the major vector of transmission of EIAV. In an attempt to control the spread of this virus, horses are tested before showing, breeding, or crossing state lines. If a horse is found to be seropositive, its movement is severely restricted; the horse must be euthanized or quarantined with a 200-yard barrier for the rest of its life. However, because testing is not yet mandatory for all horses, it is estimated that over 80% have never been tested; this pool of horses may be a major reservoir for the virus. Efforts are underway to encourage, and in some states mandate, testing of all equids to better control this disease and reduce the rate of infection. ... One way to improve testing compliance is to develop better, faster assays. Current official diagnostic assays for EIAV include agar gel immunodiffusion (AGID) as reported in Coggins, et al., Cornell Vet USA LX: 330 (1970), competitive ELISA (C-ELISA), and synthetic antigen ELISA (SA-ELISA). The first two assays detect antibodies to the major core protein p26, which has a well conserved structure but is a relatively poor immunogen compared to the envelope proteins, gp90 and gp45. SA-ELISA detects antibodies to gp45 and is approved for use, but can have a lower sensitivity. The major drawbacks of the AGID test are the length of time it takes to test the samples and the technical difficulty in interpreting the results. ELISA-based tests can be completed in several hours, but in a recent study the C-ELISA had a 2% false positive rate, as reported in Issel, EIA-Hotzone Project, U of Kentucky. Web site: http://www.delphion.com/details?pn=US06350574__ ·
Formulation for treating thalassemia and a process for preparing the same Inventor(s): Rattan; Khanna Sushil (Delhi, IN), Ghansham; Dass (Delhi, IN), Harsh; Priyadarshi (Allahabad, IN), Sudarshan; Kumar (New Delhi, IN), Kumar; Sarkar Ajit (New Delhi, IN) Assignee(s): Council of Scientific and Industrial Research (New Delhi, IN) Patent Number: 5,665,392 Date filed: July 11, 1995 Abstract: A pharmaceutical formulation useful for treating patients suffering from thalassemia, which comprises powder of Anemonin Pretensis in an amount in the range of 0.02 to 0.12 wt % of the formulation, quinine sulphate in an amount in the range of 0.0005 to 0.003 wt % of the formulation, distilled or demineralised water in an amount in
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the range of 0 to 40 wt % of the formulation and, ethanol in an amount in the range of 99.88 to 60 wt % of the formulation; and a process for preparing the formulation by mixing the above ingredients. Excerpt(s): This invention relates to a formulation for iron-chelation. The formulation of the present invention is useful for treating patients suffering from the disease of Thalassemia. ... This invention relates particularly to a formulation having increased therapeutic efficacy useful for the treatment of patients suffering from the disease of Thalassemia. ... Thalassemia is a dreaded disease among children. The disease is caused due to hereditary disorders connected with defective hemoglobin synthesis, characterised by hypochromia, microcytosis, haemolysis and a variable degree of anaemia. Thalassemia involves a heterogeneous group of molecular defects with a wide spectrum of clinical expressions. Web site: http://www.delphion.com/details?pn=US05665392__ ·
Iron complexes of hydroxy pyridones useful for treating iron deficiency anemia Inventor(s): Kontoghiorghes; George (London, GB2), Silver; Jack (London, GB2), Hider; Robert C. (Clacton, GB2), Stockham; Michael A. (Saffron Walden, GB2) Assignee(s): National Research Development Corporation (London, GB2) Patent Number: 4,550,101 Date filed: March 24, 1983 Abstract: Pharmaceutical compositions containing an iron complex of a 3-hydroxypyrid2-one or 3-hydroxypyrid-4-one in which the hydrogen atom attached to the nitrogen atom is replaced by an aliphatic hydrocarbon group and, optionally, in which one or more of the hydrogen atoms attached to ring carbon atoms are also replaced by an aliphatic hydrocarbon group, are of value for the treatment of iron deficiency anemia. Excerpt(s): This invention relates to iron compounds for use in pharmaceutical compositions for the treatment of iron deficiency anaemia. ... An adequate supply of iron to the body is an essential requirement for tissue growth in both man and animals. Although there is normally an ample amount of iron in the diet, the level of absorption of iron from food is generally low so that the supply of iron to the body can easily become critical under a variety of conditions. Iron deficiency anaemia is commonly encountered in pregnancy and may also present a problem in the newly born, particularly in certain animal species such as the pig. Moreover, in certain pathological conditions there is a mal distribution of body iron leading to a state of chronic anaemia. This is seen in chronic diseases such as rheumatoid arthritis, certain haemolytic diseases and cancer. ... Although a wide range of iron compounds is already marketed for the treatment of iron deficiency anaemia the level of iron uptake by the body from these compounds is often quite low, necessitating the administration of relatively high dosage levels of the compound. The administration of high dose, poorly absorbed, iron complexes may cause siderosis of the gut wall and a variety of side effects such as nausea, vomiting, constipation and heavy malodorous stools. Web site: http://www.delphion.com/details?pn=US04550101__
Patents 365
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Iron-pyridone complexes for anemia Inventor(s): Silver; Jack (London, GB2), Kontoghiorghes; George (London, GB2), Hider; Robert C. (St. Osyth, Clacton, GB2), Stockham; Michael A. (Saffron Walden, GB2) Assignee(s): National Research Development Corporation (London, GB2) Patent Number: 4,650,793 Date filed: March 22, 1984 Abstract: Pharmaceutical compositions containing an iron complex of a 3-hydroxypyrid2-one or 3-hydroxypyrid-4-one in which the hydrogen atom attached to the nitrogen atom is replaced by an aliphatic acyl group, by an aliphatic hydrocarbon group, or by an aliphatic hydrocarbon group substituted by one or, except in the case of ionizable groups, more than one substituent selected from aliphatic acyl, alkoxy, aliphatic amine, aliphatic amide, carboxy, aliphatic ester, halogen, hydroxy and sulpho groups and, optionally, in which one or more of the hydrogen atoms attached to ring carbon atoms are replaced by one of said substituents, by an aliphatic hydrocarbon group, or by an aliphatic hydrocarbon group substituted by an alkoxy, aliphatic ester, halogen or hydroxy group, but excluding compounds in which said replacement of hydrogen atoms in the compound is effected only by aliphatic hydrocarbon groups, are of value for the treatment of iron deficiency anemia. Excerpt(s): This invention relates to iron compounds for use in pharmaceutical compositions for the treatment of iron deficiency anaemia. ... An adequate supply of iron to the body is an essential requirement for tissue growth in both man and animals. Although there is normally an ample amount of iron in the diet, the level of absorption of iron from food is generally low so that the supply of iron to the body can easily become critical under a variety of conditions. Iron deficiency anaemia is commonly encountered in pregnancy and may also present a problem in the newly born, particularly in certain animal species such as the pig. Moreover, in certain pathological conditions there is a maldistribution of body iron leading to a state of chronic anaemia. This is seen in chronic diseases such as rheumatoid arthritis, certain haemolytic diseases and cancer. ... Although a wide range of iron compounds is already marketed for the treatment of iron deficiency anaemia, the level of iron uptake by the body from these compounds is often quite low, necessitating the administration of relatively high dosage levels of the compound. The administration of high dose, poorly absorbed, iron complexes may cause siderosis of the gut wall and a variety of side effects such as nausea, vomiting, constipation and heavy malodorous stools. Web site: http://www.delphion.com/details?pn=US04650793__
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Iron-pyridone complexes for anemia Inventor(s): Stockham; Michael A. (Saffron Walden, GB), Silver; Jack (London, GB), Hider; Robert C. (St. Osyth Clacton, GB), Kontoghiorghes; George (London, GB) Assignee(s): British Technology Group Ltd. (London, GB) Patent Number: RE36,831 Date filed: February 17, 1995 Abstract: Pharmaceutical compositions containing an iron complex of a 3-hydroxypyrid2-one or 3-hydroxypyrid-4-one in which the hydrogen atom attached to the nitrogen atom is replaced by an aliphatic acyl group, by an aliphatic hydrocarbon group, or by an
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aliphatic hydrocarbon group substituted by one or, except in the case of ionizable groups, more than one substituent selected from aliphatic acyl, alkoxy, aliphatic amine, aliphatic amide, carboxy, aliphatic ester, halogen, hydroxy and sulpho groups and, optionally, in which one or more of the hydrogen atoms attached to ring carbon atoms are replaced by one of said substituents, by an aliphatic hydrocarbon group, or by an aliphatic hydrocarbon group substituted by an alkoxy, aliphatic ester, halogen or hydroxy group, but excluding compounds in which said replacement of hydrogen atoms in the compound is effected only by aliphatic hydrocarbon groups, are of value for the treatment of iron deficiency anemia. Excerpt(s): This invention relates to iron compounds for use in pharmaceutical compositions for the treatment of iron deficiency anaemia. ... An adequate supply of iron to the body is an essential requirement for tissue growth in both man and animals. Although there is normally an ample amount of iron in the diet, the level of absorption of iron from food is generally low so that the supply of iron to the body can easily become critical under a variety of conditions. Iron deficiency anaemia is commonly encountered in pregnancy and may also present a problem in the newly born, particularly in certain animal species such as the pig. Moreover, in certain pathological conditions there is a maldistribution of body iron leading to a state of chronic anaemia. This is seen in chronic diseases such as rheumatoid arthritis, certain haemolytic diseases and cancer. ... Although a wide range of iron compounds is already marketed for the treatment of iron deficiency anaemia, the level of iron uptake by the body from these compounds is often quite low, necessitating the administration of relatively high dosage levels of the compound. The administration of high dose, poorly absorbed, iron complexes may cause siderosis of the gut wall and a variety of side effects such as nausea, vomiting, constipation and heavy malodorous stools. Web site: http://www.delphion.com/details?pn=US0RE36831__ ·
L-glutamine therapy for sickle cell diseases and thalassemia Inventor(s): Zerez; Charles R. (Culver City, CA), Tanaka; Kouichi R. (Rancho Palos Verdes, CA), Niihara; Yukaka (Rolling Hills Estates, CA) Assignee(s): Harbor-UCLA Research and Education Institute (Torrance, CA) Patent Number: 5,693,671 Date filed: May 1, 1996 Abstract: A method and kit for treating patients suffering from sickle cell disease and thalassemia. The method includes regularly administering a safe and pharmacologically effective amount of L-glutamine based compound to a patient to reduce pain, requirement for pain killers, and increase energy and activity levels. Excerpt(s): This invention relates to treatments and therapies for anemia conditions and diseases of the blood, and more particular is a therapy for sickle cell diseases and thalassemia by administration of L-glutamine and L-glutamine based compounds. ... Sickle cell diseases and thalassemia are some of the most common and devastating hereditary disorders of the blood. Sickle cell disease include diseases which cause sickling of the red blood cells, and includes sickle cell anemia (which results from two hemoglobin S genes), sickle .beta.-thalassemia (one hemoglobin S and one .beta.thalassemia gene), and hemoglobin SC disease (one hemoglobin S and one hemoglobin C), and the somewhat rare disease hemoglobin C Harlem. Thalassemia includes .alpha.thalassemia and .beta.-thalassemia. These hereditary diseases have significant morbidity
Patents 367
and mortality and affect individuals of African American heritage, as well as those of Mediterranean, Middle Eastern, and South East Asian descent. .beta.-thalassemia (also known as Cooley's anemia, erythroblastic anemia, hereditary leptocytosis and Mediterranean disease) in particular affects Eastern descent. These diseases commonly cause severe pain in sufferers in part due to ischemia caused by the damaged red blood cells blocking free flow through the circulatory system. ... No safe and effective therapies for these diseases are available. In the past several years, hydroxyurea has been used in an increasing number of sickle cell anemia patients. However, hydroxyurea is a chemotherapeutic agent with myleosuppressive effects and its long term safety is still unknown. An ideal agent would be one that is readily available, affordable, effective and safe even with chronic use. Web site: http://www.delphion.com/details?pn=US05693671__ ·
L-threonate ferrous, as well as pharmaceutical composition and use for improving and treating human anemia thereof Inventor(s): Wang; Zhiwen (Rm. 602,Unit 6, No. 31 Bldg. Dongwangzhuang Xiaoqu East Rd., Haidiang District, Beijing 100083, CN), Kou; Fuping (Rm. 602,Unit 6, No. 31 Bldg. Dongwangzhuang Xiaoqu East Rd., Haidiang District, Beijing 100083, CN), Yu; Kai (Rm. 602,Unit 6, No. 31 Bldg. Dongwangzhuang Xiaoqu East Rd., Haidiang District, Beijing 100083, CN) Assignee(s): none reported Patent Number: 6,313,170 Date filed: February 29, 2000 Abstract: A compound of ferrous L-threonate with structure (I), its compostions and methods useful for iron supplementation for mammals, particularly for human body to improve and treat nutritional iron-deficiency anemia, blood loss anemia and hemolytic anemia. Excerpt(s): This invention relates to a new derivative of L-threonic acid as a pharmaceutical active compound. More specifically, the invention concerns ferrous Lthreonate, a method of making the same, a pharmaceutical composition thereof. In a further aspect, this invention relates to use of ferrous L-threonate for the preparation of a pharmaceutical composition for improving and treating the anemia diseases, particularly, nutritional iron-deficiency anemia (IDA) (hypoferric anemia), blood-loss anemia (hemorrhagic anemia) and hemolytic anemia. ... L-threonic acid is one of metabolites of vitamin C. It is reported that some physiological functions of vitamin C were exerted very possibly by some of its metabolites, for example, L-threonic acid and the like. In the other hand, the existing of these compounds could profoundly influence the uptake and utilization of vitamin C. ... Calcium L-threonate is a derivative of Lthreonic acid. Calcium L-threonate can improve uptake of vitamin C by the lymphoma cells and can be used as the high efficient calcium nutrient for preventing and treating varied diseases caused by calcium deficiency (Chinese Patent, ZL 96 06507.9). Also, calcium L-threonate is useful for allaying inflammation and reducing blood pressure. But there was no report for other salts of L-threonic acid and their use as drugs on treating diseases. Web site: http://www.delphion.com/details?pn=US06313170__
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Method and composition for the diagnosis of equine infectious anemia virus disease by using the recombinant capsid protein virus (p26) Inventor(s): Fortes Ferraz; Isabella Bias (Belo Horizonte MG, BR), Pimenta Dos Reis; Jenner Karlisson (Belo Horizonte MG, BR), Kroon; Erna Geessien (Belo Horizonte MG, BR), Cerqueira Leite; Romulo (Belo Horizonte MG, BR), Peregrino Ferreira; Paulo Cesar (Belo Horizonte MG, BR) Assignee(s): Universidade Federal de Minas Gerais (Belo Horizonte MG, BR) Patent Number: 6,596,846 Date filed: January 16, 2001 Abstract: The present invention relates to a method and kit for detecting antibodies in clinical samples of animals infected with equine infectious anemia virus using the immunodiagnosis with the recombinant viral antigen p26. The antigen was bound to solid supports (microtitter plates, tubes, beads or nitrocellulose papers or nylon) and reacted with the test serum. After incubation with conjugated anti-equine immunoglobulin-enzyme the reaction was revealed with a solution composed of the substrate of the enzyme used in the conjugate (cromogene). After development of the reaction (color formation) it was stopped with acid solution and measured. The immunoassay may be a direct second antibody immunoassay, a one or two step sandwich immunoassay. Excerpt(s): The present invention relates to a method of detecting antibodies against core antigen of equine infectious anemia virus (EIAV), using as antigen the recombinant protein (p26) in immunoenzymatic assays. More particularly, it relates to the use of recombinant protein p26 in kits for diagnosis of equine infectious anemia (EIA). ... The equine infectious anemia (EIA) is one of the oldest diseases caused by virus, having been described for the first time in France by LIGNEE, Rec. Med Vet., 20:30, 1843, and recognized as viral disease by VALLEE and CARRE. Acad. Sci., 139:331-333, 1904. The disease affects exclusively the members of the family Equidae presenting a worldwide distribution and of great economical importance consequently. ... The EIA virus (EIAV) is classified as a lentivirus of the Retroviridae family (CHARMAN et al. J. Virol. 19(2):1073-1076, 1976), it is genetic and antigenically related to the other lentiviruses that are characterized by developing persistent infection in host. The EIA has played an especially important role in comparative virology and in the studies of the acquired immunodeficiency syndrome (AIDS). Besides their morphological identity, both viruses are similar in terms of nucleotide sequences that code for structural surfaces' proteins. This group of viruses present genetic and antigenic variants during persistent infections, which are associated to the immunresponse scape (MONTAGNIER et al. Ann. Virol., 135:119-134, 1984, MONTELARO et al. J. Biol. Chem., 259:10539-10544, 1984, RUSHLOW et al. Virology, 155:309-321, 1986, STREICHER et al. J. Am. Med. Assoc. 256:2390-2391, 1986, STOLER et al. J. Am. Med. Assoc. 256:2360-2364, 1986 and HAHN et al. Science, 232:1548-1553, 1986. Web site: http://www.delphion.com/details?pn=US06596846__
Patents 369
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Method for the direct analysis of sickle cell anemia Inventor(s): Wilson; John T. (Richmond County, GA), Wilson; Lois B. (Richmond County, GA), Geever; Robert F. (Aiken County, SC) Assignee(s): Medical College of Ga. Research Inst., Inc. (Augusta, GA) Patent Number: 4,395,486 Date filed: August 19, 1981 Abstract: A direct diagnosis of sickle cell anemia by a restriction endonuclease assay with an enzyme which recognizes the nucleotide base sequence CTNAG (where N is any base), such as Dde I, for the sickle cell allele (.beta..sup.s gene) through molecular hybridization. Following enzyme cleavage, the resulting DNA restriction fragments are separated by molecular weight and transferred to filter paper. A probe is utilized for hybridization that is complementary to the 5' end of the .beta. globin gene. The banding pattern of individuals with normal hemoglobin shows two bands (approximately 175 bp and 201 bp), sickle cell trait individuals exhibit an additional band (approximately 376 bp) and individuals with sickle cell anemia show the band at approximately 376 bp with a concommitant loss of the band at approximately 175 bp. Prenatal and postnatal diagnosis of sickle cell anemia is possible with the present method. Excerpt(s): This invention relates to a diagnosis of sickle cell anemia and, more particularly, to a direct analysis of human hemoglobin genes by the use of restriction endonuclease Dde I and molecular hybridization procedures to detect sickle cell anemia. ... Sickle cell anemia is a debilitating genetic disorder that affects two of every thousand Blacks born in the United States. The disease is also prevalent in the Mediterranean area, as well as India. It is characterized by general weakness and pains in muscles and joints and can be fatal, frequently at an early age; victims do not live much beyond the age of 30. The disorder is caused by a single nucleotide base mutation in the globin gene which converts the glutamic acid codon (GAG) at amino acid position 6 to one for valine (GTG). That chemical abnormality produces red blood cells which are distorted into an inflexible sickle shape that can clog capillaries, blocking the flow of blood to the tissues. ... The current test for sickle cell anemia diagnosis in fetuses is performed on samples of fetal blood obtained by fetoscopy. Through this procedure, a small sample of blood is taken from the fetus through the umbilical cord and then analyzed for sickle cells. The mutant protein migrates differently on the gel than the normal protein. While generally accurate, this diagnostic method is dangerous as it can cause a spontaneous abortion of the fetus 10 to 20% of the time. Web site: http://www.delphion.com/details?pn=US04395486__
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Method for treating sickle cell anemia Inventor(s): Pilley; Gerard A. (Sceaux, FR) Assignee(s): Laboratories Innothera, S.A. (Arcueil, FR) Patent Number: 4,385,064 Date filed: March 16, 1981 Abstract: A method for the treatment of the acute pain crises of sickle cell anemia has been found which comprises the administration of the citrate or the oxalate salt of the 2hexahydro-1H-azepin-1-yl)ethyl ester of .alpha.-cyclohexyl-3-thiopheneacetic acid.
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Excerpt(s): Sickle cell anemia is a disorder in which the hemoglobin of the blood is primarily hemoglobin S. Hemoglobin S differs from normal hemoglobin in that valine is substituted for the normal glutamic acid in the 6-position of the .beta.-polypeptide chains of hemoglobin. As a result of this structural difference, the reduced hemoglobin S molecules then tend to stack into filaments which further aggregate into the elongated sickled cell. ... Spontaneous sickling of such red cells occur when the concentration is sufficiently high but it is further facilitated by anoxia, acidosis, hyperthemia or excessive chilling. Thus, factors such as fever, an infection, or exposure to cold contribute to the formation of reduced hemoglobin S thus increasing the concentration of this material with a resultant increase in sickling. The sickling process is generally reversible although it does eventually reach a point at which it is irreversible. When the irreversible stage is passed, the cells involved are removed from the circulation resulting in a deficiency of such cells in the circulation and chronic hemolytic anemia. As a consequence, the ordinary symptoms associated with anemia would be observed. In addition, the cells formed deposit on the walls of the blood vessels and this would then impede circulation in the blood vessels and bring about painful vaso-occlusive crises. An increase in blood viscosity also occurs. ... Previous treatments of sickle cell anemia have been purely symptomatic involving the administration of sedatives to alleviate the pain or, when a prolonged severe painful crisis is involved, by the administration of multiple packed cell transfusion which serves to reduce the proportion of circulating sickling prone red cells below a level that can be induced to sickle. Web site: http://www.delphion.com/details?pn=US04385064__ ·
Method for treating sickle-cell anemia Inventor(s): Giudicelli; Don Pierre Rene Lucien (Fontenay-sous-Bois, FR), Najer; Henry (Paris, FR) Assignee(s): Synthelabo (Paris, FR) Patent Number: 4,021,559 Date filed: December 30, 1974 Abstract: The invention provides a new method for treating sickle-cell anemia, by administering to an affected patient the vincamine salt of 6,7-dihydroxycoumarin-4methylsulphonic acid. Excerpt(s): The invention relates to the treatment of sickle-cell anemia. It provides a new method for treating a patient suffering from this disease, which comprises administering to the said patient the vincamine salt of 6,7-dihydroxycoumarin-4methylsulphonic acid. This compound has been described in U.S. Pat. No. 3,438,988, issued Apr. 15, 1969. ... Sickle-cell anemia is a genotypical disease characterized by periodic crises. Presently, there is no specific treatment for it. And, till recently, it was even difficult to give the affected patients true remissions. The currently used drug was urea, but it is badly tolerated. ... Since 1972, following clinical studies made at the assignee's instigation, it is known that the alkaloid vincamine itself gives very good results in the sickle-cell anemia patients. (see : Societe Francaise d'Hematologie, Abidjan meeting, held on Nov. 23.sup.rd 1972, in Nouvelle Revue Francaise d'Hematologie, 1973, Vol. 13, No. 2, p. 274-277). Web site: http://www.delphion.com/details?pn=US04021559__
Patents 371
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Method of producing a recombinant non-glycosylated gp90 of equine infectious anemia virus (EIAV), and product thereof Inventor(s): Leite; Romulo C. (Minas Gerais, BR), Dos Reis; Jenner K. P. (Minas Gerais, BR), Kroon; Erna G. (Minas Gerais, BR), Ferreira; Paulo C. P. (Minas Gerais, BR), Ferraz; Isabella B. F. (Minas Gerais, BR) Assignee(s): Universidade Federal de Minas Gerais-UFMG (Belo Horizonte-Minas Gerais, BR) Patent Number: 6,444,442 Date filed: August 29, 2000 Abstract: The present invention describes recombinant gp90 envelop protein derived from the equine infectious anemia virus, their corresponding encoding recombinant DNA molecule and the process of production of the recombinant protein produced through genetic engineering techniques, to be used in diagnosis, vaccination or in research. Excerpt(s): The present invention refers to the general field of the technology of the DNA recombinant proteins, for the production of the gp90 envelope protein of Equine Infectious Anemia virus (EIAV), to be used in diagnosis, vaccination, antibody production or in research field. ... The equine infectious anemia (EIA) is one of the oldest diseases caused by virus, having been described for the first time in France by LIGNEE, Rec. Med. Vet, 20:30, 1843, and recognized as viral disease by VALLEE and CARRE. Acad. Sci., 139:331-333, 1904. The disease affects exclusively the members of the family Equidae presenting a worldwide distribution and consequently of great economical importance. ... The transmission of EIAV occurs mainly by arthropods vectors (tabanideos) by inoculating the virus into the animal's blood stream when feeding themselves (mechanical transmission) justifying the high prevalence of EIA in hot areas favorable to the life cycle of of these vectors ISSEL et al. Vet. 17:251-286, 1988. EIA can also be transmitted by the placenta and colostro of mare with high virus titers, and by needles and surgical instruments contaminated with blood COGGINS Comparative diagnosis of viral diseases, N.Y., 4:646-658, 1981. The disease present the acute forms, subacute, chronic and mainly inaparent or assimptomaticxn lSSEL & COGGINS, J. Am. Vet. Med. Assoc. 174(7):727-33, 1979, and the most prominent signs are the feverish episodes, anemia hemolitica, anorexia, fast weight loss and ventral edema. Web site: http://www.delphion.com/details?pn=US06444442__
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Method of treating anemia Inventor(s): Armstrong; Jay J. (Bensalem, PA) Assignee(s): American Home Products Corporation (Madison, NJ) Patent Number: 5,561,138 Date filed: December 13, 1994 Abstract: This invention provides a method of treating immune related anemia in a mammal which comprises administering rapamycin to said mammal orally, parenterally, intravascularly, intranasally, intrabronchially, transdermally, rectally. Excerpt(s): Anemia is defined as a reduction in the hemoglobin concentration of the blood, usually associated with a reduction of total circulating red cell mass. Regardless of the cause, anemia decreases the oxygen-carrying capacity of the blood, and when
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severe enough, causes clinical symptoms and signs. ... Clinically, anemia is characterized by pallor of the skin and mucus membranes, and by manifestations of hypoxia, most commonly weakness, fatigue, lethargy, or dizziness. Myocardial hypoxia may produce hyperdynamic circulation with an increase in heart rate and stroke volume. Ejection type flow murmurs may develop, and if the anemia is severe enough, cardiac failure may ensue. ... Anemias are generally classified in one of two ways: either by etiological classification (based on the cause) or by morphologic classification (based on changes in shape and size). Etiological classification is more commonly employed. The invention covered by this application is primarily concerned with anemias implicating the immune system. Web site: http://www.delphion.com/details?pn=US05561138__ ·
Method of treating sickle cell anemia Inventor(s): Abraham; Donald J. (Murrysville, PA), Kennedy; Paul E. (Lawrence, KS) Assignee(s): University of Pittsburgh (Pittsburgh, PA) Patent Number: 4,887,995 Date filed: January 22, 1985 Abstract: A method of treating a person for sickle cell anemia including administering to the patient's blood a therapeutically effective dosage of ethacrynic acid. The dosage may be administered to blood removed from the patient which blood after addition of the compound is restored to the patient or by other means such as orally. Excerpt(s): This invention relates to a method of treating sickle cell anemia and, more specifically, it relates to a method of resisting sickling of hemoglobin in a sickle cell anemia patient. ... Sickle cell anemia is a hereditary blood disease which can afflict African, Mediterranean and Mideastern peoples. The anemia results from the physical aggregation of a mutant hemoglobin protein constituent in red blood cells. This aggregation results in a distortion in shape of deoxygenated red blood cells and causes impairment of flow of the blood through the capillaries (sickle cell "crises"). As the principal function of hemoglobin is to transport oxygen from the lungs to body tissues, efficient flow of oxygen throughout the body's tissues is impeded by the anemia due to a lower number of red blood cells. Sickle cell anemia also may have an indirect effect on the heart, lungs, kidneys, spleen, hips and brain. Sickle cell anemia crises can be extremely painful, can result in infections such as pneumonia, can result in skin ulceration, can contribute to strokes and seizures in the one afflicted and can also result in the development of chronic bone infections. ... In general, the result of the differences between cells containing hemoglobin A, the normal hemoglobin, and hemoglobin S, the sickle cell hemoglobin, is that the former cell is generally flexible and bioconcave discoid in shape, while the latter is more rigid and crescent shaped and typically has pointed ends. This rigidity and distortion in shape causes the cells to be lodged in the capillary. Hemoglobin molecules contain two beta polypeptide chains and two alpha polypeptide chains. In the sickle cell hemoglobin, a mutation is present in the beta chains. More specifically, the sixth amino acid of each beta chain is changed from glutamic acid to valine. As a result of this mutation, hemoglobin S upon deoxygenation polymerizes and causes the cell to assume the elongated, sickle-like configuration. As the sickle cells have a much shorter life span than normal red cells, the effect on the body is to deplete the total volume of blood cells thereby creating an anemic condition. Web site: http://www.delphion.com/details?pn=US04887995__
Patents 373
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Method of treating sickle cell disease or thalassemia Inventor(s): Utterback; Barbara Gail (Avon, IN), Um; Suzane Lee (Indianapolis, IN), Yan; Sau-Chi Betty (Indianapolis, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 6,372,213 Date filed: November 22, 1999 Abstract: The present invention provides a method of treatment of sickle cell disease (SCD) or thalassemia with protein C. The claimed invention provides a needed therapy for potentially serious and debilitating disorders while avoiding complications such as bleeding tendency, toxicity and general side effects of currently available anti-coagulant agents. Excerpt(s): This invention relates to medical science particularly the treatment of sickle cell disease or thalassemia with protein C. ... Protein C is a vitamin K dependent serine protease and naturally occurring anticoagulant that plays a role in the regulation of hemostasis by inactivating Factors Va and VIIIa in the coagulation cascade. Human protein C circulates as a 2-chain zymogen, but functions at the endothelial and platelet surface following conversion to activated protein C (aPC) by limited proteolysis with thrombin in complex with the cell surface membrane protein, thrombomodulin. ... In conjunction with other proteins, aPC functions as perhaps the most important downregulator of blood coagulation resulting in protection against thrombosis. In addition to its anti-coagulation functions, aPC hasanti-inflammatory effects through its inhibition of cytokine generation (e.g. TNF and IL-1) and also exerts profibrinolytic properties that facilitate clot lysis. Thus, the protein C enzyme system represents a major physiological mechanism of anti-coagulation, anti-inflammation, and fibrinolysis. Web site: http://www.delphion.com/details?pn=US06372213__
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Methods for treatment of sickle cell anemia Inventor(s): Vassilev; Vassil P. (San Diego, CA), Chen; Long-Shiuh (San Diego, CA), Lai; Ching-San (San Diego, CA) Assignee(s): Medinox, Inc. (San Diego, CA) Patent Number: 6,355,661 Date filed: March 1, 2001 Abstract: The preparation and use of a protected organic aldehyde is described wherein bioavailability of the orally administered therapeutic aldehyde is improved. The protected aldehyde is prepared by reacting the aldehyde with a protecting group, for example, condensing the aldehyde chemically with a thiazolidine-4-carboxylic acid. The improved bioavailability of such orally administered drugs increases the feasibility of delivering sufficient amounts of vanillin or other therapeutic organic aldehydes in vivo to prevent sickling in sickle cell anemia. Combination therapy is also described wherein a protected organic aldehyde is administered to a subject in treatment of sickle cell anemia in conjunction with one or more other drugs, such as pain killers, used in treatment of the symptoms of sickle cell anemia or sickle cell disease.
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Excerpt(s): The present invention generally relates to methods for treating anemia. More specifically, the present invention relates to methods for treating sickle cell anemia using protected forms(s) of organic aldehydes. ... Sickle cell disease is a hemolytic disorder, which affects, in its most severe form, approximately 80,000 patients in the United States (see, for example, D. L. Rucknagel, in R. D. Levere, Ed., Sickle Cell Anemia and Other Hemoglobinopathies, Academic Press, New York, 1975, p.1). The disease is caused by a single mutation in the hemoglobin molecule; .beta.6 glutamic acid in normal adult hemoglobin A is changed to valine in sickle hemoglobin S. (see, for example, V. M. Ingram in Nature, 178:792-794 (1956)). Hemoglobin S has a markedly decreased solubility in the deoxygenated state when compared to that of hemoglobin A. Therefore, upon deoxygenation, hemoglobin S molecules within the erythrocyte tend to aggregate and form helical fibers that cause the red cell to assume a variety of irregular shapes, most commonly in the sickled form. After repeated cycles of oxygenation and deoxygenation, the sickle cell in the circulation becomes rigid and no longer can squeeze through the small capillaries in tissues, resulting in delivery of insufficient oxygen and nutrients to the organ, which eventually leads to local tissue necrosis. The prolonged blockage of microvascular circulation and the subsequent induction of tissue necrosis lead to various symptoms of sickle cell anemia, including painful crises of vasoocclusion. ... Now, most patients with sickle cell disease can be expected to survive into adulthood, but still face a lifetime of crises and complications, including chronic hemolytic anemia, vaso-occlusive crises and pain, and the side effects of therapy. Currently, most common therapeutic interventions include blood transfusions, opioid and hydroxyurea therapies (see, for example, S. K. Ballas in Cleveland Clin. J. Med., 66:48-58 (1999). However, all of these therapies are associated with some undesirable side-effects. For example, repeated blood transfusions are known to be associated with the risks of transmission of infectious disease, iron overload, and allergic and febrile reactions. Complications of opioid therapy may include addiction, seizures, dependency, respiratory depression and constipation. Web site: http://www.delphion.com/details?pn=US06355661__ ·
Pharmaceutical composition for the treatment of the anemia of malignant tumors Inventor(s): Ono; Masayoshi (Saitama, JP), Akamatsu; Ken-ichi (Tokyo, JP) Assignee(s): Chugai Seiyaku Kabushiki Kaisha (Tokyo, JP) Patent Number: 4,745,099 Date filed: February 3, 1986 Abstract: A pharmaceutical composition for the treatment of the anemia of malignant tumors comprising a therapeutically effective amount of human erythropoietin (EPO) in a parenterally acceptable vehicle is disclosed. Human EPO may be extracted from human urine or also be prepared by expressing in a host cell the gene coding for the amino acid sequence of human EPO. Excerpt(s): The present invention relates to a pharmaceutical composition for the treatment of the anemia of malignant tumors that comprises a therapeutically effective amount of human erythropoietin (hereinafter referred to as "human EPO") in a parenterally acceptable vehicle. ... The term "human EPO" as used hereinafter means a polypeptide having the amino acid sequence inherent in human beings, with or without sugar chains. Examples of the human EPO include one that is derived from human urine (hereinafter referred to as "human urinary EPO"), one obtained by expressing in a host cell the gene coding for the amino acid sequence of human EPO (this type of
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human EPO is hereinafter referred to as "human rEPO"), one obtained from a tissue culture of human kidney cancer cells, and one obtained by cultivating a hybridoma resulting from cell fusion of a human cell line having the ability to produce human EPO. The term "erythropoietin" (hereinafter referred to as "EPO") will mean a trace physiologically active substance that acts on erythroblastic stem cells present not only in humans but also in other animals so as to accelerate the differentiation of such stems cells into mature erythrocytic cells, and proliferation of the latter. While numerous studies on human urinary EPO have been reported, the pharmaceutical utility of human EPO still remains unknown in many respects. ... High incidence of anemia as one of the complications in cancer-bearing patients has been known for many years (see, for example, Miller, A. et al.; J. Clin. Invest. 35, 1248 (1956)), and severe anemia associated with malignancy is of particular clinical concern in the treatment of the disease. Many hypotheses have been proposed for explaining the mechanism behind the development of anemia, and they include the blockade of iron in the reticuloendothelial system due to abnormal iron metabolism, impaired iron release, spleen involvement, impaired EPO production, hemolysis, and disorders in hemopoietic stem cells. In the case of the anemia of malignant tumors, possible causes include hemorrhage resulting from abnormal tumor growth, the blockade of reticuloendothelial iron release, infiltration of bone marrow with tumor cells, hemolysis due to impaired microvessels and autoimmune diseases, bone marrow suppression resulting from treatment with antitumor agents or radiotherapy, as well as chronic inflammation. The plasma EPO levels in cancer-bearing patients have been reported to be equal to or lower than normal levels (see, for example, Zucker, S. et al., J. Clin. Invest., 53, 1132 (1974); Douglas, S. W. et al., Blood, 45, 55 (1975); Firat, D. et al., Cancer Res., 31, 1355 (1971); Ward, H. P. et al., J. Clin. Invest., 50, 332 (1971); and Degowin, R. L. et al., J. Lab. Clin. Med., 94, 303 (1979)). However, in the absence of any corelation between the decrease in the plasma EPO levels and the degree of anemia in malignancy and in view of the fact that most cancerbearing patients suffer from dysfunction of bone marrow, some researchers propose that the principal cause of the anemia of malignancy is not impaired erythropoietin production but more probably is impaired erythropoietic ability in the bone marrow due to hyporesponsiveness to EPO. Therefore, in view of the proposed mechanism for the development of anemia in malignancy, it has been very doubtful that administration of human EPO to patients with the anemia of malignancy is effective for the purpose of treating the disease. As already mentioned, numerous papers exist that report the various functions of human urinary EPO but nobody has demonstrated by in vivo experimentation with humans or animals that human urinary EPO and other types of human EPO are effective as therapeutic agents for the treatment of anemia in malignancy. Web site: http://www.delphion.com/details?pn=US04745099__ ·
Pharmaceutical composition for the treatment of the anemia of rheumatoid arthritis Inventor(s): Cynshi; Osamu (Tokyo, JP), Mizuno; Koji (Saitama, JP) Assignee(s): Chugai Seiyaku Kabushiki Kaisha (Tokyo, JP) Patent Number: 4,732,889 Date filed: February 3, 1986 Abstract: A pharmaceutical composition for the treatment of the anemia of rheumatoid arthritis comprising a therapeutically effective amount of human erythropoietin (EPO) in a parenterally acceptable vehicle is disclosed. Human EPO may be extracted from
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human urine or also be prepared by expressing in a host cell the gene coding for the amino acid sequence of human EPO. Excerpt(s): The present invention relates to a pharmaceutical composition for the treatment of the anemia of rheumatoid arthritis that comprises a therapeutically effective amount of human erythropoietin (hereinafter referred to as "human EPO") in a parenterally acceptable vehicle. ... The term "human EPO" as used hereinafter means a polypeptide having the amino acid sequence inherent in human beings, with or without sugar chains. Examples of the human EPO include one that is derived from human urine (hereinafter referred to as "human urinary EPO"), one obtained by expressing in a host cell the gene coding for the amino acid sequence of human EPO (this type of human EPO is hereinafter referred to as "human rEPO"), one obtained from a tissue culture of human kidney cancer cells, and one obtained by cultivating a hybridoma resulting from cell fusion of a human cell line having the ability to produce human EPO. The term "erythropoietin"(hereinafter referred to as "EPO") will mean a trace physiologically active substance that acts on erythroblastic stem cells present not only in humans but also in other animals so as to accelerate the differentiation of such stems cells into mature erythrocytic cells, and proliferation of the latter. While numerous studies on human urinary EPO have been reported, the pharmaceutical utility of human EPO still remains unknown in many respects. ... High incidence of anemia as one of the complications in patients with rheumatoid arthritis has been known for many years (see, for example, Nilsson, F., Acta. Med. Scand. Suppl., 210, 193 (1948), and Roberts, F. D. et al.; Blood, 21, 470 (1983)), and severe anemia associated with rheumatoid arthritis is of particular clinical concern in the treatment of the disease. Web site: http://www.delphion.com/details?pn=US04732889__ ·
Pharmaceutical composition of BUF-5 for treating anemia Inventor(s): Washitake; Masayo (Kawasaki, JP), Ejima; Daisuke (Kawasaki, JP), Koyama; Naoto (Kawasaki, JP), Eto; Yuzuru (Kawasaki, JP), Shibai; Hiroshiro (Kawasaki, JP) Assignee(s): Ajinomoto Company, Inc. (Tokyo, JP) Patent Number: 5,200,395 Date filed: October 29, 1991 Abstract: The polypeptides BUF-4 and BUF-5 may be used to treat osteoporosis, cancer, and anemia, and pharmaceutical compositions containing BUF-4 and/or BUF-5 are disclosed. Excerpt(s): The present invention relates to pharmaceutical compositions containing as an effective ingredient, at least one substance selected from the polypeptides BUF-4 and BUF-5 (hereafter referred to as BUF-4 and BUF-5), more particularly, to pharmaceutical compositions containing, as an effective ingredient, at least one substance selected from BUF-4 and BUF-5 which exhibit therapeutic effects on any of osteoporosis, anemia, and cancer and methods of treating osteoporosis, anemia, and cancer by administering of BUF-4 or BUF-5. ... With the increased population of aged people, the number of patients with osteoporosis has also recently increased, resulting in a serious social problem. The number of patients suffering from osteoporosis in Japan, is currently estimated to be approximately 4 million people. Osteoporosis is a disease which results in a decrease in the amount of bone or skeletal tissue atrophy. The disease is extremely dangerous in that as the amount of bone decreases, the trabecula becomes narrow which causes bones to become fragile, and as the result, the vertebra, femur, cervical vertebra,
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etc. are broken. ... The disease is roughly classified into two types: (1) post-menopausal osteoporosis found in women after menopause and (2) senile osteoporosis found in aged people irrespective of sex. Web site: http://www.delphion.com/details?pn=US05200395__ ·
Proteins encoded by chicken anemia virus DNA and diagnostic kits and vaccines employing said proteins Inventor(s): De Boer; Gerden F. (Lelystad, NL), Noteborn; Mathews H. M. (Leiden, NL) Assignee(s): Leadd, bv (NL) Patent Number: 6,238,669 Date filed: August 13, 1997 Abstract: Circular double-stranded replication intermediates were identified in lowmolecular-weight DNA of cells of the avian leukemia virus-induced lymphoblastoid cell line 1104-X-5 infected with chicken anemia virus (CAV). To characterize the genome of CAV, we cloned linearized CAV DNA into the vector pIC20H. Transfection of the circularized cloned insert into chicken cell lines caused a cytopathogenic effect, which was arrested when a chicken serum with neutralizing antibodies directed against CAV was added. The 2,319-bp cloned CAV DNA contained all the genetic information needed for the complete replication cycle of CAV. The CAV genome probably contains only one promoter region and only one poly(A) addition signal. Southern blot analysis using oligomers derived from the CAV DNA sequence showed that infected cells contained double- and single-stranded CAV DNAs, whereas purified virus contained only the minus strand. The CAV DNA sequence has three partially overlapping major reading frames coding for putative peptides of 51.6, 24.0, and 13.6 kDa. The claimed invention is directed toward immunogenic and vaccine compositions comprising these novel peptides. Excerpt(s): This invention is in the fields of genetic engineering (gene manipulation) by means of the recombinant DNA (and RNA) technology, diagnostics and immunization/vaccination. More in particular, the invention relates to the detection, cloning and sequence analysis of the Chicken Anemia Virus (CAV) DNA genome and applications thereby made possible. ... The CAV virus that has not been classified so far causes infectious anemia in chicken. The virus was first isolated in Japan in 1979 and was given its name because of the serious anemia caused by it in young chicks (Yuasa, et al., (1979) Avian Diseases 23:366-385). The other symptoms of CAV infection are the atrophy of the bone marrow and destruction of lymphocytes in the thymus. Lesions occur in the spleen and liver. ... Day-old chicks are most susceptible. In these animals lethargy, anorexia and a passing anemia are observed from 4 to 7 days after inoculation with CAV and about half of the animals die between 2 and 3 weeks after infection. With increasing age the natural resistance also increases. Upon infection at the age of seven days the chicks only develop a passing anemia after infection, and upon infection of 14 days old animals no anemia follows. Web site: http://www.delphion.com/details?pn=US06238669__
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Rapid method for diagnosing the various forms of alpha-thalassemia Inventor(s): Tang; Delia C. (Bethesda, MD), Rodgers; Griffin P. (Kensington, MD) Assignee(s): The United States of America as represented by the Department of Health and (Washington, DC) Patent Number: 6,322,981 Date filed: July 16, 1999 Abstract: The present invention relates to the simultaneous and specific identification of the variant forms of .alpha.-thalassemia. This invention utilizes simple and readily available equipment to rapidly identify, diagnose and differentiate the different forms of .alpha.-thalassemia. Specifically, the present invention relates to a simple and rapid nonradioisotopic technique for the diagnosis and differentiation of the common forms of .alpha.-thalassemia has been developed. This approach works on any biological tissue including blood, wherein the assay works equally well with fresh blood and dried blood samples stored on filter paper. Excerpt(s): The present invention relates to the field of diagnostic methodologies. More particularly, the invention is related to a simple, inexpensive and rapid method for detecting thalassemias and monitoring therapeutic effects on the disease. ... The .alpha.thalassemia (".alpha.-thal") are common genetic disorders that result from reduced synthesis of the a globin chains of fetal (.alpha..sub.2.gamma..sub.2, HbF) and adult (.alpha..sub.2.beta..sub.2, HbA) hemoglobin (Weatherall and Clegg, 1981; Higgs et al., 1989, Higgs and Weatherall, 1993). The normal human .alpha. globin gene cluster is located on the short arm of chromosome 16 (Breuning et al., 1987; Buckle et al., 1988). In .alpha.-thal syndromes, .alpha.-globin synthesis is either diminished or absent due to either deletional or non-deletional abnormalities involving the .alpha.-globin genes (Higgs et al., 1989; Higgs and Weatherall, 1993). Diploid cells have four .alpha.-chain genes (i.e., .alpha..alpha./.alpha..alpha.). The severity of the hematological and clinical picture is directly proportional to the number of involved .alpha.-globin genes and thus the deletion of one, two, three, or all four of these .alpha. genes attribute to mild to complete a chain deficiencies syndromes. ... The deletion of .alpha.-chain at birth results in the formation of a .gamma. chain tetramer, Hb Bart's (.gamma..sub.4). The percentage of Hb Bart's present corresponds to the degree of .alpha. chain deficiency (Cong & Shong, 1982; Liang et al., 1985; Higgs et al., 1989; Higgs and Weatherall, 1993). The .alpha.-thal-2 genotype has been found to have one of the two genes deleted, thug these heterozygotes (.alpha..alpha./-.alpha.) possess a mild .alpha. chain deficiency resulting from the presence of only three .alpha. chain genes and have not more than 2% Hb Bart's at birth (Higgs et al., 1989). Homozygotes (-.alpha./-.alpha.), as well as .alpha.thal-1 heterozygotes (.alpha..alpha./--), possess moderate a chain deficiency resulting from the presence of only two .alpha. chain genes and have approximately 5% Hb Bart's at birth (Higgs and Weatherall, 1993). While Hb H disease is a heterozygosity for .alpha.-thal-2 in association with an .alpha.-thal-1 heterozygosity (--/-.alpha.), a severe .alpha. chain deficiency occurs due to the deletion of three .alpha. chain genes (Higgs et al., 1989; Higgs and Weatherall, 1993). The .alpha.-thal-1 homozygotes (--/--), which lack any functional .alpha. genes, present with Hb Bart's is known as hydrops fetalis syndrome and results in intra-uterine or early post-delivery death to the fetus (Lie-Injo & Hie, 1960; Higgs et al., 1989). Mother bearing fetuses with homozygous .alpha.-thal-1 (--/--) are at high risk for obstetrical complications, such pregnancy induced hypertension, eclampsia, and/or death. Web site: http://www.delphion.com/details?pn=US06322981__
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Recombinant chicken anemia virus particle Inventor(s): De Boer; Gerden F. (Lelystad, NL), Noteborn; Mathews H.M. (Leiden, NL) Assignee(s): Leadd BV (NL) Patent Number: 5,958,424 Date filed: August 13, 1997 Abstract: Recombinant genetic information (DNA or RNA), comprising a Chicken Anemia Virus (CAV)-specific nucleotide sequence and the use thereof for diagnostics, vaccination or protein production. Recombinant CAV protein and the use thereof for diagnostics, vaccination or production of CAV-specific antibodies. The use of CAVspecific antibodies thus obtained. Excerpt(s): This invention is in the fields of genetic engineering (gene manipulation) by means of the recombinant DNA (and RNA) technology, diagnostics and immunization/vaccination. More in particular, the invention relates to the detection, cloning and sequence analysis of the Chicken Anemia Virus (CAV) DNA genome and applications thereby made possible. ... The CAV virus that has not been classified so far causes infectious anemia in chicken. The virus was first isolated in Japan in 1979 and was given its name because of the serious anemia caused by it in young chicks (Yuasa, et al., (1979) Avian Diseases 23:366-385). The other symptoms of CAV infection are the atrophy of the bone marrow and destruction of lymphocytes in the thymus. Lesions occur in the spleen and liver. ... Day-old chicks are most susceptible. In these animals lethargy, anorexia and a passing anemia are observed from 4 to 7 days after inoculation with CAV and about half of the animals die between 2 and 3 weeks after infection. With increasing age the natural resistance also increases. Upon infection at the age of seven days the chicks only develop a passing anemia after infection, and upon infection of 14 days old animals no anemia follows. Web site: http://www.delphion.com/details?pn=US05958424__
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Reduction of the severity 3'-azido-3'-deoxythymidine-induced benzylacyclouridine
anemia
using
Inventor(s): Chu; Ming Y. W. (Four Azalea Ct., Barrington, RI 02806), Wiemann; Michael C. (11 Villa Ave., Providence, RI 02906), Calabresi; Paul (27 Glen Ave., Barrington, RI 02806) Assignee(s): none reported Patent Number: 4,874,602 Date filed: February 22, 1988 Abstract: A method of reducing anemia caused by the administration of 3'-azido-3'deoxythymidine to an animal which comprises treating said animal with a compound which inhibits the enzyme uridine phosphorylase in order to increase cellular uridine levels is disclosed. A particularly-effective compound is 5-benzylacyclouridine. Excerpt(s): 3'-Azido-3'-deoxythymidine (AZT) is the only drug which is commercially available for the treatment of the acquired immune deficiency syndrome (AIDS) or symptomatic advanced AIDS-related complex (ARC). AZT inhibits the human immunodifficiency virus reverse transcriptase. ... The main toxic affect of AZT in
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patients receiving the drug is severe anemia, often associated with megaloblastic bone marrow (Yarchoan, et al., Lancet, 1986, 1:575. ... In studies carried out in vitro to "rescue" human bone marrow progenitor (HBMP) cells using potential rescue agents, Sommadossi, et al., found that uridine and cytidine could reverse the toxic effect of AZT in HBMP cells. Web site: http://www.delphion.com/details?pn=US04874602__ ·
Reduction of the severity of 3'-azido-3'-deoxythymidine-induced anemia using a combination of benzylacyclouridine and dipyridamole Inventor(s): Wiemann; Michael C. (11 Villa Ave., Providence, RI 02906), Darnowski; James W. (6 Calderone St., Barrington, RI 02806), Calabresi; Paul (27 Glen Ave., Barrington, RI 02806) Assignee(s): none reported Patent Number: 4,950,466 Date filed: June 22, 1988 Abstract: The invention is directed to a method of inhibiting anemia caused by the administration of AZT to a patient which comprises administering to said patient an effective anemia-inhibiting amount of a combination of dipyridamole and 5benzylacyclouridine. The invention is further directed to a pharmaceutical composition comprising as the active pharmaceutical agent a combination of dipyridamole and 5benzylacyclouridine in association with a pharmaceutically acceptable carrier or diluent. Excerpt(s): 3'-Azido-3'-deoxythymidine (AZT) is the only drug which is commercially available for the treatment of the acquired immune deficiency syndrome (AIDS) or symptomatic advanced AIDS-related complex (ARC). AZT inhibits the human immunodifficiency virus reverse transcriptase. ... The main toxic affect of AZT in patients receiving the drug is severe anemia, often associated with a megaloblastic bone marrow (Yarchoan, et al., Lancet, 1986, 1:575). ... It has been found that administration of a combination of BAU and dypyridamole to animals receiving AZT reduces the severity of AZT-induced anemia. Animals which were treated with AZT and with a combination of BAU and dipyridamole did not develop severe suppression of hemoglobin or hematocrit as did animals treated only with AZT. Administration of a combination of BAU/DPR is expected to produce a rise in the reticulocyte count, hemoglobin and hematocrit of patients which have previously been made anemic by administration of AZT. Web site: http://www.delphion.com/details?pn=US04950466__
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Remedy for anemia and arthritis Inventor(s): Cheng; Theodore (1209 W. Wynnewood Rd., Wynnewood, PA 19096) Assignee(s): none reported Patent Number: 4,767,626 Date filed: February 27, 1986 Abstract: A method for the treatment of anemia associated with viral and bacterial infection in a patient wherein symptoms of rheumatoid arthritis are present, by administering to the patient an effective amount of a composition capable of increasing
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thyroxine in the blood stream of said patient and thereby increasing stem cells in the blood stream. The composition preferably comprises fat soluble alkaloid extracts from the root of Zanthoxylum Simulans. Excerpt(s): The present invention relates to a method and composition for the alleviation of certain symptoms associated with rheumatoid arthritis. Also, the present invention is concerned with a method for diagnosing and monitoring patients suffering from rheumatoid arthritis. More particularly, the present invention relates to the treatment of anemia associated with rheumatoid arthritis. A still further part of the invention is the treatment of anemia which results from bacterial or viral infections and indicates also the presence of arthritis. ... There have been a number of investigations which indicate that certain bacterial and viral infections contribute to a subsequent development of the syndrome of rheumatoid arthritis as well as mild anemia. Some of these reports have indicated that there is a high incidence of anemia in patients which are suffering from rheumatoid arthritis. Such anemia is characterized as being moderately hypochromic and normocytic. ... Freireich et al, in the article entitled "Radioactive Iron Metabolism & Erythrocyte Studies of the Mechanism of the Anemia Associated With Rheumatoid Arthritis", J. Clinical Investigation 36: 1055 (1957), reported the mechanism of said anemia in arthritic patients, appears to be the rate of said red cell destruction was increased while the rate of said red cell synthesis was comparable to normal. Said anemia results because erythropoiesis fails to increase in order to compensate for said increased rate of red cell destruction. Said erythropoiesis, includes the synthesis of stem cells maturing into red blood cells in the bone marrow and in said blood stream with its continuous division and differentiation, appears to be self-regulating and also under the influence of thyrotropin, a thyroid hormone. Web site: http://www.delphion.com/details?pn=US04767626__ ·
Screening test for beta-thalassemia trait and a diagnostic kit for its individualization Inventor(s): De Matteis; Maria C. (Piazza Isotta Nogarola, 15 - 37131 Verona, IT) Assignee(s): none reported Patent Number: 4,604,350 Date filed: April 15, 1983 Abstract: A screening test for beta-thalassemia trait carriers is carried out by mixing 10 .mu.l of blood of the patient with 2 ml of an aqueous solution prepared from glycerol, sodium chloride, sodium dihydrogen phosphate, disodium hydrogen phosphate, sodium azide, Acid Green 5 to obtain a suspension. A well cluster, having several wells is used. The suspension is formed in one well and the turbidity is determined by placing a reading scale under the cluster. Excerpt(s): Hemolysis of the erythrocytes by glycerol has been studied by many authors, among whom: M. H. Jacobs, et al, J. Exper. Zool. 113, 272, (1950); J. Kroes, et al, Biochim. Biophys. Acta 249, 647, (1971); T. J. Moore, J. Lipid Res. 9, 642 (1968); J. De Gier, et al, Biochim. Biophis, Acta 49, 286 (1961) and Experientia 22, 20 (1966); J. M. C. Wessels, et al, Biochim. Biophys. Acta 291, 178-196 (1973). E. L. Gottfried and N. A. Robertson, Blood 40, 940 (1972), J. Lab. Clin. Med. 83, 323-333 (1974) and 84, 746-751, describe methods for screening erythrocyte abnormalities like the thalassemia trait carriers, iron deficiency anemia, hereditary spherocytosis, sickle-cell anemia, based on the lysis time of the erythrocytes suspended in a 0.3M aqueous buffered solution of glycerol (glycerol lysis test, GLT). ... The present invention is based on a similar principle bar is far more
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reliable and simpler. A. Zanella et al, British Journal of Haematology, 45, 481-6 (1980), describes a modification of GLT, named Acidified Glycerol Lysis Test (AGLT) as a screening test for hereditary spherocytosis. ... The object of the present invention is to provide a screening test for beta-thalassemia trait carriers with a diagnostic kit for its diagnosis. Web site: http://www.delphion.com/details?pn=US04604350__ ·
Sickle cell anemia control Inventor(s): Chima; Oji A. (Little Rock, AR) Assignee(s): Norris; Jerome J. (Rockville, MD) Patent Number: 4,904,678 Date filed: August 25, 1987 Abstract: Method of providing anti-sickling of red blood cells in sickle cell anemia patients without hemolyzing said cells, using thiocyanates alone, or together with Vitamin B.sub.6. Excerpt(s): Sickle cell anemia is a blood disorder characterized by anemia arising from low levels of hemoglobin and hematocrit (packed red cell volume). ... This form of anemia is a hereditary defect resulting from a genetic mutation, wherein a hemoglobin variant (sickle cell) is synthesized instead of the normal adult hemoglobin. In the generic sense, sickle cell disease applies to disorders characterized by human red blood cells, which contain an abnormal hemoglobin, that has been designated hemoglobin S. ... When deprived of oxygen, sickle cell hemoglobin becomes insoluble, and forms hemoglobin crystals. These crystals form rigid rods which distort the normally, nearly spherical red blood cells to the sickle shaped forms. It has been found that sickle cells are more fragile than normal red blood cells, and the abnormal shapes of these cells cause them to be easily hemolyzed (broken) in circulating blood. Web site: http://www.delphion.com/details?pn=US04904678__
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Sickle cell anemia treatment Inventor(s): Goodman; Steven R. (Mobile, AL) Assignee(s): South Alabama Medical Science Foundation (Mobile, AL) Patent Number: 6,087,398 Date filed: March 1, 1996 Abstract: The present invention provides a method of treating sickle cell anemia comprising the step of administering to an individual in need of said treatment a therapeutically acceptable dose of reducing agent. In yet another embodiment of the present invention, there is provided a method of pharmacologically correcting a posttranslational modification of the .beta.-actin protein in sickled erythrocytes, comprising the step of contacting said sickled erythrocytes with a pharmacologically effective dose of a reducing agent. In still yet another embodiment of the present invention, there is provided a method of identifying a drug for use in treating sickle cell anemia. Any drug which hastens the HDSS Core Skeleton dissociation rate is tested by the in vitro ternary complex dissociation assay to test whether its effect is on HDSS beta-actin. Furthermore, drugs can be tested by the oxygenation-deoxygenation cycling assay for its ability to
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block ISC formation in vitro. Finally, drugs can be tested for ability to cause the conversion of preformed ISCs back to the biconcave shape. Excerpt(s): The present invention relates generally to the fields of molecular hematology and protein chemistry. More specifically, the present invention relates to a novel treatment for sickle cell anemia. ... Hemoglobinopathies encompass a number of anemias of genetic origin in which there is decreased production and/or increased destruction (hemolysis) of red blood cells. The blood of normal adult humans contains hemoglobin (designated as HbA) which contains two pairs of polypeptide chains designated alpha and beta. Fetal hemoglobin (HbF), which produces normal red blood cells, is present at birth, but the proportion of HbF decreases during the first months of life and the blood of a normal adult contains only about 2% HbF. There are genetic defects which result in the production by the body of abnormal hemoglobins with a concomitant impaired ability to maintain oxygen concentration. Among these genetically derived anemias are included thalassemia, Cooley's Disease and, most importantly, sickle-cell anemia (HbS disease). ... Sickle-cell anemia is an inherited chronic hemolytic anemia characterized by sickle-shaped red blood cells present in part of the offspring of parents who are both heterozygotes to the abnormal gene which causes the sickling disease. This disease is recessive, and heterozygotes carrying this gene show no blatant anemia or similar abnormality. Thus, only about 25% of the children of parents who are both heterozygous are expected to be homozygotic to this abnormal gene and will develop sickle cell anemia and eventually sickling crisis (aplastic crisis). Few homozygotes live past 40 years of age and many show abnormal body growth patterns. The gene which characterizes sickling trait causes valine to be substituted for glutamic acid in the sixth position of the beta chain, thus producing HbS rather than HbA. Deoxygenated HbS is much less soluble than deoxy HbA and it forms a semisolid gel of rodlike tactoids, thus causing the red blood cells produced from HbS to assume a sickle shape. These abnormally shaped red blood cells form a sort of sludge. In addition, these HbS red blood cells are more fragile than normal red blood cells and hemolyze more easily, thus leading eventually to anemia. The clinical manifestations of an aplastic crisis in sickle-cell homozygotes include arthralgia with fever, jaundice, aseptic necrosis of the femoral head, chronic punched-out ulcers about the ankles plus episodes of severe abdominal pain with vomiting. Thrombosis and/or infarction may also be present. Laboratory findings include a monocytic anemia with an RBC count in the range 2-3 times. Early death, usually before 40, is caused by intercurrent infections (especially tuberculosis), multiple pulmonary emboli or thrombosis of a vessel supplying a vital area. In the past, treatment of sickle-cell anemia was symptomatic only. Web site: http://www.delphion.com/details?pn=US06087398__ ·
Simple, rapid and reliable method for detecting thalassemia Inventor(s): Huang; Shu-Zhen (Shanghai, CN), Schechter; Alan N. (Bethesda, MD), Rodgers; Griffin P. (Silver Spring, MD) Assignee(s): The United States of America as represented by the Department of Health (Washington, DC) Patent Number: 5,281,519 Date filed: October 23, 1992
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Abstract: A simple, rapid and reliable method for diagnosis of thalassemia is described. The method comprises amplification of the cDNA by polymerase chain reaction and determining the ratio between .alpha. and .beta. hemoglobin chain mRNAs. Excerpt(s): The present invention is related generally to diagnostic methodologies. More particularly, the present invention is related to a simple, inexpensive and rapid method for detecting thalassemias and monitoring therapeutic effects on the disease. ... The thalassemias represent a heterogeneous group of diseases, characterized by the absence or diminished synthesis of one or the other of the globin chains of hemoglobin A. In .alpha.-thalassemia, .alpha.-chain synthesis is decreased or absent; whereas in .beta.thalassemia, .beta.-chain synthesis is diminished or absent. Numerous molecular defects account for the various thalassemias. The degree of clinical expression is generally dictated by the nature and severity of the underlying globin gene (DNA) defect. Thalassemia major (homozygous .beta.-thalassemia) defines the most severe variety of the disease. Thalassemia intermedia and thalassemia minor refer to the heterozygous state, generally associated with milder clinical manifestations. ... Beta-thalassemia is an autosomal recessive disorder characterized by absent (.beta..sup.o) or decreased (.beta..sup.+) synthesis of the .beta.-globin chain. Thalassemia is found in almost all population and ethnic groups around the world. It has been estimated that 3% of the world's population or 150 million people carry .beta.-thalassemia genes. Indeed, it is among the most common genetic diseases in the world. Alpha thalassemia, the corresponding disorder of .alpha. hemoglobin chain is also of great prevalence, especially in the Orient. Web site: http://www.delphion.com/details?pn=US05281519__ ·
Trace element composition for iron deficiency anemia Inventor(s): Fouad; M. Taher A. (Layton, UT) Assignee(s): Kelatron Pharmaceutical Division of Intermountain Laboratories Inc. (Ogden, UT) Patent Number: 4,208,405 Date filed: February 12, 1979 Abstract: An improved dietary supplement for mammals, the dietary supplement includ the essential dietary trace metals, iron, copper and molybdenum. These metals are provided in a highly bioavailable state such as peptide and polypeptide chelates. This invention also includes a method for using natural proteinaceous starting materials for producing the peptide and polypeptide ligands for the chelates. The proteinaceous starting materials are obtained from a primary grown yeast, an isolated vegetable protein, dessicated tissues of animal origin and the like which, upon hydrolysis, yields the peptide and polypeptide ligands suitable for forming chelates with the iron, copper and molybdenum. The metals are each separately chelated with the peptide and polypeptide ligands and thereafter combined in the suitable ratios to form the dietary supplement. The dietary supplement is adsorbed on a suitable food product and provided in an effective amount for consumption in iron deficiency anemia. Excerpt(s): This invention relates to dietary supplements and, more particularly to a dietary supplement including the metals iron, copper and molybdenum and its use in iron deficiency anemia. ... Although more than 100 elements are known, certain trace elements perform functions which are indispensable to maintaining life. These trace elements are directly involved in the cellular physiochemical reactions and are,
Patents 385
therefore, referred to as essential elements. Accordingly, essential elements are those fulfilling certain criteria outlined as follows: (a) the element is present in all healthy tissue of all organisms; (b) its concentration in these healthy tissues is relatively constant; and (c) withdrawal of the element produces similar structural and physiological abnormalities in different species, the abnormalities being prevented or reversed by addition of such elements. ... Trace elements fulfilling the above-mentioned properties as essential elements are, in alphabetical order: chromium, cobalt, copper, fluorine, iodine, iron, manganese, molybdenum, nickel, selenium, silicon, tin, vanadium and zinc. Each element exhibits a spectrum of actions that depend, in part, on (a) the amount or dose and (b) the nutritional state of the cell or the recipient regarding that element. The concentration of essential elements is internally controlled by chemical mechanism which tends to restore the correct concentration of these elements thus leading to a normal or symmetrical distribution pattern. Accordingly, increasing amounts of certain elements result in stimulating biological response until a certain plateau is reached. If intake of these elements exceed the foregoing plateau, a pharmacological action followed by toxic effects will appear. Web site: http://www.delphion.com/details?pn=US04208405__ ·
Treating anemia using recombinant adeno-associated virus virions comprising an EPO DNA sequence Inventor(s): Podsakoff; Gregory M. (Fullerton, CA), Kurtzman; Gary J. (Menlo Park, CA) Assignee(s): Avigen, Inc. (Alameda, CA), Johns Hopkins University (Baltimore, MD) Patent Number: 5,846,528 Date filed: January 16, 1997 Abstract: The use of recombinant adeno-associated virus (AAV) virions for delivery of DNA molecules to muscle cells and tissue in the treatment of anemia is disclosed. The invention allows for the direct, in vivo injection of recombinant AAV virions into muscle tissue, e.g., by intramuscular injection, as well as for the in vitro transduction of muscle cells which can subsequently be introduced into a subject for treatment. The invention provides for sustained, high-level expression of a delivered nucleotide sequence encoding erythropoietin, and for in vivo secretion thereof from transduced muscle cells such that systemic delivery is achieved. Excerpt(s): The present invention relates generally to DNA delivery methods. More particularly, the invention relates to the use of recombinant adeno-associated virus (AAV) virions for in vitro and in vivo delivery of erythropoietin (EPO) to muscle cells and tissue for the treatment of anemia. The method provides for sustained, high-level expression of EPO. ... The production of red blood cells in mammals, erythropoiesis, is under the control of the hormone erythropoietin (EPO). EPO is normally present in low concentrations in plasma, where it is sufficient to maintain equilibrium between normal blood cell loss (i.e., through aging) and red blood cell production. ... Anemia is a decrease in red blood cell mass caused by decreased production or increased destruction of red blood cells. EPO is currently used for treatment of the anemias associated with end-stage renal failure and acquired immunodeficiency syndrome (AIDS), particularly in subjects who are being treated with zidovudine (AZT). EPO is also used for amelioration of the anemia associated with cancer chemotherapy. Web site: http://www.delphion.com/details?pn=US05846528__
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Treatment of sickle cell anemia crises with fructose-1, 6-diphosphate as an analgesic drug Inventor(s): Markov; Angel K. (Jackson, MS), Fox; Anthony W. (Rancho LaCosta, CA), Marangos; Paul J. (Encinitas, CA) Assignee(s): Cypros Pharmaceutical Corp. (Carlsbad, CA) Patent Number: 6,074,658 Date filed: October 3, 1997 Abstract: Fructose-1,6-diphosphate (FDP) has been shown, in double-blinded controlled clinical trials on patients with sickle cell anemia, to substantially reduce the pain suffered by such patients during the recurrent ischemic crises that are caused by red blood cell sickling. Tests on patients who have been hospitalized for such crises demonstrated that when they received an intravenous injection of FDP, they reported substantially lower pain levels during their hospital stays than control groups that received identical treatment without any FDP. Apparently, FDP has never previously been used or even tested in human clinical trials, to treat sickle cell anemia. In addition, FDP has never previously been reported to have any analgesic (pain-reducing) activity. Excerpt(s): This invention relates to the use of a naturally occurring sugar-phosphate compound called fructose-1,6-diphosphate, for treating the sporadic crises that arise in people suffering from sickle cell anemia. ... Accordingly, sickle cell anemia and 1,6-FDP have both been studied extensively. However, there apparently has never been any prior effort to treat sickle cell anemia, using 1,6-FDP. ... This genetic mutation is relatively common in Africa, since a person who carries a single copy of the mutated gene has a relatively high resistance to malaria, without suffering from major adverse health effects. Accordingly, it has been estimated that roughly 30% of all people native to Nigeria (as just one example) carry at least one such gene (Barnhart et al 1976). About 8% of African-Americans also carry at least one such gene, although local populations often contain higher levels. The gene which disposes red blood cells to sickling is often referred to as HbS, where "Hb" refers to hemoglobin, and "S" refers to sickling. By contrast, a normal, healthy, adult hemoglobin is usually referred to as HbA. Web site: http://www.delphion.com/details?pn=US06074658__
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Treatment of sickle cell anemia crises with fructose-1,6-diphosphate as an analgesic drug Inventor(s): Marangos; Paul J. (Encinitas, CA), Fox; Anthony W. (Rancho LaCosta, CA), Markov; Angel K. (Jackson, MS) Assignee(s): Questcor Pharmaceuticals, Inc. (Union City, CA) Patent Number: 6,312,707 Date filed: June 12, 2000 Abstract: Fructose-1,6-diphosphate (FDP) has been shown, in double-blinded controlled clinical trials on patients with sickle cell anemia, to substantially reduce the pain suffered by such patients during the recurrent ischemic crises that are caused by red blood cell sickling. Tests on patients who have been hospitalized for such crises demonstrated that when they received an intravenous injection of FDP, they reported substantially lower pain levels during their hospital stays than control groups that received identical treatment without any FDP. Apparently, FDP has never previously
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been used or even tested in human clinical trials, to treat sickle cell anemia. In addition, FDP has never previously been reported to have any analgesic (pain-reducing) activity. Excerpt(s): This invention relates to the use of a naturally occurring sugar-phosphate compound called fructose-1,6-diphosphate, for treating the sporadic crises that arise in people suffering from sickle cell anemia. ... Accordingly, sickle cell anemia and 1,6-FDP have both been studied extensively. However, there apparently has never been any prior effort to treat sickle cell anemia, using 1,6FDP. ... This genetic mutation is relatively common in Africa, since a person who carries a single copy of the mutated gene has a relatively high resistance to malaria, without suffering from major adverse health effects. Accordingly, it has been estimated that roughly 30% of all people native to Nigeria (as just one example) carry at least one such gene (Barnhart et al 1976). About 8% of African-Americans also carry at least one such gene, although local populations often contain higher levels. The gene which disposes red blood cells to sickling is often referred to as HbS, where "Hb" refers to hemoglobin, and "S" refers to sickling. By contrast, a normal, healthy, adult hemoglobin is usually referred to as HbA. Web site: http://www.delphion.com/details?pn=US06312707__
Patent Applications on Anemia 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 anemia: ·
Anemia Inventor(s): Naylor, Stuart ; (Oxford, GB), Binley, Katie (Mary) ; Kingsman, Susan Mary ; (Oxford, GB)
(Oxford, GB),
Correspondence: FROMMER LAWRENCE & HAUG; 745 FIFTH AVENUE- 10TH FL.; NEW YORK; NY; 10151; US Patent Application Number: 20030143202 Date filed: February 1, 2002 Abstract: Disclosed is a vector containing a nucleic acid sequence encoding erythropoietin (Epo) in operable linkage with an HRE expression control sequence, as well as uses thereof; for instance, in preparing a medicament, as well as in methods for treating anemia in a patient in need thereof. The method can involve administering to the patient a vector comprising a nucleic acid sequence encoding erythropoietin (Epo) in operable linkage with an HRE expression control sequence, wherein expression of Epo is physiologically regulated such that hematocrit levels of the patient are corrected and maintained. Excerpt(s): This application claims priority from British Application No.______, filed Jan. 31, 2002 (UK Attorney Docket No. P013473GB). ... Reference is made to: U.S. Pat. No. 6,265,390 (Methods For Expressing Nucleic Acid Sequences Using Nucleic Acid Constructs Comprising Hypoxia Response Elements), filed Feb. 22, 1999, U.S. Pat. No. 5,942,434 (Nucleic Acid Constructs Comprising Hypoxia Response Elements), filed Dec. 12, 1996, PCT/GB95/00322, filed Feb. 15, 1995 and published Aug. 17, 1995 as WO 10
This has been a common practice outside the United States prior to December 2000.
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95/21927 (Targeting Gene Therapy), GB application serial no. 9402857, filed Feb. 15, 1994, and WO 00/17371, filed Sep. 22, 1999; nationally processed in the U.S. as U.S. Ser. No. 09/787,562. ... Each of the foregoing applications and patents and articles, and each document cited or referenced in each of the foregoing applications and patents and articles, including during the prosecution of each of the foregoing applications and patents ("application and article cited documents"), and any manufacturer's instructions or catalogues for any products cited or mentioned in each of the foregoing applications and patents and articles and in any of the application and article cited documents, are hereby incorporated herein by reference. Furthermore, all documents cited in this text, and all documents cited or referenced in documents cited in this text, and any manufacturer's instructions or catalogues for any products cited or mentioned in this text or in any document hereby incorporated into this text, are hereby incorporated herein by reference. Documents incorporated by reference into this text or any teachings therein may be used in the practice of this invention. Documents incorporated by reference into this text are not admitted to be prior art. Furthermore, authors or inventors on documents incorporated by reference into this text are not to be considered to be "another" or "others" as to the present inventive entity and vice versa, especially where one or more authors or inventors on documents incorporated by reference into this text are an inventor or inventors named in the present inventive entity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Composition and method for treating autoimmune hemolytic anemia Inventor(s): Kappler, John ; (Denver, CO), Jordan, Michael ; (Denver, CO), Marrack, Philippa ; (Denver, CO) Correspondence: SHERIDAN ROSS PC; 1560 BROADWAY; SUITE 1200; DENVER; CO; 80202 Patent Application Number: 20030118637 Date filed: November 27, 2002 Abstract: Disclosed are a composition and method to treat or prevent antibody-induced anemia and particularly, autoimmune hemolytic anemia. The composition comprises a bisphosphonate and a pharmaceutically acceptable carrier. In a preferred embodiment, the composition comprises clodronate and a liposome carrier. Excerpt(s): This application claims the benefit of priority under 35 U.S.C. .sctn.119(e) from U.S. Provisional Application Serial No. 60/334,326, filed Nov. 29, 2001. The entire disclosure of U.S. Provisional Application Serial No. 60/334,326 is incorporated herein by reference. ... This invention generally relates to a method of treating antibodyinduced anemia, and particularly, autoimmune hemolytic anemia. The invention includes the administration of a bisphosphonate to a patient having such a disease, and particularly, liposomal clodronate. The invention also relates to compositions comprising a bisphosphonate and a second agent for the treatment of antibody-induced anemia. ... Autoimmune hemolytic anemia (AIHA) is an autoimmune disease in which antibodies against the patients own red blood cells (RBC's) lead to their premature destruction (Ware et al., Autoimmune Hemolytic Anemia. In: David G Nathan, Stuart H Orkin, ed. Hematology of Infancy and Childhood (5.sup.th ed). Philadelphia: W. B. Saunders; 1998:499-522, incorporated by reference herein in its entirety). Anemia can be sudden and life threatening, or more gradual in onset. Though most cases are idiopathic, association with other forms of autoimmunity, malignancy, or infection is common (Ware et al., ibid.; Schreiber J Rheumatol. 7:395-397 (1980); Diehl et al., Semin
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Oncol. 25:80-97 (1998); Saif, AIDS Patient Care STDS. 15:217-224 (2001)). AIHA occurs in both children and adults, with a wide age distribution. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Diagnostic method of hemolytic anemia Inventor(s): Han, Kyung-Ja ; (Seoul, KR) Correspondence: BIRCH STEWART KOLASCH & BIRCH; PO BOX 747; FALLS CHURCH; VA; 22040-0747; US Patent Application Number: 20020127617 Date filed: December 27, 2001 Abstract: This invention is related to the diagnostic method of hemolytic anemia, which allows early diagnosis of hemolytic anemia and discrimination of significant schistocytes from insignificant old schistocytes by utilizing the flow cytometric detection of damaged RBCs using anti-Hb in a hypotonic solution compared to saline solution, in the case of the presence of schistocytes in the peripheral blood, such as microangiopathic hemolytic anemia (MAHA).This method does not require the washing or lysing steps, and get the result within 20 minutes easily. In detail, two microliter of peripheral blood isolated from a patient was stained with PE conjugated antihemoglobin (anti-Hb) antibody in 0.6% NaCl for 15 minutes at room temperature. Then, without wash, 3 ml of saline were added and analyzed by flow cytometry.Therefore, compared with the counting schistocytes on the stained blood smears the time-consuming and hard to distinguish schistocytes from indented normal red cells (RBCs), this invention provides here a new quick and accurate diagnostic method of hemolytic anemia by flow cytometry using antihemoglobin (anti-Hb) antibody which detect only newly produced damaged RBCs and discriminate significant from insignificant old schistocytosis.Key word: red blood cell (RBC), hemolytic anemia, red blood cell (RBC) test. Excerpt(s): This invention is related to the diagnostic method of hemolytic anemia, which allows early diagnosis of hemolytic anemia and discrimination of significant schistocytes from insignificant old schistocytes by utilizing the flow cytometric detection of damaged RBCs using anti-Hb in a hypotonic solution compared to saline solution, in the case of the presence of schistocytes in the peripheral blood, such as microangiopathic hemolytic anemia (MAHA). ... The conventional method for red blood cell (RBC) test involving microscopic examination of blood smears isolated form patients, has a limit for the accurate diagnosis of hemolytic anemia, such as hard to distinguish schistocytes from indented normal red cells(RBCs), especially newly produced damaged RBCs from insignificant old schistocytosis. The presence of schistocytes in the peripheral blood is a cardinal sign of microangiopathic hemolytic anemia(MAHA), and is also important in many other diseases associated with intravascular hemolysis including disseminated intravascular coagulation. The only available method to confirm the presence of schistocytes is microscopic examination of the blood smears after Romanovsky stain, and this is the only method of the quantitative analysis of schistocytes also. However, it is labor intensive, timeconsuming, and hard to distinguish schistocytes from indented normal red cells(RBCs). Sometimes, the patients, who received splenectomy revealed marked poikilocytosis including schistocytes without any significant clinical signs of hemolysis. Therefore, it is needed to develop a new method to detect and quantitate schistocytes in the peripheral blood, preferentially, newly produced schistocytes with clinical significance from the
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old one without clinical significance. In extravascular hemolysis, frequently poikilocytosis including spherocytosis and elliptocytosis is associated, Although specific laboratory tests for individual disease like antiglobulin test in autoimmune hemolytic anemia is available, early diagnosis of extravascular hemolysis is very difficult. ... This invention is related to the diagnostic method of hemolytic anemia, which allows early diagnosis of hemolytic anemia and discrimination of significant schistocytes from insignificant old schistocytes by utilizing the flow cytometric detection of damaged RBCs using anti-Hb in a hypotonic solution compared to saline solution, in the case of the presence of schistocytes in the peripheral blood, such as microangiopathic hemolytic anemia (MAHA). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Erythropoietin dosing regimen for treating anemia Inventor(s): Farrell, Francis ; (Doylestown, PA) Correspondence: AUDLEY A. CIAMPORCERO JR.; JOHNSON & JOHNSON; ONE JOHNSON & JOHNSON PLAZA; NEW BRUNSWICK; NJ; 08933-7003; US Patent Application Number: 20030134795 Date filed: November 26, 2002 Abstract: The present invention provides a new subcutaneous injection dosing regimen for erythropoietin to treat anemia. The new erythropoietin treatment regimen of the present invention results in improved hemoglobin levels with less frequent dosing. Excerpt(s): The present invention provides a method to treat anemia whereby an alternate dosing regimen is used to raise and maintain hemoglobin levels with dosing intervals greater than one week after the hemoglobin level was elevated with weekly administration. ... Erythropoietin (EPO) is a glycoprotein hormone secreted by the kidneys in response to tissue hypoxia, which stimulates red blood cell production in the bone marrow (1). The gene for EPO has been cloned and expressed in Chinese hamster ovary cells (2,3). This recombinant human erythropoietin (epoetin alfa, rhEPO) has an amino acid sequence identical to that of human urinary erythropoietin, and the two are indistinguishable on the basis of functional and immunological assays, although differences exist regarding protein glycosylation, affecting in vivo efficacy (4,5). ... In clinical trials to date, rhEPO has been evaluated in normal subjects as well as in patients with various anemic conditions (6,7). EPO induces a brisk hematologic response in normal human volunteers, provided that adequate supplies of iron are available to support increased hemoglobin synthesis (8). The majority of trials have investigated the safety and effectiveness of rhEPO in the treatment of chronic renal failure maintained on dialysis and in those not yet on maintenance dialysis. Other indications approved in the US include anemia secondary to chemotherapy treatment in cancer and anemia associated with zidovudine treatment of human immunodeficiency virus infection. Worldwide, EPO has been used to treat anemia associated with rheumatoid arthritis, prematurity, myelofibrosis, sickle cell anemia, bone marrow transplantation, thermal injury, .beta.-thalassemia, as a facilitator of presurgical autologous blood donation, and use as a presurgical adjuvant (6,7). Although rhEPO is generally well tolerated, occasional skin rashes and urticaria have been observed suggesting allergic hypersensitivity to some components of the Epoetin alfa formulation, likely human serum albumin. Further, despite blood screening, there exists a risk of infection with a transmissible agent when a pharmaceutical agent is formulated using human blood
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products. Therefore pharmaceutical formulations of rhEPO that are stable and are free of human blood products, such as albumin are needed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Immunostimulatory nucleic acids for the treatment of anemia, thrombocytopenia, and neutropenia Inventor(s): Petersen, Deanna M. ; (Newton, MA), Schetter, Christian ; (Hilden, DE), Bratzler, Robert L. ; (Concord, MA) Correspondence: WOLF GREENFIELD & SACKS, PC; FEDERAL RESERVE PLAZA; 600 ATLANTIC AVENUE; BOSTON; MA; 02210-2211; US Patent Application Number: 20020165178 Date filed: June 28, 2001 Abstract: The invention involves administration of an immunostimulatory nucleic acid alone or in combination with an anemia, thrombocytopenia, or neutropenia medicament for the treatment or prevention of anemia, thrombocytopenia, and neutropenia in subjects. The agents in combination are administered in synergistic amounts or in various dosages or at various time schedules. The invention also relates to kits and compositions concerning the combination of immunostimulatory nucleic acids and anemia, thrombocytopenia, or neutropenia drugs. Excerpt(s): This application claims benefit of U.S. Provisional Application No. 60/214,368, filed Jun. 28, 2000. ... The present invention relates to immunostimulatory nucleic acids, compositions thereof and methods of using the immunostimulatory nucleic acids in the treatment of anemia, thrombocytopenia, and neutropenia. ... Hematopoiesis, the formation of blood cells, represents a complex physiologic phenomenon whereby blood cells of various lineages arise from common progenitor cells called hematopoietic stem cells. Hematopoietic development is regulated by colony-stimulating factors (CSFs), which promote colony formation and proliferation of cells of various lineages, and by potentiators, which potentiate maturation or differentiation. Many of the factors involved in hematopoiesis affect more than a single lineage. For example, erythropoietin (EPO) stimulates both erythrocyte and platelet production. Similarly, some factors can be classified both as CSF and as potentiator. For example, thrombopoietin (TPO) was reported to possess both megakaryocyte-CSF (Meg-CSF) and megakaryocyte potentiator (Meg-Pot) activity in the development of megakaryocytes in vivo. In addition, many factors are involved in the development of any given cell lineage. Thus Meg-CSFs reportedly include interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF) and stem cell factor, and Meg-Pots reportedly include IL-6, IL-7, IL-11, erythropoietin (EPO) and leukemia inhibitory factor (LIF). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of treating anemia caused by ribavirin treatment of hepatitis C using erythropoietin alpha Inventor(s): Dieterich, Douglas T. ; (Garden City, NY) Correspondence: FROMMER LAWRENCE & HAUG; 745 FIFTH AVENUE- 10TH FL.; NEW YORK; NY; 10151; US Patent Application Number: 20030032590 Date filed: May 21, 2001 Abstract: Claimed and disclosed in a new use for a previously approved drug: erythropoietin. The present invention teaches using Erythropoetin to treat anemia caused by the combined treatment of Ribavirin and alpha-interferon. Erythropoetin has previously been approved for the treatment of anemia caused by cancer chemotherapy, renal failure and HIV. It has not been used for anemia caused by ribavirin. Ribavirin is part of a two-drug regimen now used to treat hepatitis C along with alpha interferon. The principal side effect of ribavirin is a hemolytic anemia. In the past, mangement of that anemia was done by dose reduction of the ribavirin, sometimes resulting in reversal of part of the anemia. It has become particularly important in light of new data, to maximize the dose of ribavirin given to persons undergoing treatment for hepatitis C to ensure a successful eradication of hepatitis C. Excerpt(s): The present invention is directed to a new use for Erythropoetin ("EPO"), such as EPO alpha, for treating hepatitis C and/or anemia caused by hepatitis C treatment. Accordingly, the invention involves using EPO with hepatitis C treatment, such as Ribavirin ("RBV") and/or interferon such as alpha-interferon (".alpha.-IFN" or "IFN"); and thus, the invention pertains to methods involving administration of EPO, RBV and .alpha.-IFN, or EPO and RBV, and compositions and kits containing EPO, RBV and .alpha.-IFN or EPO and RBV. ... Various documents are cited herein, e.g., in the text and/or in a reference section. There is no admission that any of the various documents cited in this text are prior art as to the present invention. Any document having as an author or inventor person or persons named as an inventor herein is a document that is not by another as to the inventive entity herein. All documents cited in this text ("herein cited documents") and all documents cited or referenced in herein cited documents are hereby incorporated herein by reference. All specifications, manufacturer's data sheets, and the like for products referenced herein, and all documents cited therein, are hereby incorporated herein by reference. ... Erythropoietin ("EPO") is one of the red blood cell stimulating factors in the human body. Recombinant technology has made manufacture of this stimulating factor colony possible and its use in treating anemia caused by cancer chemotherapy, acquired immune deficiency syndrome ("AIDS") and renal failure. The recombinant product has been shown to be biologically identical to human erythropoietin. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 393
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METHOD OF TREATING SICKLE CELL DISEASE OR THALASSEMIA Inventor(s): YAN, SAU-CHI BETTY ; (INDIANAPOLIS, IN), UTTERBACK, BARBARA GAIL ; (AVON, IN), UM, SUZANE LEE ; (INDIANAPOLIS, IN) Correspondence: ELI LILLY AND COMPANY; LILLY CORPORATE CENTER; DROP CODE 1104; INDIANAPOLIS; IN; 46285; US Patent Application Number: 20020012662 Date filed: November 22, 1999 Abstract: The present invention provides a method of treatment of sickle cell disease (SCD) or thalassemia with protein C. The claimed invention provides a needed therapy for potentially serious and debilitating disorders while avoiding complications such as bleeding tendency, toxicity and general side effects of currently available anticoagulant agents. Excerpt(s): This application claims priority of U.S. Provisional Application Serial No. 60/109,474 filed Nov. 23, 1998. ... This invention relates to medical science particularly the treatment of sickle cell disease or thalassemia with protein C. ... Protein C is a vitamin K dependent serine protease and naturally occurring anticoagulant that plays a role in the regulation of hemostasis by inactivating Factors Va and VIIIa in the coagulation cascade. Human protein C circulates as a 2-chain zymogen, but functions at the endothelial and platelet surface following conversion to activated protein C (aPC) by limited proteolysis with thrombin in complex with the cell surface membrane protein, thrombomodulin. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for treatment of sickle cell anemia Inventor(s): Chen, Long-Shiuh ; (San Diego, CA), Vassilev, Vassil P. ; (San Diego, CA), Lai, Ching-San ; (Encinitas, CA) Correspondence: Stephen E. Reiter; Foley & Lardner; P.O. Box 80278; San Diego; CA; 92138-0278; US Patent Application Number: 20030022923 Date filed: March 12, 2002 Abstract: The preparation and use of a protected organic aldehyde is described wherein bioavailability of the orally administered therapeutic aldehyde is improved. The protected aldehyde is prepared by reacting the aldehyde with a protecting group, for example, condensing the aldehyde chemically with a thiazolidine-4-carboxylic acid. The improved bioavailability of such orally administered drugs increases the feasibility of delivering sufficient amounts of vanillin or other therapeutic organic aldehydes in vivo to prevent sickling in sickle cell anemia. Combination therapy is also described wherein a protected organic aldehyde is administered to a subject in treatment of sickle cell anemia in conjunction with one or more other drugs, such as pain killers, used in treatment of the symptoms of sickle cell anemia or sickle cell disease. Excerpt(s): The present invention generally relates to methods for treating anemia. More specifically, the present invention relates to methods for treating sickle cell anemia using protected forms(s) of organic aldehydes. ... Sickle cell disease is a hemolytic disorder, which affects, in its most severe form, approximately 80,000 patients in the United States (see, for example, D. L. Rucknagel, in R. D. Levere, Ed., Sickle Cell Anemia and Other
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Hemoglobinopathies, Academic Press, New York, 1975, p.1). The disease is caused by a single mutation in the hemoglobin molecule; .beta.6 glutamic acid in normal adult hemoglobin A is changed to valine in sickle hemoglobin S. (see, for example, V. M. Ingram in Nature, 178:792-794 (1956)). Hemoglobin S has a markedly decreased solubility in the deoxygenated state when compared to that of hemoglobin A. Therefore, upon deoxygenation, hemoglobin S molecules within the erythrocyte tend to aggregate and form helical fibers that cause the red cell to assume a variety of irregular shapes, most commonly in the sickled form. After repeated cycles of oxygenation and deoxygenation, the sickle cell in the circulation becomes rigid and no longer can squeeze through the small capillaries in tissues, resulting in delivery of insufficient oxygen and nutrients to the organ, which eventually leads to local tissue necrosis. The prolonged blockage of microvascular circulation and the subsequent induction of tissue necrosis lead to various symptoms of sickle cell anemia, including painful crises of vasoocclusion. ... Now, most patients with sickle cell disease can be expected to survive into adulthood, but still face a lifetime of crises and complications, including chronic hemolytic anemia, vaso-occlusive crises and pain, and the side effects of therapy. Currently, most common therapeutic interventions include blood transfusions, opioid and hydroxyurea therapies (see, for example, S. K. Ballas in Cleveland Clin. J. Med., 66:48-58 (1999). However, all of these therapies are associated with some undesirable side-effects. For example, repeated blood transfusions are known to be associated with the risks of transmission of infectious disease, iron overload, and allergic and febrile reactions. Complications of opioid therapy may include addiction, seizures, dependency, respiratory depression and constipation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Suppressors of anemia and appetite suppressors and methods for suppressing anemia and suppressing appetite Inventor(s): Sakai, Ryousei ; (Kawasaki-shi, JP), Toue, Sakino ; (Kawasaki-shi, JP), Miura, Makoto ; (Kawasaki-shi, JP), Kimura, Takeshi ; (Kawasaki-shi, JP), Kawamata, Yasuko ; (Kawasaki-shi, JP) Correspondence: OBLON SPIVAK MCCLELLAND MAIER & NEUSTADT PC; FOURTH FLOOR; 1755 JEFFERSON DAVIS HIGHWAY; ARLINGTON; VA; 22202; US Patent Application Number: 20030018075 Date filed: May 31, 2002 Abstract: The present invention provides a method for suppressing hemolytic anemia by selectively ameliorating reticulocyte increase and iron deposition on spleen caused as the side effects of methionine. The present invention also provides an appetite suppressor with reduced such side effects, where threonine is used as the effective ingredient of the suppressor of hemolytic anemia due to methionine and a combination of methionine and threonine is used as the effective ingredient of the appetite suppressor. Excerpt(s): This application claims priority to Japanese Patent Application No. 2001165242, which was filed on May 31, 2001, and Internal Japanese Patent Application No. 2002-150918, which was filed on May 24, 2002, both of which are incorporated herein by reference in their entirety. ... The present invention relates to novel suppressors of anemia and novel appetite suppressors. More specifically, the present invention relates to agents for the prophylaxis (prevention), amelioration (improvement) and/or therapeutic treatment of anemia due to or caused by methionine (methionine-induced
Patents 395
anemia). The present invention also relates to methionine-containing appetite suppressors, which exhibit a reduced tendency to elicit anemia. The present invention further relates to feeds, nutritional supplements, foods or drinks, and/or pharmaceutical agents, which contain methionine and in which the tendency or action of methionine to elicit hemolytic anemia is ameliorated or reduced (improved). The present invention additionally relates to methods for suppressing methionine-induced anemia. The present invention also relates to methods for suppressing the appetite. ... Methionine belongs to a group of sulfur-containing amino acids and is one of the essential amino acids for humans. Methionine is nutritionally important. It is known that methionine is abundantly present in animal-derived proteins but is present in lesser amounts in plant-derived proteins. Methionine is medicinally used in amino acid infusions and general amino acid formulations in blends with other essential amino acids. Methionine is also used in therapeutic agents for liver diseases such as chronic or acute hepatitis and liver cirrhosis and in agents for the detoxification of chemicals, owing to its anti-fatty liver action and detoxification action (see "General Review of Amino Acid Industry (Aminosan Kogyo no Zenyou)," CMC, pp. 29-39, 1988). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html ·
Use of anti-TNF antibodies as drugs in treating septic disorders of anemic patients Inventor(s): Fischkoff, Steven A. ; (Short Hills, NJ), Barchuk, William T. ; (Madison, NJ), Teoh, Leah S. ; (Wayne, NJ) Correspondence: John D. Conway; Abbott Bioresearch Center, Inc.; 100 Research Drive; Worcester; MA; 01605-4314; US Patent Application Number: 20030012786 Date filed: May 23, 2002 Abstract: The instant invention is directed to treating an anemic patient having elevated levels of IL-6 by administering a TNF antagonist. It is also directed to treating sepsis in a patient by administering a TNF antagonist. Excerpt(s): The present invention relates to the use of TNF antagonists for treating septic disorders in anemic patients. ... It is known that the term tumor necrosis factor (TNF) embraces two cytotoxic factors (TNF-.alpha. and TNF-.beta.) which are mostly produced by activated lymphocytes and monocytes. ... EP 260,610 describes, for example, antiTNF antibodies which are said to be usable for inactivating TNF in disorders associated with an increase in TNF in the blood, such as septic shock, transpant rejection, allergies, autoimmune diseases, shock lung, coagulation disturbances or inflammatory bone disorders. 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 anemia, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/main/patents.htm. Under “Services,” click on “Search Patents.” You will see two broad options: (1) Patent Grants, and (2) Patent Applications. To see a list of granted patents, perform the following steps: Under “Patent Grants,” click “Quick Search.”
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Then, type “anemia” (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 anemia. You can also use this procedure to view pending patent applications concerning anemia. Simply go back to the following Web address: http://www.uspto.gov/main/patents.htm. Under “Services,” click on “Search Patents.” Select “Quick Search” under “Patent Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON ANEMIA Overview This chapter provides bibliographic book references relating to anemia. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on anemia 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 “anemia” (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 anemia: ·
Clinical Practice Guidelines for the Treatment of Anemia of Chronic Renal Failure Source: New York, NY: National Kidney Foundation. 1997. 174 p. Contact: Available from National Kidney Foundation. 30 East 33rd Street, New York, NY 10016. (800) 622-9010. Fax (212) 689-9261. PRICE: $13.00. ISBN: 0962972177. Summary: In March 1995, the National Kidney Foundation Dialysis Outcomes Quality Initiative (NKF-DOQI) was established, with the objective of improving patient outcomes and survival by providing recommendations for optimal clinical practices in four areas: hemodialysis adequacy, peritoneal dialysis adequacy, vascular access, and the treatment of anemia of chronic renal failure (CRF). This document presents 28 clinical practice guidelines for anemia. They are categorized in seven sections: anemia workup, target hematocrit and hemoglobin, iron support, administration of Epoetin (erythropoietin), inadequate epoetin response, the role of red blood cell transfusions, and possible adverse effects related to epoetin therapy. Each guideline is accompanied
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by a rationale, enabling dialysis caregivers to make informed decisions about the proper care plan for each individual patient. This document also includes a list of acronyms and abbreviations, a description of the guideline development methodology, endnotes, references, biographical sketches of the NKF-DOQI anemia work group members, and a complete listing of the articles reviewed by the anemia work group. 1 figure. 9 tables. 349 references. (AA-M). ·
Fanconi anemia: A handbook for families and their physicians Source: Eugene, OR: Fanconi Anemia Research Fund. 1993. 84 pp. Contact: Available from Fanconi Anemia Research Fund/Support Group, 1902 Jefferson Street, Two, Eugene, OR 97405. Telephone: (541) 687-4658 or (800) 828-4891 / fax: (541) 687-0548 / e-mail:
[email protected] / Web site: http://www.rio.com/~fafund. Available at no charge to any Fanconi anemia-affected family. Summary: This handbook is a lay guide to the inherited disorder Fanconi anemia. The topics covered are the definition, characteristics, and diagnosis of the disorder; treatments and therapies; continuing scientific study; and coping. The appendices contain lists of support resources for families and Fanconi anemia family support groups throughout the world.
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 PrintÒ). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “anemia” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “anemia” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “anemia” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): ·
A Benefit-Cost Analysis of Nutritional Interventions for Anemia Reduction (World Bank Staff Working Papers, No 801) by Henry M. Levin; ISBN: 0821307223; http://www.amazon.com/exec/obidos/ASIN/0821307223/icongroupinterna
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Acquired immune hemolytic anemias by Lawrence D. Petz; ISBN: 0443080518; http://www.amazon.com/exec/obidos/ASIN/0443080518/icongroupinterna
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Against All Odds: The Story of My Battle With Sickle Cell Anemia by Janice Gillespie (1994); ISBN: 0966054903; http://www.amazon.com/exec/obidos/ASIN/0966054903/icongroupinterna
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Anemia by B. A. Floyd (2002); ISBN: 1403360855; http://www.amazon.com/exec/obidos/ASIN/1403360855/icongroupinterna
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Anemia & Heavy Menstrual Flow: A Self-Help Program (The Women's Health Series) by Susan M. Lark; ISBN: 0917010493; http://www.amazon.com/exec/obidos/ASIN/0917010493/icongroupinterna
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Anemia (Hematology Series, Unit 1); ISBN: 0683159216; http://www.amazon.com/exec/obidos/ASIN/0683159216/icongroupinterna
Books 399
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Anemia in Teens by David J. Gerrick; ISBN: 0916750051; http://www.amazon.com/exec/obidos/ASIN/0916750051/icongroupinterna
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Anemia in Women: Self-Help and Treatment by Joan, Md. Gomez (2003); ISBN: 0897933664; http://www.amazon.com/exec/obidos/ASIN/0897933664/icongroupinterna
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Anemia y Homeopatica by Gilberto Quintero Ramirez (1997); ISBN: 8180564053; http://www.amazon.com/exec/obidos/ASIN/8180564053/icongroupinterna
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Anemia: A Guide to Causes, Treatment and Prevention by Jill Davies; ISBN: 0722528469; http://www.amazon.com/exec/obidos/ASIN/0722528469/icongroupinterna
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Anemia: Exercise in Clinical Problem (1987); ISBN: 068316855X; http://www.amazon.com/exec/obidos/ASIN/068316855X/icongroupinterna
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Anemia: Facts About Low Blood by David Steinberg; ISBN: 0721686125; http://www.amazon.com/exec/obidos/ASIN/0721686125/icongroupinterna
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Anemia: From Molecule to Medicine by Isaias, Raw; ISBN: 0316734810; http://www.amazon.com/exec/obidos/ASIN/0316734810/icongroupinterna
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Anemias Case Studies: A Compilation of 49 Clinical Studies by Robert H. Kough; ISBN: 0874881994; http://www.amazon.com/exec/obidos/ASIN/0874881994/icongroupinterna
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Aplastic anemia : pathophysiology and approaches to therapy; ISBN: 0387097724; http://www.amazon.com/exec/obidos/ASIN/0387097724/icongroupinterna
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Aplastic Anemia : Pathophysiology and Treatment by Hubert Schrezenmeier (Editor), Andrea Bacigalupo (Editor) (2000); ISBN: 0521641012; http://www.amazon.com/exec/obidos/ASIN/0521641012/icongroupinterna
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Aplastic anemia : proceedings of the First International Conference on Aplastic Anemia, held September 3-4, 1976, Kyoto; ISBN: 0839112297; http://www.amazon.com/exec/obidos/ASIN/0839112297/icongroupinterna
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Aplastic anemia : stem cell biology and advances in treatment : proceedings of the Third International Conference on Aplastic Anemia, held in Airlie, Virginia, June 2628, 1983; ISBN: 084510148X; http://www.amazon.com/exec/obidos/ASIN/084510148X/icongroupinterna
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Aplastic Anemia and Other Bone Marrow Failure Syndromes by Nasrollah T. Shahidi (Editor); ISBN: 0387970304; http://www.amazon.com/exec/obidos/ASIN/0387970304/icongroupinterna
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Aplastic Anemia and Other Bone Marrow Failure Syndromes (1990); ISBN: 3540970304; http://www.amazon.com/exec/obidos/ASIN/3540970304/icongroupinterna
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Aplastic Anemia: Acquired and Inherited by Neal S. Young, Blanche P. Alter (Contributor); ISBN: 0721637027; http://www.amazon.com/exec/obidos/ASIN/0721637027/icongroupinterna
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Aplastic Anemia: Stem Cell Biology and Advances in Treatment: Proceedings of the Third International Conference on Aplastic Anemia by International Conference on Aplastic Anemia, et al; ISBN: 0471834394; http://www.amazon.com/exec/obidos/ASIN/0471834394/icongroupinterna
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Astronauts Anemia Possible Mechanisms of Pathogenesis (Hematology Reviews and Communications Series) by V. M. Gavrilov; ISBN: 9057022540; http://www.amazon.com/exec/obidos/ASIN/9057022540/icongroupinterna
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Back to Our Roots: Cooking for Control of Sickle Cell Anemia and Cancer Prevention by Dawud Ujamaa; ISBN: 1884938019; http://www.amazon.com/exec/obidos/ASIN/1884938019/icongroupinterna
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Clinical Aspects and Laboratory: Iron Metabolism, Anemias: Novel Concepts in the Anemias of Malignancies and Renal and Rheumatoid Diseases by M. Iron Metabolism, Anemias Wick, et al (2003); ISBN: 3211006958; http://www.amazon.com/exec/obidos/ASIN/3211006958/icongroupinterna
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Control of Nutritional Anemia With Special Reference to Iron Deficiency: Proceedings of the Iaea-Usaid-Who Joint Meeting,Geneva, 1974 (Technical Report Series No. 580) by Iaea Usaid Who Joint Meeting Staff; ISBN: 9241205806; http://www.amazon.com/exec/obidos/ASIN/9241205806/icongroupinterna
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Cooley's Anemia: Seventh Symposium (Annals of the New York Academy of Sciences) by Alan Cohen (Editor), Mass.) Cooley's Anemia Symposium 1997 Cambridge (1998); ISBN: 1573311227; http://www.amazon.com/exec/obidos/ASIN/1573311227/icongroupinterna
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Diet, Demography, and Disease: Changing Perspectives of Anemia (Foundations of Human Behavior) by Patricia Stuart-MacAdam (Editor), Susan Kent (Editor) (1992); ISBN: 0202011895; http://www.amazon.com/exec/obidos/ASIN/0202011895/icongroupinterna
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Diseases Explained: Anemia by Lexi-Comp; ISBN: 1930598432; http://www.amazon.com/exec/obidos/ASIN/1930598432/icongroupinterna
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Dr. Susan Lark's Heavy Menstrual Flow & Anemia Self Help Book: Effective Solutions for Premenopause, Bleeding Due to Fibroid Tumors, Hormonal Imbalance, Endometriosis, Endometrial Cancer, and Low Blood Count by Susan M. Lark; ISBN: 0890877742; http://www.amazon.com/exec/obidos/ASIN/0890877742/icongroupinterna
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Dying in the City of the Blues: Sickle Cell Anemia and the Politics of Race and Health by Keith Wailoo; ISBN: 0807825840; http://www.amazon.com/exec/obidos/ASIN/0807825840/icongroupinterna
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Erythropoietin in Renal and Non-Renal Anemias: Update on Basic Research and Clinical Applications (Contributions to Nephrology; Vol 88) by International Workshop on Treatment of Anemia With Recombinant Human E, et al (1991); ISBN: 3805552726; http://www.amazon.com/exec/obidos/ASIN/3805552726/icongroupinterna
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Everything You Need to Know About Anemia (Need to Know Library) by Allison J. Ross; ISBN: 0823932184; http://www.amazon.com/exec/obidos/ASIN/0823932184/icongroupinterna
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Fanconi Anemia: Clinical, Cytogenetic, and Experimental Aspects by T.M. SchroederKurth, et al; ISBN: 038750401X; http://www.amazon.com/exec/obidos/ASIN/038750401X/icongroupinterna
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Ferritin in Iron Metabolism: Diagnosis of Anemias by M. Pinggera (1996); ISBN: 3211827064; http://www.amazon.com/exec/obidos/ASIN/3211827064/icongroupinterna
Books 401
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Fifth Cooley's Anemia Symposium; ISBN: 0897662857; http://www.amazon.com/exec/obidos/ASIN/0897662857/icongroupinterna
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Fifth Cooley's Anemia Symposium (Annals of the New York Academy of Sciences, Vol 445) by N.Y.)/ Cooley's Anemia Symposium / Bank, Arthur/ Anderson, W. French/ Zaino, Edward C./ New York Academy of Sciences Cooley's Anemia Symposium 1984 New York, Arthur Bank (1985); ISBN: 0897662849; http://www.amazon.com/exec/obidos/ASIN/0897662849/icongroupinterna
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Fourth Cooley's Anemia Symposium; ISBN: 0897660773; http://www.amazon.com/exec/obidos/ASIN/0897660773/icongroupinterna
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Hemolytic anemia in disorders of red cell metabolism by Ernest Beutler; ISBN: 0306311127; http://www.amazon.com/exec/obidos/ASIN/0306311127/icongroupinterna
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Hypovolemic Anemia of Trauma: The Missing Blood Syndrome by C. Robert Valeri, Mark D. Altschule (1981); ISBN: 0849353890; http://www.amazon.com/exec/obidos/ASIN/0849353890/icongroupinterna
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Immune hemolytic Anemias by Lawrence D. Petz, George Garratty; ISBN: 0443085595; http://www.amazon.com/exec/obidos/ASIN/0443085595/icongroupinterna
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Immune Hemolytic Anemias (Methods in Hematology Vol 12) by Hugh Chaplin (Editor); ISBN: 0443083207; http://www.amazon.com/exec/obidos/ASIN/0443083207/icongroupinterna
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In the Blood: Sickle Cell Anemia and the Politics of Race (Critical Histories) by Melbourne Tapper (1999); ISBN: 0812234715; http://www.amazon.com/exec/obidos/ASIN/0812234715/icongroupinterna
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Iron Deficiency Anemia: Recommended Guidelines for the Prevention, Detection, and Management Among U.S. Children and Women of Childbearing Age by Robert O. Earl (Editor), et al; ISBN: 0309049873; http://www.amazon.com/exec/obidos/ASIN/0309049873/icongroupinterna
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Iron Metabolism, Anemias, Diagnosis and Therapy: Novel Concepts in the Anemias of Renal and Rheumatoid Disease by M. Wick, et al (2000); ISBN: 3211833579; http://www.amazon.com/exec/obidos/ASIN/3211833579/icongroupinterna
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Iron, Anemia, and Old Age by J. Andrews (Editor) (1971); ISBN: 3805508891; http://www.amazon.com/exec/obidos/ASIN/3805508891/icongroupinterna
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Iron-deficiency anemia in mink fed raw marine fish; a five year study. Eisenmangelanämie beim Nerz nach Verfütterung von rohen Meeresfischen; ISBN: 3490402154; http://www.amazon.com/exec/obidos/ASIN/3490402154/icongroupinterna
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Is Menstruation Obsolete: How Suppressing Menstruation Can Help Women Who Suffer from Anemia, Endometriosis, or PMS by Elsimar M. Coutinho, Sheldon J. Segal (2003); ISBN: 0195162560; http://www.amazon.com/exec/obidos/ASIN/0195162560/icongroupinterna
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Laboratory investigation of drug-induced immune hemolytic anemia and/or positive direct antiglobulin tests by George Garratty; ISBN: 0914404539; http://www.amazon.com/exec/obidos/ASIN/0914404539/icongroupinterna
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Let's Talk About Sickle Cell Anemia (Let's Talk Library) by Melanie Apel Gordon; ISBN: 082395417X; http://www.amazon.com/exec/obidos/ASIN/082395417X/icongroupinterna
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Management Guidelines for the Treatment of Renal Anemia by M. Wolfson (Editor), W.M. Bennett (Editor); ISBN: 3805552769; http://www.amazon.com/exec/obidos/ASIN/3805552769/icongroupinterna
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Measurements of Iron Status: A Report of the International Nutritional Anemia Consultative Group (Inacg by James D. Cook (Editor), et al (1985); ISBN: 0935368477; http://www.amazon.com/exec/obidos/ASIN/0935368477/icongroupinterna
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Natural Ways to Relieve Heavy Menstrual Flow and Anemia: Effective Treatment of Premenopausal Symptoms, Hormone Imbalance-Related Bleeding, Low Blood Count and Fibroid Tumors by Susan M. Lark; ISBN: 0879837616; http://www.amazon.com/exec/obidos/ASIN/0879837616/icongroupinterna
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Nutritional Anemias by Usha Ramakrishnan (Editor); ISBN: 0849385695; http://www.amazon.com/exec/obidos/ASIN/0849385695/icongroupinterna
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Nutritional Anemias: Proceedings of the Who Expert Committee, Geneva, 1971 (Technical Report Series No. 503) by Who Staff; ISBN: 9241205032; http://www.amazon.com/exec/obidos/ASIN/9241205032/icongroupinterna
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Ontogeny of Hematopoiesis, Aplastic Anemia by E. Gluckman (Editor), L. Coulombel (Editor) (1995); ISBN: 2855986265; http://www.amazon.com/exec/obidos/ASIN/2855986265/icongroupinterna
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Overcoming Chronic Fatigue: Effective Self-Help Options to Relieve the Fatigue Associated With Cfs, Candida, Allergies, Pms, Menopause, Anemia, Low Thyroid and Depression ((Good Health Guide Ser.: Women's Self Care Library)) by Susan M. Lark; ISBN: 0879837160; http://www.amazon.com/exec/obidos/ASIN/0879837160/icongroupinterna
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Pernicious anemia by Lawrence Kass; ISBN: 0721652956; http://www.amazon.com/exec/obidos/ASIN/0721652956/icongroupinterna
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Refractory anemia by Lawrence Kass; ISBN: 0398033412; http://www.amazon.com/exec/obidos/ASIN/0398033412/icongroupinterna
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Renal Anemia: Conflicts and Controversies by Onyekachi Ifudu (Editor) (2002); ISBN: 1402006780; http://www.amazon.com/exec/obidos/ASIN/1402006780/icongroupinterna
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Severe Anemia in Pregnancy: Report of a Workshop Held at the Institute of Child and Mother Health in Dhaka, Bangladesh by Erick Boy Gallego (Editor) (2000); ISBN: 1894217128; http://www.amazon.com/exec/obidos/ASIN/1894217128/icongroupinterna
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Sickle Cell Anemia by Ronald L. Nagel MD, Samuel Charache MD; ISBN: 0865420602; http://www.amazon.com/exec/obidos/ASIN/0865420602/icongroupinterna
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Sickle Cell Anemia by Anthony Cerami; ISBN: 089388068X; http://www.amazon.com/exec/obidos/ASIN/089388068X/icongroupinterna
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Sickle Cell Anemia by David Gerrick; ISBN: 068589679X; http://www.amazon.com/exec/obidos/ASIN/068589679X/icongroupinterna
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Sickle Cell Anemia (A Venture Book) by George W. Beshore (Editor); ISBN: 0531125106; http://www.amazon.com/exec/obidos/ASIN/0531125106/icongroupinterna
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Sickle Cell Anemia (Diseases and People) by Alvin Silverstein, et al; ISBN: 0894907115; http://www.amazon.com/exec/obidos/ASIN/0894907115/icongroupinterna
Books 403
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Sickle cell anemia and other hemoglobinopathies; ISBN: 0124447503; http://www.amazon.com/exec/obidos/ASIN/0124447503/icongroupinterna
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Sickle Cell Anemia: Preliminary Survey by Lenwood G. Davis; ISBN: 0686203976; http://www.amazon.com/exec/obidos/ASIN/0686203976/icongroupinterna
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Sickle-Cell Anemia and Thalassemia: A Primer for Health Care Professionals by R.G. Huntsman; ISBN: 0921037007; http://www.amazon.com/exec/obidos/ASIN/0921037007/icongroupinterna
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Sixth Cooley's Anemia Symposium; ISBN: 0897666364; http://www.amazon.com/exec/obidos/ASIN/0897666364/icongroupinterna
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Sixth Cooley's Anemia Symposium (Annals of the New York Academy of Sciences, Vol 612) by Arthur Bank (Editor) (1991); ISBN: 0897666356; http://www.amazon.com/exec/obidos/ASIN/0897666356/icongroupinterna
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Tanya's Daddy: A Story About Sickle-Cell Anemia by Peter Anderson, et al; ISBN: 0865434573; http://www.amazon.com/exec/obidos/ASIN/0865434573/icongroupinterna
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The 2002 Official Patient's Sourcebook on Sickle Cell Anemia by Icon Health Publications, et al (2002); ISBN: 0597831572; http://www.amazon.com/exec/obidos/ASIN/0597831572/icongroupinterna
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The Disguised Disease, Anemia by Lawrence Galton; ISBN: 0517521261; http://www.amazon.com/exec/obidos/ASIN/0517521261/icongroupinterna
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The Drug Etiology of Agranulocytosis and Aplastic Anemia (Monographs in Epidemiology and Biostatistics, Vol. 18) by David W. Kaufman, et al (1991); ISBN: 0195059832; http://www.amazon.com/exec/obidos/ASIN/0195059832/icongroupinterna
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The Early Life of Jeomie East: Struggling With Sickle Cell Anemia by Phyllis East (2002); ISBN: 0759668019; http://www.amazon.com/exec/obidos/ASIN/0759668019/icongroupinterna
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The Hereditary Hemolytic Anemias by William C. Mentzer, Gail M. Wagner (Editor); ISBN: 0443082421; http://www.amazon.com/exec/obidos/ASIN/0443082421/icongroupinterna
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The Iron Disorders Institute Guide to Anemia by Cheryl D. Garrison (Editor), et al (2003); ISBN: 1581822995; http://www.amazon.com/exec/obidos/ASIN/1581822995/icongroupinterna
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Treatment of Renal Anemia (Blood Purification) by Bernard Canaud (Editor), KarlMartin Koch (Editor); ISBN: 3805553447; http://www.amazon.com/exec/obidos/ASIN/3805553447/icongroupinterna
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Treatment of Renal Anemia With Recombinant Human Erythropoietin (Contributions to Nephrology, Vol 66) by K. Kuhn, et al (1988); ISBN: 3805547641; http://www.amazon.com/exec/obidos/ASIN/3805547641/icongroupinterna
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Understanding Anemia (Understanding Sickness & Health Series) by Ed Uthman (1998); ISBN: 1578060397; http://www.amazon.com/exec/obidos/ASIN/1578060397/icongroupinterna
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What You Can Do About Anemia (The Dell Medical Library) by Marilynn Larkin; ISBN: 0440214092; http://www.amazon.com/exec/obidos/ASIN/0440214092/icongroupinterna
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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 “anemia” (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 ·
A program for collaborative research in the nutritional anemias in Latin America. Author: Finch, Clement A.,; Year: 1966; Washington, Pan American Health Organization, 1964
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A study on a substance eluted from erythrocytes of patients with rheumatoid arthritis and patients with hemolytic anemia. Author: Blodgett, Randolph C.,; Year: 1931; [Minneapolis] 1963
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Anemia in chronic pyelonephritis and in renal failure of analgesic abusers, with special reference to signs of microangiopathic hemolytic anemia. [Translated by Aino Wuolle]. Author: Forsström, Jorma.; Year: 1946; Turku, 1968
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Anemia problems in rheumatoid arthritis. Author: Nilsson, Fried Alvar,; Year: 1948; Uppsala, Appelbergs boktryckeriaktiebolag, 1948
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Disturbances in heme synthesis; special considerations of the sideroachrestic anemias and erythropoietic porphyrias, by Ludwig Heilmeyer, with the collaboration of Roman Clotten and Ludwig Heilmeyer, Jr. Author: Heilmeyer, Ludwig,; Year: 1963; Springfield, Ill., Thomas [c1966]
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Fatal aplastic anemia and chloramphenicol. Report to the California State Assembly and Senate by the California Medical Association and State Department of Public Health, with cooperation and assistance of the California Pharmaceutical Association. Author: California Medical Association.; Year: 1964; [Berkeley, California Dept. of Public Health, 1967]
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On the differential diagnosis between pernicious tapeworm anemia and cryptogenetic pernicious anemia in carriers of Diphyllobothrium latum. Author: Hirvonen, Martti.; Year: 1962; Helsinki [1947]
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Pernicious anemia; a study of 117 cases, by Birger Strandell. Author: Strandell, Birger.; Year: 1935; Stockholm, P. A. Norstedt; söner, 1931
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Studies in anemia of injury. [Tr. from the Swedish]. Author: Gelin, Lars-Erik.; Year: 1935; Stockholm, 1956
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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Chapters on Anemia In order to find chapters that specifically relate to anemia, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and anemia 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 and language you prefer, and the format option “Book Chapter.” Type “anemia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on anemia: ·
Occult Bleeding and Iron Deficiency Anemia Source: in Edmundowicz, S.A., ed. 20 Common Problems in Gastroenterology. New York, NY: McGraw-Hill, Inc. 2002. p. 137-144. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Website: www.bookstore.mcgraw-hill.com. PRICE: $45.00;plus shipping and handling. ISBN: 0070220557. Summary: Occult bleeding refers to the chemical detection of blood in stools without any grossly visible blood. Such a chronic loss of small volumes of blood via the gastrointestinal (GI) tract will eventually result in iron deficiency anemia. This chapter on occult bleeding and iron deficiency anemia is from a book that focuses on the most common gastroenterological problems encountered in a primary practice setting. The chapter is organized to support rapid access to the information necessary to evaluate and treat most patients with this problems. Topics include detection, clinical presentation, physical findings, the differential diagnosis, and patient evaluation and management. The author notes that iron deficiency anemia can also occur with problems not related to the gut (e.g., due to excessive menstrual losses or poor long term iron intake). Barring such circumstances, patients who have iron deficiency anemia or occult bleeding should be evaluated for a GI source of blood loss. When the causative lesions are identifiable, further loss of blood can usually be averted by endoscopic therapy. In the appropriate clinical setting, individuals with an unidentifiable source of blood loss may need push enteroscopy, intraoperative enteroscopy, or angiography. The chapter includes an outline for quick reference, the text itself, a diagnostic and treatment algorithm, and selected references. 3 figures. 2 tables. 15 references.
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Anemia Correction and Cardiac Function: Coronary Artery Disease and LeftVentricular Hypertrophy Source: in Koch, K.M. and Stein, G., eds. Pathogenetic and Therapeutic Aspects of Chronic Renal Failure. New York, NY: Marcel Dekker, Inc. 1997. p. 225-232. Contact: Available from Marcel Dekker, Inc. 270 Madison Avenue, New York, NY 10016. (212) 696-9000. Fax (212) 685-4540. PRICE: $115.00. ISBN: 0824798945. Summary: This chapter on anemia correction and cardiac function is from a book based on an international workshop, Chronic Renal Failure: Pathogenetic and Therapeutic Aspects, held in Berlin in May 1996. The author explores the role of renal anemia and the effects of erythropoietin (EPO)-induced recompensation of anemia in dialysis patients with left-ventricular hypertrophy (LVH) and coronary artery disease (CAD). Both of these diseases are characterized by a reduced coronary reserve and episodes of myocardial ischemia. The author examines the indirect evidence available from
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morphological (echocardiographic) studies and functional studies. The adverse effect of chronic ischemic disease in dialysis patients is mediated by heart failure, which is a strong predictor of earlier death. Recompensation (correction) of renal anemia by EPO to a target hematocrit of 35 percent initiates a slow and moderate echocardiographic regression of LVH, primarily by normalizing diastolic dimensions, and increases crucial coronary reserve in CAD. Induction of arterial hypertension by EPO (a side effect of the drug) may counteract those effects and should by avoided by appropriate antihypertensive agents. 1 figure. 20 references. ·
Overview of the Management of Anemia in End-Stage Renal Disease Source: in American Dietetic Association. Clinical Guide to Nutrition Care in End-Stage Renal Disease. Chicago, IL: American Dietetic Association. 1994. p. 195-197. 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 item is an appendix from a manual that provides guidelines for the clinical nutrition care of patients with end-stage renal disease (ESRD). In it the author provides an overview of the management of anemia in ESRD. Topics include the use of recombinant human erythropoietin (rHuEPO) in all modes of ESRD treatment; administration of rHuEPO in hemodialysis and peritoneal dialysis patients; how rHuEPO works to stimulate red blood cell production; monitoring of patients on rHuEPO; maintaining adequate iron status with iron supplementation; and evaluating overall nutritional and biochemical parameters of patients receiving rHuEPO. 14 references.
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Nutritional Anemias Source: in Nutritional Concerns of Women. Wolinski, I. Klimis-Tavantzis, D. eds. Boca Raton, FL, CRC Press, pp. 61-88, 1996. Contact: CRC Press LLC, 2000 Corporate Blvd., NW., Boca Raton, FL 33431. Summary: Nutritional Anemias, a chapter in Nutritional Concerns of Women, focuses on the main nutritional anemia found in adult women in the United States, iron deficiency anemia. Anemia occurs when the hemoglobin in the red blood cells falls below normal. Hemoglobin is made up of iron, protoporphyrin, and globin, with iron comprising one third the weight. In iron deficiency, the supply of iron is insufficient for normal hemoglobin synthesis. The consequences of greatest concern for women with iron deficiency anemia are the potential effects on pregnancy outcome and work capacity. Very severe anemia is associated with increased maternal mortality. The major causes of iron deficiency anemia among women are inadequate iron intake, increased physiologic requirements, and excessive blood loss. Postmenopausal women are less likely to develop iron deficiency anemia. The main sources of iron in the American diet are meat, poultry and fish, eggs, vegetables, and whole, iron-enriched, and iron-fortified grain products. Iron absorption by the body varies with physiologic need. Absorption increases when iron status is reduced and decreases when iron status is adequate. The type of iron consumed is far more important than the quantity of iron in the diet. Heme iron, from the hemoglobin and myoglobin of animals, is generally well-absorbed and unaffected by factors that inhibit iron absorption. The main inhibitors of nonheme iron absorption are phytates and polyphenols. Phytates are found primarily in cereal grains, nuts, legumes, and some vegetables. Polyphenols are found in tea, vegetables, and legumes. The recommended dietary allowance (RDA) for iron for women of
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childbearing age is 15 milligrams per day for nonpregnant and lactating women and 30 milligrams per day for pregnant women. The loss of blood during menstruation causes a loss of iron and the effect of this loss depends on the quantity of blood lost and the iron stores of the individual. Pathological blood loss from parasitic infection and gastrointestinal lesions can also be significant and contribute to iron deficiency anemia. A diagnosis of anemia alone has often been used as the screening test for iron deficiency anemia. Anemia is commonly diagnosed on the basis of a hemoglobin concentration or hematocrit level that is below a specific cutoff value for the population under study. Iron deficiency anemia is prevented by maintaining a balance between iron intake and iron requirement and loss. Women at risk should be counseled on dietary strategies to prevent anemia and should be treated and followed up if anemia presents during evaluation. A brief summary of the megaloblastic anemias caused by folate and vitamin B-12 deficiencies is also included. Folate and vitamin B-12 deficiency anemias are rare in the United States, but the associated deficiencies do occur among specific groups of women. Women of low socioeconomic status who are pregnant are at greatest risk for folate deficiency and women with impaired absorption of vitamin B-12 and strict vegetarian women who consume no animal products are at greatest risk for vitamin B12 deficiency. Folate deficiency and folate deficiency anemia are prevented by providing adequate dietary folate to meet requirements. This is accomplished through a choice of folate rich foods and minimal processing of the foods before consumption. 2 figures, 10 tables, 102 references.
Directories In addition to the references and resources discussed earlier in this chapter, a number of directories relating to anemia have been published that consolidate information across various sources. The Combined Health Information Database lists the following, which you may wish to consult in your local medical library:12 ·
9Health Fair Referral Guide Source: Denver, CO, Nine Health Services, Inc., 216 p., 1994. Contact: Nine Health Services, Inc., 825 East Speer Boulevard, Suite 200, Denver, CO 80218. (303) 698-4455. Summary: 9Health Fair Referral Guide is a publication of Nine Health Services, Inc. in Denver, Colorado, and is primarily used as a resource guide by health professionals at 9Health Fairs across Colorado. The Guide was compiled as a general reference with an emphasis on agencies that serve individuals and families on a limited income. It does, however, have resources for all income levels. Each resource listed in the Referral Guide includes an address, phone number, available services and resources, and cost. Resources are listed in each of the following categories: Crisis and emergency numbers, acquired immune deficiency syndrome (AIDS), alopecia areata, Alzheimer's disease, arthritis, blood pressure screenings, cancer, cardiovascular, cerebral palsy, chiropractic, clinics, cystic fibrosis, dental care, dermatology, diabetes, disabled resources, eating disorders, epilepsy, general consumer information and education, government agencies,
12 You will need to limit your search to “Directory” and “anemia” using the "Detailed Search" option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find directories, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Select your preferred language and the format option “Directory.” Type “anemia” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months.
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hearing, home health care, hospitals in metro Denver, immunizations, intestinal diseases, kidney disease, leukemia, living wills and related issues, lupus, medical societies, mental health, migrant health program, multiple sclerosis, muscular dystrophy, nutrition, orthodontics, ostomies, Parkinson's disease, physical therapy, podiatry, post-polio, prostate and testicular cancer, rehabilitation centers, respiratory diseases, runaways and shelters, safety, senior services, sexuality and family planning, sexually transmitted diseases, sickle cell anemia, shelter, smoking withdrawal and smokeless tobacco, social services agencies, speech and language, sports medicine, stress and grief, substance abuse (including alcohol and drug), suicide prevention, transplant resources, transportation, victim assistance, vision, and weight control. Resources are also listed for the following Colorado regions: Central and Mountain area, Eastern, Northern, Southern, and Western. Information numbers and referral services are also listed. ·
Directory of genetic service providers Source: Austin, TX: Texas Department of Health. 1992. 89 pp. Contact: Available from Texas Department of Health, Bureau of Chronically Ill and Disabled Children's Services, 1100 West 49th Street, Austin, TX 78756. Telephone: (512) 458-7111. Summary: This directory lists genetic service providers in Texas. It is organized by category of service including medical genetics programs, biochemical genetics laboratories, cytogenetics laboratories, DNA laboratories, and sickle cell anemia programs. Each entry includes the program name, address, phone, program director, contact person, and a list of the clinical services provided. Many of the entries include information about cost reimbursement. [Funded by the Maternal and Child Health Bureau].
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CHAPTER 8. MULTIMEDIA ON ANEMIA Overview In this chapter, we show you how to keep current on multimedia sources of information on anemia. 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 anemia is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “anemia” 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 “anemia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on anemia: ·
HGB E, anemia and basic genetics Source: Providence, RI: Providence Ambulatory Health Care Foundation. n.d. 1 videotape. Contact: Available from Media Consultants, 18 Stillwater Road, Smithfield, RI 02917. Telephone: (401) 232-0412 / fax: (401) 231-4462. $8.00 plus $2.00 shipping and handling. Summary: This videotape provides information on hemoglobin E, anemia, and basic genetics. It is supplemented by three pamphlets: 'Questions about Thalassemia,' Questions about Hemoglobin E,' and 'Genetics: The story of genes.' The tapes and pamphlets are available in English, Laotian, and Cambodian. [Funded by the Maternal and Child Health Bureau].
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Audio Recordings The Combined Health Information Database contains abstracts on audio productions. To search CHID, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find audio 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 “Sound Recordings.” Type “anemia” (or synonyms) into the “For these words:” box. The following is a typical result when searching for sound recordings on anemia: ·
[Digestive Disease Week 1992 Sessions Audiocassettes] Source: Timonium, MD: Milner-Fenwick, Inc. 1992. (audiocassettes). Contact: Available from AGA Audiovisual Materials in Gastroenterology and Liver Disease. c/o Milner Fenwick, Inc., 2125 Greenspring Drive, Timonium, MD 21093-3100. PRICE: $15 per cassette; discount available for series purchase. Summary: These audiocassettes reproduce clinical symposia, research forums, and lectures sponsored by Digestive Disease Week (DDW). Topics available include the pathogenesis, diagnosis, and treatment of gastroesophageal reflux disease (GERD); controversial issues in acute pancreatitis; the epidemiology, pathogenetic mechanisms, and molecular biology of Helicobacter pylori; the physiological and psychological basis for functional gastrointestinal pain; the management of esophageal varices; obesity, weight loss, and gallstones; therapy of inflammatory bowel disease (IBD); and clinical management strategies for anemia, colon polyps, dyspepsia of unknown cause, dysphagia, achalasia, motility disorders, and liver enzyme abnormalities. Topics in lectures include: alcoholic hepatitis; vitamin status and the elderly; erythromycin, macrolides and motilin as prokinetic agents; gallbladder mucosal function; Crohn's disease; and antibiotic selection for gastroenterology practice.
Bibliography: Multimedia on Anemia The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in anemia (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on anemia (for more information, follow the hyperlink indicated): ·
An Approach to the diagnosis of anemia from the peripheral blood counts and smear examination: microcytic and hypochromic anemias [motion picture] Source: National Medical Audiovisual Center in cooperation with New Jersey College of Medicine and Dentistry; Year: 1972; Format: Motion picture; Atlanta: The Center, [1972]
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An Approach to the diagnosis of anemia from the peripheral blood counts and smear examination: nomenclature and definition of terminology [motion picture] Source: National Medical Audiovisual Center, in cooperation with the New Jersey College of Medicine and Dent; Year: 1972; Format: Motion picture; Atlanta: The Center, [1972]
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An Approach to the diagnosis of anemia from the peripheral blood counts and smear examination: poikilocytosis and red cell inclusions [motion picture] Source: National
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Medical Audiovisual Center in cooperation with New Jersey College of Medicine and Dentistry; Year: 1972; Format: Motion picture; Atlanta: The Center, [1972] ·
An Approach to the problem of hemolytic anemia [slide] Source: American Society of Hematology; produced by Audiovisual Services, McMaster University; Year: 1973; Format: Slide; [Seattle]: The Society: [for sale by University of Washington Health Sciences Center for Educational Resources,] 1973
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Anemia and iron metabolism [slide] Source: Perry G. Rigby and James O. Armitage; Year: 1973; Format: Slide; New York: Medcom, c1973
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Anemia in the first week of life [slide] Source: developed at an NMAC Workshop under the auspices of The Audiovisual Committee of the Association of Medical School Pediatric Department Chairmen; Year: 1973; Format: Slide; Atlanta: National Medical Audiovisual Center, 1973
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Anemia of chronic disease [videorecording] Source: [Stanley P.] Balcerzak; produced by Ohio State University, Medical Audiovisual and Television Center; Year: 1971; Format: Videorecording; [Columbus, Ohio]: The Center, c1971
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Bone marrow interpretation in selected anemias [videorecording] Source: American Society of Clinical Pathologists; Year: 1976; Format: Videorecording; Chicago: The Society, c1976
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Care of patients with anemias and polycythemia [filmstrip] Source: Evanston Hospital School of Nursing, McGaw Medical Center; produced by American Journal of Nursing Co., Educational Services Division; Year: 1974; Format: Filmstrip; New York: The Company, c1974
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Hereditary anemias [slide] Source: R. M. Bannerman; Year: 1974; Format: Slide; New York: Medcom, c1974
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Iron deficiency anemia [videorecording] Source: [Albert F.] LoBuglio; produced by Ohio State University, Medical Audiovisual and Television Center; Year: 1971; Format: Videorecording; [Columbus, Ohio]: The Center, c1971
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Morphological and etiological classification of anemias [slide] Source: Dept. of Medical Technology, School of Health Related Professions, SUNYAB and Empire State Association of Medical Technologists, Niagara Frontier Chapter; Year: 1977; Format: Slide; Buffalo: Communications in Learning, 1977
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Nutritional anemias: part one, hypochromic anemia [motion picture] Source: Wayne State University School of Medicine; produced by Rex Fleming; Year: 1965; Format: Motion picture; Detroit: The University; [Atlanta: for loan by National Medical Audiovisual Center], c1965
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Nutritional anemias: part two, megaloblastic anemia [motion picture] Source: Wayne State University School of Medicine; produced by Rex Fleming; Year: 1965; Format: Motion picture; Detroit: The University; [Atlanta: for loan by National Medical Audiovisual Center], c1965
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Pathogenesis of anemia [motion picture] Source: Emory University School of Medicine and National Medical Audiovisual Center; Year: 1969; Format: Motion picture; Atlanta: The Center; [Washington: for sale by National Audiovisual Center], 1969
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Refractory anemia [slide] Source: Department of Medical Education at the Millard Fillmore Hospital in cooperation with the School of Medicine State University of New York at Buffalo; Year: 1976; Format: Slide; Buffalo: Communications in Learning, 1976
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Sickle cell: anemia or trait, the problem explained [videorecording] Source: Virginia Sickle Cell Anemia Awareness Program of the Medical College of Virginia/VCU; produced by Visual Education Dept., Medical College of Virginia; Year: 1978; Format:
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Videorecording; Richmond: The College: [for loan or sale by its Learning Resource Centers], 1978 ·
Sickle cell anemia [videorecording]: the facts Source: Virginia Sickle Cell Anemia Awareness Program of the Medical College of Virginia/VCU; produced by Visual Education Dept., Medical College of Virginia; Year: 1978; Format: Videorecording; Richmond: The College: [for loan or sale by its Learning Resource Centers], 1978
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The Black male with sudden anemia [slide] Source: University of Michigan Medical Center, Independent Study Unit, Dept. of Postgraduate Medicine and Health Professions Education; Year: 1972; Format: Slide; [Ann Arbor]: The Univ.: [for sale by Univ. of Michigan Medical Center Media Library], c1972
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The Clinical diagnosis of anemia [slide] Source: American Society of Hematology, National Slide Bank; Year: 1974; Format: Slide; Seattle: The Society: [for loan and sale by Univ. of Washington Health Sciences Center for Educational Resources, 1974]
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X-ray findings associated with acquired hemolytic anemia [videorecording] Source: M. I. Goldstein; produced by Ohio State University, Medical Audiovisual and Television Center; Year: 1972; Format: Videorecording; [Columbus, Ohio]: The Center, c1972
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X-ray findings related to hypochronic anemia [videorecording] Source: M. I. Goldstein; produced by Ohio State University, Medical Audiovisual and Television Center; Year: 1972; Format: Videorecording; [Columbus, Ohio]: The Center, c1972
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X-ray findings related to megaloblastic anemia [videorecording] Source: M. I. Goldstein; produced by Ohio State University, Medical Audiovisual and Television Center; Year: 1972; Format: Videorecording; [Columbus, Ohio]: The Center, c1972
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CHAPTER 9. PERIODICALS AND NEWS ON ANEMIA Overview In this chapter, we suggest a number of news sources and present various periodicals that cover anemia.
News Services and Press Releases One of the simplest ways of tracking press releases on anemia 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 “anemia” (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 anemia. 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 “anemia” (or synonyms). The following was recently listed in this archive for anemia: ·
Decitabine boosts HbF levels in sickle cell anemia patients Source: Reuters Industry Breifing Date: August 20, 2003 http://www.reutershealth.com/archive/2003/08/20/business/links/20030820drgd008 .html
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Medicare rate lower for Amgen anemia drug vs JJ Source: Reuters Industry Breifing Date: August 06, 2003
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Medicare coverage for Amgen anemia drug unchanged Source: Reuters Medical News Date: August 06, 2003
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Anemia in elderly increases risk of physical decline and loss of independence Source: Reuters Medical News Date: July 25, 2003
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Anemia hastens physical decline in elderly Source: Reuters Health eLine Date: July 25, 2003
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Anemia increases risk of death in patients with severe heart failure Source: Reuters Medical News Date: June 24, 2003
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Darbepoetin alfa effective for anemia in lymph malignancies Source: Reuters Industry Breifing Date: June 16, 2003
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Altana anemia drugs sale to fetch $22 mln Source: Reuters Industry Breifing Date: June 16, 2003
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Folate supplementation may mask pernicious anemia in sickle cell disease Source: Reuters Medical News Date: May 28, 2003
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Mutations in Fanconi's anemia genes linked to pancreatic cancer Source: Reuters Medical News Date: May 27, 2003
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Anemia common among diabetics Source: Reuters Medical News Date: April 10, 2003
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Hydroxyurea therapy may increase sickle cell anemia survival Source: Reuters Medical News Date: April 02, 2003
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FDA uncovers contaminated lots of fake anemia drug Source: Reuters Health eLine Date: March 11, 2003
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Immunosuppressive therapy for aplastic anemia often produces excellent results Source: Reuters Industry Breifing Date: March 06, 2003
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Anemia appears to increase mortality risk in heart failure patients Source: Reuters Medical News Date: February 25, 2003
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Partial splenectomy effective for congenital hemolytic anemias Source: Reuters Medical News Date: January 31, 2003
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Almost all children experience anemia after renal transplantation Source: Reuters Industry Breifing Date: January 03, 2003
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Gender difference found in sickle cell anemia Source: Reuters Health eLine Date: December 23, 2002
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Study quantifies anemia in chronic heart failure patients Source: Reuters Medical News Date: November 22, 2002
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Treatment of anemia may resolve restless legs syndrome Source: Reuters Medical News Date: November 14, 2002
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Treating anemia may resolve restless legs syndrome Source: Reuters Health eLine Date: November 14, 2002
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Caution recommended in epoetin use for anemia in hematologic malignancy Source: Reuters Industry Breifing Date: October 24, 2002
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Anemia common in kids in federal nutrition program Source: Reuters Health eLine Date: October 15, 2002
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Ion-channel therapy for sickle cell anemia given US fast-track status Source: Reuters Medical News Date: October 07, 2002
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Icagen sickle cell anemia therapy wins US fast-track status Source: Reuters Industry Breifing Date: October 07, 2002
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Darbepoetin alfa curbs anemia in lung cancer patients Source: Reuters Industry Breifing Date: September 04, 2002
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Darbepoetin safe and effective for chemotherapy-related anemia Source: Reuters Industry Breifing Date: August 20, 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 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 “anemia” (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
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you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “anemia” (or synonyms). If you know the name of a company that is relevant to anemia, 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 “anemia” (or synonyms).
Newsletters on Anemia Find newsletters on anemia 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 “anemia.” 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 “anemia” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: ·
Nutrition and WIC Update Source: Topeka, KS, Kansas Department of Health and Environment, 4 p., October 1993. Contact: Kansas Department of Health and Environment, Landon State Office Building, 900 Southwest Jackson, Topeka, KS 66612. Summary: The quarterly newsletter Nutrition and WIC Update offers information about the Special Supplemental Food Program for Women, Infants and Children (WIC) in Kansas. This issue highlights the 1992 Pediatric Nutrition Surveillance System for Kansas, which provides ongoing data on the health status of Kansas WIC children. Demographic data from the survey indicate that 68,605 records were placed in the system. Of those, 71 percent were primarily white, followed by blacks (14.4 percent), Hispanic Americans (11.7 percent), Asian Americans (1.8 percent), and Native Americans (1.1 percent). Anthropometric data showed that in 1992, the prevalence of short stature, a measure of chronic undernutrition, was 7.1 percent, a drop of 0.6 percent from the previous year and less than the national average of 8.6 percent. Birthweight data indicate that in Kansas, the 1992 prevalence of 8.9 percent is a decrease from 1991 (9.1 percent) and is below the national average of 9.4 percent. Screening for the risk of anemia showed a continued downward trend in children seen with low hemoglobin or hematocrit values. Finally, in 1992, increasing breast feeding incidence and duration were seen: 57.8 percent of infants on WIC were breast fed at hospital discharge and nearly all of them continued at 1 week; at 6 months, 28.9 percent were still being breast fed. Another article concerns the iron needs of the breast-fed infant. It states that exclusively breast-fed term infants should receive iron-rich weaning foods by age 6 months, and preterm and low-birth-weight, breast-fed infants should receive iron supplements by age 2 months. The possible need for new growth charts for breast-fed infants is discussed. Because of the slower growth velocity of breast-fed infants after the first 2-3 months, they often appear to be faltering when their growth is plotted on
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current growth charts. The World Health Organization is exploring the development of new growth charts for breast-fed infants. In the meantime, the article urges health care providers counseling parents to be aware of the differences in growth patterns of breastfed and formula-fed infants. ·
Nutrition Update Source: Atlanta, GA, Georgia Department of Human Resources, Division of Public Health, Maternal and Child Health Branch, Office of Nutrition, 2 p., July-August 1993. Contact: Georgia Department of Human Resources, Division of Public Health, Maternal and Child Health Branch, Office of Nutrition, Two Peachtree Street, NE., Atlanta, GA 30303. Summary: The Nutrition Update newsletter offers counseling tips from the Office of Nutrition of the Georgia Department of Human Resources. This issue discusses the Georgia Nutrition Surveillance System. Under cooperative agreements with the Centers for Disease Control and Prevention, two separate nutrition surveillance systems were established: The Pediatric Nutrition Surveillance System and the Pregnancy Nutrition Surveillance System. Both gather nutritional risk information from participants in the Supplemental Food Program for Women, Infants and Children (WIC). Georgia has been part of the pediatric system since 1986, with a systematic method for identifying and tracking six nutritional risk factors among infants and children ages 0 to 60 months. The risk factors are low birthweight, short stature, overweight, underweight, low hemoglobin, and low hematocrit. Since 1988, there has been a decline in the percent prevalence of all six nutrition risk indicators. The pregnancy nutrition surveillance system, initially implemented in Georgia in 1991 with six pilot sites, is currently in 20 districts statewide. Information on nutritional and behavioral risk factors affecting pregnancy outcome, such as prepregnancy weight status, weight gain during pregnancy, anemia, smoking, alcohol use, medical care, parity, and breast feeding trends, is obtained from WIC participants. Both surveillance systems allow state and local health departments to evaluate and monitor existing maternal and child health programs to plan appropriate nutrition-related health activities. In Georgia, health officials plan to use the surveillance data to determine staff training and education needs; enhance fiscal accountability, including personnel allocation; develop patient education programs and materials; and disseminate information to appropriate private, public, and legislative officials.
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 “anemia” (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 anemia: ·
Anemia-Related Fatigue: Feeling Tired Isn't Always Normal Source: PKR Progress. 15(3): 10. Fall-Winter 2000.
Periodicals and News 419
Contact: PKD Foundation. 4901 Main Street, Suite 200, Kansas City, MO 64112-2634. (800) 753-2873. E-mail:
[email protected]. Summary: This article from a newsletter for patients with polycystic kidney disease (PKD) explores the problem of anemia related fatigue in patients with kidney diseases. The author notes that since basic treatments are available for PKD, health care providers and researchers are now turning their attention to quality of life medical issues such as anemia. Anemia develops in virtually all patients with renal failure during the course of their disease. Health care providers now know that by intervening earlier in the disease process (in patients with chronic kidney disease who are not yet on dialysis), patients can realize a number of benefits and enhance their overall well being. The kidneys produce about 90 percent of the body's supply of the hormone erythropoietin (EPO); EPO is a major catalyst in the production of red blood cells in the bone marrow, so a reduction in EPO due to kidney disease usually results in fewer red blood cells and insufficient oxygen reaching the body tissues. The author explains the two primary diagnostic tests used to check for anemia, hematocrit (HCT) and hemoglobin. Anemia related fatigue is often described as a total lack of energy or debilitating exhaustion that can last days, weeks, or months. Fatigue can also have mental and emotional effects. The author cautions that because of its gradual onset and insidious nature, fatigue is often overlooked, underrecognized, and undertreated. Readers are encouraged to work with their physicians to address any problems or symptoms of fatigue. ·
Anemia Management: Preparing the Body and Mind for Rehabilitation Source: Renal Rehabilitation Report. 6(3): 4. May-June 1998. Contact: Available from Life Options Rehabilitation Program. Medical Education Institute, Inc, 414 D'Onofrid Drive., Suite 200, Madison, WI 53719. (608) 833-8033. Email:
[email protected]. Summary: This brief article reviews the importance of addressing problems with anemia in dialysis patients, before attempting renal rehabilitation. When left untreated, anemia produces physiological abnormalities, such as cardiac problems, disruption of muscle metabolism, and decreased mental function. Dialysis patients who suffer from anemia are likely to experience symptoms that include shortness of breath, chest pain, fatigue, inability to concentrate, and exercise intolerance. As long as these symptoms persist, making progress toward rehabilitation goals is difficult, if not impossible. The author discusses how treating anemia can prepare the body and the mind for rehabilitation. One section briefly covers the use of recombinant human erythropoietin (EPO) to treat anemia; the indications for iron therapy are also noted. The author concludes by encouraging dialysis providers to implement facility-based protocols for anemia management. 4 references.
Academic Periodicals covering Anemia Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to anemia. In addition to these sources, you can search for articles covering anemia 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.”
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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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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 Institute13: ·
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/
13
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.14 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:15 ·
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
14 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). 15 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 “anemia” 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 “anemia” (or synonyms) into the “For these words:” box. The following is a sample result: ·
Iron deficiency anemia: Recommended guidelines for the prevention, detection, and management among U.S. children and women of childbearing age Source: Washington, DC: National Academy Press. 1993. 126 pp. Contact: Available from National Academy Press, 2101 Constitution Avenue, N.W., Lockbox 285, Washington, DC 20002 / Web site: http://www.nap.edu. $29.00 plus $4.00 shipping and handling; prepayment required by check, money order, or credit card; purchase orders accepted. Summary: This report summarizes information related to public health measures for the prevention, detection, and management of iron deficiency anemia. It presents recommended guidelines as they apply in primary health care and public health clinic settings, and makes recommendations for research. The report identifies and addresses aspects that differ between the two target populations (infants and children, and women of childbearing age), as well as those common to both groups, and briefly considers family-oriented approaches. This report is intended to provide a frame of reference for health professionals and to assist the Centers for Disease Control and Prevention with preparing guidelines for prevention and control of iron deficiency anemia.
The NLM Gateway16 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.17 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “anemia” (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. 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). 16 17
Physician Resources 427
Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 115572 1999 675 794 27 119067
HSTAT18 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.19 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.20 Simply search by “anemia” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
Coffee Break: Tutorials for Biologists21 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.22 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.23 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/.
Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. The HSTAT URL is http://hstat.nlm.nih.gov/. 20 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. 21 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 22 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. 23 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. 18 19
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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/.
The Genome Project and Anemia In the following section, we will discuss databases and references which relate to the Genome Project and anemia.
Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).24 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “anemia” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for anemia: ·
Adenosine Deaminase, Elevated, Hemolytic Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?102730
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Adenosine Triphosphatase Deficiency, Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?102800
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Alpha-thalassemia Myelodysplasia Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?300448
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Alpha-thalassemia Myelodysplasia Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?300449
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Alpha-thalassemia/mental Retardation Syndrome, X-linked Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?301040
24 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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·
Anemia and Triphalangeal Thumbs Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?205600
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Anemia, Autoimmune Hemolytic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?205700
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Anemia, Congenital Hypoplastic, with Multiple Congenital Anomalies/mental Retardation Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604315
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Anemia, Congenital Sideroblastic, B6-nonresponsive Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?205950
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Anemia, Dyserythropoietic Congenital, Type I Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?224120
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Anemia, Dyserythropoietic Congenital, Type II Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?224100
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Anemia, Dyserythropoietic Congenital, Type Iii Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?105600
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Anemia, Familial Pyridoxine-responsive Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?206000
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Anemia, Hypochromic Microcytic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?206100
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Anemia, Microcytic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?206200
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Anemia, Nonspherocytic Hemolytic, Associated with Abnormality of Red Cell Membrane Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?206300
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Anemia, Nonspherocytic Hemolytic, Possibly due to Defect in Porphyrin Metabolism Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?206400
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Anemia, Sideroblastic, and Spinocerebellar Ataxia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?301310
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Anemia, Sideroblastic, X-linked Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?301300
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Cystic Fibrosis with Helicobacter Pylori Gastritis, Megaloblastic Anemia, and Subnormal Mentality Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?219721
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Diamond-blackfan Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?205900
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Diamond-blackfan Anemia 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606129
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Diamond-blackfan Anemia with Microtia and Cleft Palate Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606164
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Diamond-blackfan Anemia, Autosomal Dominant Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?105650
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Dyserythropoietic Anemia with Thrombocytopenia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?300367
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·
Dyserythropoietic Anemia, Congenital, Irish or Weatherall Type Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603902
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Fanconi Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?227650
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Fanconi Anemia Complementation Group a Gene Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607139
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Fanconi Anemia Zinc Finger Protein Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605859
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Fanconi Anemia, Complementation Group B Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?227660
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Fanconi Anemia, Complementation Group C Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?227645
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Fanconi Anemia, Complementation Group D1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605724
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Fanconi Anemia, Complementation Group D2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?227646
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Fanconi Anemia, Complementation Group E Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600901
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Fanconi Anemia, Complementation Group F Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603467
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Gamma-glutamylcysteine Synthetase Deficiency, Hemolytic Anemia due to Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?230450
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Glutathione Synthetase Deficiency of Erythrocytes, Hemolytic Anemia due to Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?231900
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Heinz Body Anemias Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?140700
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Hemolytic Anemia with Thermal Sensitivity of Red Cells Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?235370
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Hemolytic Anemia, Congenital, with Emphysema and Cutis Laxa Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?235360
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Hemolytic Anemia, Lethal Congenital Nonspherocytic, with Genital and Other Abnormalities Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600461
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Hemolytic Poikilocytic Anemia due to Reduced Ankyrin Binding Sites Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?141700
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Hexokinase Deficiency Hemolytic Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?235700
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Homocystinuria-megaloblastic Anemia due to Defect in Cobalamin Metabolism, Cble Complementation Type Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?236270
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Lymphopenic Hypergammaglobulinemia, Antibody Deficiency, Autoimmune Hemolytic Anemia, and Glomerulonephritis Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?247800
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Megaloblastic Anemia 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?261100
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Myopathy with Lactic Acidosis and Sideroblastic Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600462
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Pernicious Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?170900
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Pernicious Anemia, Congenital, due to Defect of Intrinsic Factor Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?261000
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Sickle Cell Anemia Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603903
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Sideroblastic Anemia with Erythrocyte Dimorphism Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?182170
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Sideroblastic Anemia, Autosomal Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?269950
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Systemic Lupus Erythematosus with Hemolytic Anemia, Susceptibility To, 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607279
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Thiamine-responsive Megaloblastic Anemia Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?249270
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Uridine 5-prime Monophosphate Hydrolase Deficiency, Hemolytic Anemia due to Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?266120
Genes and Disease (NCBI - Map) The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: ·
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
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Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier
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disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html ·
Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
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Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html
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Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html
Entrez Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: ·
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “anemia” (or synonyms) into the search box and click “Go.”
Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database25 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database26 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. 25 Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 26 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “anemia” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
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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 anemia 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 anemia. 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 anemia. 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 “anemia”:
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Guides on anemia Anemia http://www.nlm.nih.gov/medlineplus/anemia.html
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Other Guides Amphetamine Abuse http://www.nlm.nih.gov/medlineplus/amphetamineabuse.html Anemia http://www.nlm.nih.gov/medlineplus/anemia.html Bone Marrow Diseases http://www.nlm.nih.gov/medlineplus/bonemarrowdiseases.html High Risk Pregnancy http://www.nlm.nih.gov/medlineplus/highriskpregnancy.html Sickle Cell Anemia http://www.nlm.nih.gov/medlineplus/sicklecellanemia.html
Within the health topic page dedicated to anemia, the following was listed: ·
General/Overviews Anemia Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00321 Anemia: When Low Blood Iron is the Cause Source: American Academy of Family Physicians http://familydoctor.org/healthfacts/009/index.html
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Diagnosis/Symptoms Ferritin Test Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/ferritin/test.html Hematocrit Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/hematocrit/test.html Hemoglobin Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/hemoglobin/test.html Serum Iron Test Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/serum_iron/test.html TIBC (Total Iron-Binding Capacity) & Transferrin Source: American Association for Clinical Chemistry http://www.labtestsonline.org/understanding/analytes/tibc/test.html
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Understanding Your Complete Blood Count http://www.cc.nih.gov/ccc/patient_education/pepubs/cbc97.pdf ·
Treatment Blood and Marrow Stem Cell Transplantation Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=2443 Cord Blood FAQs Source: National Marrow Donor Program http://www.marrow.org/FAQS/cord_blood_faqs.html How Is Fanconi Anemia Treated? Source: Fanconi Anemia Research Fund http://www.fanconi.org/treatment.html
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Specific Conditions/Aspects Acquired Aplastic Anemia: Basic Explanations Source: Aplastic Anemia & MDS International Foundation http://www.aplastic.org/cgi-bin/byteserver.pl/pdfs/ACQUIRED-APLASTICANEMIA-BASIC-EXPLANATIONS.pdf Anemia (Normocytic Anemia) Source: American Academy of Family Physicians http://familydoctor.org/handouts/639.html Anemia in Kidney Disease and Dialysis Source: National Kidney and Urologic Diseases Information Clearinghouse http://kidney.niddk.nih.gov/kudiseases/pubs/anemia/index.htm Aplastic Anemia Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00322 Blood Donor Anemia: Causes? Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=HQ00328 Diamond-Blackfan Anemia (DBA) Source: National Cancer Institute http://marrowfailure.cancer.gov/DBA.html Iron-Deficiency Anemia Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00323 Thalassemia (Mediterranean Anemia) Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=AN00457 Vitamin Deficiency Anemia Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00325
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What Is Fanconi Anemia and How Is It Diagnosed? Source: Fanconi Anemia Research Fund http://www.fanconi.org/WhatisFA.html ·
Children About Anemia Source: Nemours Foundation http://kidshealth.org/kid/health_problems/blood/anemia.html Anemia Source: Nemours Foundation http://kidshealth.org/parent/medical/heart/anemia.html Anemia and Iron Status Source: Centers for Disease Control and Prevention http://www.cdc.gov/nccdphp/dnpa/anemiron.htm G6PD Deficiency (Glucose-6-Phosphate Dehydrogenase) Source: Nemours Foundation http://kidshealth.org/parent/general/aches/g6pd.html Iron-Deficiency Anemia Source: Nemours Foundation http://kidshealth.org/parent/medical/heart/ida.html Symptoms of Anemia Source: American Academy of Pediatrics http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZ6G06JL5C&s ub_cat=107 Thalassemia Source: March of Dimes Birth Defects Foundation http://www.marchofdimes.com/professionals/681_1229.asp
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Latest News Anemia Elevates Risk of Physical Decline in Older People Source: 07/25/2003, National Institute on Aging http://www.nih.gov/news/pr/jul2003/nia-25.htm
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Organizations Fanconi Anemia Research Fund http://www.fanconi.org/ National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/
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Research Anemia Elevates Risk of Physical Decline in Older People Source: National Institute on Aging http://www.nih.gov/news/pr/jul2003/nia-25.htm
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Pregnancy Outcomes in Women with Aplastic Immunosuppression Source: American College of Physicians http://www.annals.org/cgi/content/full/137/3/I-34
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Reversibility of Liver Scarring in Patients Who Are Cured of Thalassemia Source: American College of Physicians http://www.annals.org/cgi/content/full/136/9/I36 ·
Statistics FASTATS: Anemia Source: National Center for Health Statistics http://www.cdc.gov/nchs/fastats/anemia.htm
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Teenagers Understanding Anemia Source: Nemours Foundation http://kidshealth.org/teen/diseases_conditions/blood/anemia.html
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Women Anemia Source: National Women's Health Information Center http://www.4woman.gov/faq/anemia.htm Keeping the Blood and Lymphatic System Healthy Source: American Medical Women's Association http://www.amwa-doc.org/publications/WCHealthbook/bloodamwa-ch29.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 anemia. 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: ·
Anemia in AIDS: Getting Your Energy Back Contact: Ortho Pharmaceutical Corporation, Biotech Division, PO Box 300, Raritan, NJ, 08869-0602, (908) 218-7010.
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Summary: This brochure discusses anemia and its treatment in Persons with AIDS (PWA's). It explains what anemia is, and describes the two types of anemia in Acquired immunodeficiency syndrome (AIDS): Anemia caused by Human immunodeficiency virus (HIV) infection, and anemia caused by azidothymidine (AZT). ·
What You Need to Know About Anemia and Chronic Kidney Disease Source: New York, NY: National Kidney Foundation (NKF). 2002. 7 p. Contact: Available from National Kidney Foundation (NKF). 30 East 33rd Street, New York, NY 10016. (800) 622-9010. Website: www.kidney.org. PRICE: Single copy free. Summary: Anemia occurs when the red blood cells in the body are in short supply. Red blood cells carry oxygen from the lungs to all the organs and tissues, providing energy for daily activities. This brochure reviews the interplay of anemia and chronic kidney disease. The brochure describes the symptoms of anemia, its causes, why chronic kidney disease causes anemia, treatment options, the indications for dietary supplements to help treat anemia, other dietary changes that may be helpful, and complications of untreated anemia. One sidebar offers suggestions for questions to ask the health care provider about anemia. Chronic kidney disease may cause anemia because of a low level of the hormone called erythropoietin (EPO) which stimulates red blood cell production. In chronic kidney disease, iron supplements are often needed along with EPO to treat anemia. The brochure includes a brief description of the work and publications of the National Kidney Foundation (NKF, www.kidney.org).
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Anemia Source: Camp Hill, PA: Chek-Med Systems, Inc. 200x. [2 p.]. Contact: Available from Chek-Med Systems, Inc. 200 Grandview Avenue, Camp Hill, PA 17011-1706. (800) 451-5797 or (717) 761-1170. Fax (717) 761-0216. PRICE: $22.00 per pack of 50 brochures; 3 pack minimum. Summary: This brochure helps patients to understand anemia and what it means when they receive this diagnosis from their health care provider. Anemia is defined as a low red blood cell count. The red blood cell carries oxygen to the body's tissues. Inside each red cell is a protein and iron combination that is called hemoglobin that can be measured; low hemoglobin counts mean anemia. A second way to measure anemia is called the hematocrit, a test which checks how many red cells are packed into a specific amount of blood. The brochure offers the range considered normal for these two measures (different for men and women), then reviews the symptoms and the different types of anemia. Mild anemia may be symptomless, and a moderate anemia may cause some fatigue, drowsiness, or even shortness of breath on exertion. However, if the anemia occurs very slowly, the individual often can tolerate a remarkably low red blood cell count, sometimes with very few symptoms. The types of anemia are put into major categories based on cause: blood loss anemia (iron deficiency), large red blood cell anemia (macrocytic anemia), bone marrow failure, red cell destruction (hemolytic anemia), chronic kidney disease, and chronic illness and malignancies. The author of the brochure outlines the tests that may be done to determine the level of anemia and its cause, including blood studies, imaging, endoscopy, and bone marrow biopsy. A final section briefly describes the treatments that may be undertaken for anemia, stressing that taking oral iron or receiving a blood transfusion must also be accompanied by efforts to determine the underlying cause of the anemia. 2 figures.
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Getting the Most from Your Treatment: What You Need to Know about Anemia Source: New York, NY: National Kidney Foundation. 1998. 23 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: Many kidney patients develop anemia, or a low red blood cell count. For patients with kidney disease who are not yet on dialysis or those who have been receiving dialysis for some time, treating anemia is important to their health and quality of life. This booklet summarizes the problem of anemia and how to prevent and treat it. People on dialysis who have anemia are usually treated with a hormone called erythropoietin (EPO) and with extra iron. The booklet tells readers what anemia is and how it affects one's health, how anemia is treated, why iron is important in treating anemia, how treating anemia can benefit one's overall health, and additional resources that are available. Other topics include the role of diet in treating anemia, possible side effects of anemia treatment, anemia treatment during travel or illness, and payment for anemia treatment. Health benefits obtained from treating anemia can include an increase in energy level, an improvement in quality of life, a decrease in the chance of having heart problems, and an increase in one's ability to exercise. 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.
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Treating Anemia in Early Kidney Disease Source: New York, NY: National Kidney Foundation. 1994. 4 p. Contact: Available from National Kidney Foundation. 30 East 33 Street, New York, NY 10016. (800) 622-9010. PRICE: Single copy free. Summary: This brochure provides general information about the anemia often associated with early kidney disease. Written in a question-and-answer format, the brochure covers topics including reduced kidney function; causes of kidney disease; how kidney disease is treated; why people with kidney disease get anemia; how anemia can be treated; erythropoietin (EPO); side effects of EPO treatment; how kidney disease can affect the bones; diet therapy and the role of protein restriction; and the importance of exercise and maintaining overall health. The brochure encourages readers to consult their health care providers for more information and includes blank space for readers to record any questions that they may have. The brochure concludes with a brief description of the National Kidney Foundation (NKF).
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People Like Us: EPO: Treating Anemia. [Gente Como Nosotros: EPO: Tratamiento de la anemia] Source: New York, NY: National Kidney Foundation, Inc. 1994. (instructional package). Contact: Available from Amgen, Inc. 1840 DeHavilland Drive, Thousand Oaks, CA 91320-1789. (800) 282-6436. PRICE: Part of an instructional package free to dialysis centers, transplantation centers, and hospitals with dialysis or transplantation units. Summary: This videotape and booklet package is part of a patient education program designed to educate patients and their families about kidney disease and options for treatment. In this segment, erythropoietin, the medicine that helps relieve the anemia that often accompanies renal failure, is discussed. Reasons why and how it is prescribed and the role it can play in treatment are addressed. The booklet reiterates the material
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covered in the videotape and includes a quiz for self-testing, a glossary, and blank spaces to record questions and information about health care team members. (AA-M). ·
EPO: Treating Anemia in Chronic Renal Failure Source: New York, NY: National Kidney Foundation. 1990. 4 p. Contact: Available from National Kidney Foundation. 30 East 33rd Street, New York, NY 10016. (800) 622-9010. PRICE: Single copy free ($12 per 100 copies). Order Number 08-75. Summary: Written in a question-and-answer format, this brochure provides basic information about the use of erythropoietin (EPO) in treating the anemia frequently resulting from chronic renal failure. Topics covered include the development of kidney disease, obtaining and using EPO, dosage information, complications and side effects of EPO, and the impact of EPO on the daily lifestyle of the patient. The brochure notes that rehabilitation and adjustment to kidney failure require hard work, determination, and close cooperation between patient and doctor. EPO can be an important adjunct to successfully living with chronic renal failure.
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[Sickle cell anemia brochures] Source: Austin, TX: Texas Department of Health. 1990-1992. 16 items. Contact: Available from Texas Department of Health, 1100 West 49th Street, Austin, TX 78756. Telephone: (512) 458-7658 or (800) 434-4453 / fax: (512) 458-7713. Summary: This collection of informational pamphlets distributed by the Texas Department of Health includes the following titles: 'Sickle Cell Anemia: A Parent's Guide for the School Age Child;' 'The Infant and Young Child with Sickle Cell Anemia;' 'Sickle Beta+ Thalassemia;' 'Sickle Beta Zero Thalassemia;' 'Sickle Cell Anemia and Stroke;' 'Hemoglobin Sickle C Disease;' 'Hemoglobin C Disease;' 'Pain in the Child with Sickle Cell Disease;' 'Splenic Sequestration Crisis;' 'Chest Syndrome;' 'Aplastic Crisis;' 'So Your Baby Has the Sickle Cell Trait;' 'Priapism;' 'La Anemia Falciforme (Sickle Cell) En Bebes y Ninos Pequenos;' and 'Con Que Su Bebe Tiene El Rasgo de Globulos Falciformes.'.
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Facts about sickle cell anemia and sickle cell trait Source: Norfolk, VA: Society for the Aid of Sickle Cell Anemia. n.d. 2 pp. Contact: Available from Lyman Beecher Brooks Medical Center, Society for the Aid of Sickle Cell Anemia, 930 Majestic Avenue, Suite 150, Norfolk, VA 23504. Telephone: (804) 624-9225. Summary: This pamphlet provides general information on sickle cell disorders. It includes a form for readers to fill out for more information on sickle cell disorders from the Society for the Aid of Sickle Cell Anemia, which serves southeastern Virginia.
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Informacion Acerca de la Anemia Relacionada con el VIH. [About HIV-Related Anemia] Contact: National Minority AIDS Council, 1931 13th St NW, Washington, DC, 200094432, (202) 483-6622, http://www.nmac.org. Summary: This fact sheet explains anemia and how it is related to the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS). The fact
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sheet defines anemia and identifies its symptoms and its causes. It provides information concerning the epidemiology of anemia in persons with HIV/AIDS and briefly outlines the treatments available for this condition. ·
La Anemia Relacionada con el VIH: Los Datos. [HIV Related-Anemia : The Facts] Contact: National Minority AIDS Council, 1931 13th St NW, Washington, DC, 200094432, (202) 483-6622, http://www.nmac.org. Summary: This fact sheet explains anemia, as a serious complication, to persons with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS). The fact sheet defines anemia and identifies its symptoms and its causes. It provides information about the epidemiology of anemia in persons with HIV/AIDS and briefly outlines the treatments available for this condition.
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About HIV-Related Anemia Contact: National Minority AIDS Council, 1931 13th St NW, Washington, DC, 200094432, (202) 483-6622, http://www.nmac.org. Summary: This fact sheet explains anemia and how it is related to the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS). The fact sheet defines anemia and identifies its symptoms and its causes. It provides information concerning the epidemiology of anemia in persons with HIV/AIDS and briefly outlines the treatments available for this condition.
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HIV Related-Anemia : The Facts Contact: National Minority AIDS Council, 1931 13th St NW, Washington, DC, 200094432, (202) 483-6622, http://www.nmac.org. Summary: This fact sheet explains anemia, as a serious complication, to persons with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS). The fact sheet defines anemia and identifies its symptoms and its causes. It provides information about the epidemiology of anemia in persons with HIV/AIDS and briefly outlines the treatments available for this condition.
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HIV Treatment, Fatigue, and Anemia : What's the Connection? Contact: Ortho Pharmaceutical Corporation, Biotech Division, PO Box 300, Raritan, NJ, 08869-0602, (908) 218-7010. Summary: This fact sheet explains human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS)-related fatigue and anemia, and how the therapeutic drug, Procrit, assists in relieving these conditions. The fact sheet discusses that one of the side effects of the drug AZT is that it reduces the production of red blood cells; thereby depriving the body of oxygen leading to fatigue and anemia. It states that Procrit helps to keep AZT from suppressing the production of red blood cells in the bone marrow, and that adverse reactions are mainly found to be disease-related rather than a side effect of Procrit itself.
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La Anemia (un Recuento Bajo de Celulas Rojas de la Sangre). [Anemia (Low Red Blood Cell Count)] Contact: National AIDS Treatment Information Project, Beth Israel Deaconess Medical Center, Beth Israel Hospital, 330 Brookline Ave Libby Bldg 317, Boston, MA, 02215, (617) 667-5520, http://www.natip.org. Summary: This fact sheet, for persons with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS), presents information about anemia, a condition in which there are a low number of red blood cells in the body. The symptoms of anemia include fatigue, dizziness, shortness of breath, heart palpitations, and pale skin. Some of the causes of anemia (decreased red blood cell production by the bone marrow, blood loss from trauma originating from the digestive tract or uterus, and increased destruction of red blood cells) are explained in the context of HIV/AIDS. Anemia is diagnosed using a test called a complete blood count (CBC), which measures the level of hemoglobin and the concentration of red blood cells in the blood. An evaluation of the cause of anemia should include a review of all prescription, over-the counter, and complementary/alternative medications taken by HIV-positive individuals. Substance abuse, bleeding in the abdomen or uterus, microscopic examination of blood cells, bone marrow production, levels of iron, vitamin B12, and folic acid in the blood should also be evaluated. The optimal way to manage anemia is to identify and treat the cause.
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Anemia, Pernicious (B-12 Deficiency Anemia) Source: in Griffith, H.W. Instructions for Patients. 5th ed. Philadelphia, PA: W.B. Saunders Company. 1994. p. 20. Contact: Available from W.B. Saunders Company. Book Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. PRICE: $49.95. ISBN: 0721649300 (English); 0721669972 (Spanish). Summary: This fact sheet provides basic information on frequent signs and symptoms, causes, risk factors, preventive measures, etc. treatment, medication, and diet; and when to contact one's health care provider. The fact sheet is designed to be photocopied and distributed to patients as a reinforcement of oral instructions and as a teaching tool. The book in which the fact sheet appears is available in English or Spanish.
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Anemia, Iron-Deficiency Source: in Griffith, H.W. Instructions for Patients. 5th ed. Philadelphia, PA: W.B. Saunders Company. 1994. p. 19. Contact: Available from W.B. Saunders Company. Book Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. PRICE: $49.95. ISBN: 0721649300 (English); 0721669972 (Spanish). Summary: This fact sheet provides basic information on frequent signs and symptoms, causes, risk factors, preventive measures, etc. treatment, medication, and diet; and when to contact one's health care provider. The fact sheet is designed to be photocopied and distributed to patients as a reinforcement of oral instructions and as a teaching tool. The book in which the fact sheet appears is available in English or Spanish.
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Anemia, Folic-Acid Deficiency Source: in Griffith, H.W. Instructions for Patients. 5th ed. Philadelphia, PA: W.B. Saunders Company. 1994. p. 17. Contact: Available from W.B. Saunders Company. Book Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. PRICE: $49.95. ISBN: 0721649300 (English); 0721669972 (Spanish). Summary: This fact sheet provides basic information on frequent signs and symptoms, causes, risk factors, preventive measures, etc. treatment, medication, and diet; and when to contact one's health care provider. The fact sheet is designed to be photocopied and distributed to patients as a reinforcement of oral instructions and as a teaching tool. The book in which the fact sheet appears is available in English or Spanish.
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Anemia in Kidney Disease and Dialysis Source: Bethesda, MD: National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH). 2001. 4 p. Contact: Available from National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC). 3 Information Way, Bethesda, MD 20892-3580. (800) 891-5390 or (301) 654-4415. Fax (301)634-0716. E-mail:
[email protected]. Website: www.niddk.nih.gov/health/kidney/nkudic.htm PRICE: Full-text available online at no charge; single copy free; bulk orders available. Order number: KU-146. Summary: Anemia (low levels of red blood cells) is common in people with kidney disease. Healthy kidneys produce a hormone called erythropoietin (EPO) which stimulates the bone marrow to produce the proper number of red blood cells needed to carry oxygen to vital organs. Diseased kidneys, however, often do not make enough EPO. Other common causes of anemia include loss of blood from hemodialysis and low levels of iron and folic acid. This fact sheet describes anemia in kidney disease and dialysis. The presence of anemia is determined by a complete blood count (CBC), which includes a determination of hematocrit (Hct) level, which is the percentage of the blood that consists of red blood cells. Anemia can begin with chronic renal insufficiency, and tends to worsen as kidney disease progresses. Treatment includes EPO injections, and iron supplements; a few people may also need vitamin B12 and folic acid supplements to keep anemia under control and let patients feel better, live longer, and have more energy. The fact sheet concludes with a description of current research projects in this area, a brief list of resource organizations for more information, and a brief description of the National Kidney and Urologic Diseases Information Clearinghouse (NKUDIC) and its contact information. 2 figures. 1 table.
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Just the Facts: Anemia Source: Madison, WI: Life Options Rehabilitation Program. 1999. 2 p. Contact: Available from Life Options Rehabilitation Program. Medical Education Institute, Inc, 414 D'Onofrid Drive., Suite 200, Madison, WI 53719. (608) 833-8033. Email:
[email protected]. PRICE: Single copy free to health professionals only. Summary: This fact sheet is part of the Life Options Rehabilitation Program, a patient education service of Amgen, Inc. The Keys to a Long Life materials were developed to motivate patients on dialysis and teach them how to optimize their dialysis care and improve their quality of life. This fact sheet on anemia (not enough red blood cells) is
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one of six fact sheets providing general information about living well on dialysis. Each fact sheet contains research based information about the topic and why it is important for patients; simple illustrations; and a table of problems, prevention strategies, and questions for patients to ask. Topics covered in this fact sheet include the causes of anemia, the role of erythropoietin (a hormone made by healthy kidneys that tells the bone marrow to make more red blood cells), how anemia can impact quality of life and increase risk of death, treatment options for managing anemia (epoetin alfa and iron supplements), how anemia is measured, the symptoms of anemia, preventive strategies, and the role of exercise in building stamina. The fact sheet defines medical terms in nontechnical language. 'The Keys to a Long Life' materials are based on the real life experiences and advice of long term dialysis patients, as well as on data from a telephone opinion survey of dialysis patients. 1 figure. 1 table. 3 references. ·
Anemia and Kidney Disease Source: San Bruno, CA: Krames Communications. 1997. 2 p. Contact: Available from Krames Communications. 1100 Grundy Lane, San Bruno, CA 94066-3030. (800) 333-3032. Fax (415) 244-4512. PRICE: $12.50 for pad of 50 sheets. Summary: This patient education handout explains the basics of anemia and how it can become a problem for people with kidney disease. Anemia occurs when the blood does not have enough red cells; therefore, the blood cannot carry the necessary oxygen to the body. The handout lists the symptoms of anemia, including ongoing fatigue; shortness of breath; rapid, irregular heartbeat; trouble concentrating; erectile dysfunction (impotence); feeling dizzy or lightheaded; and constantly feeling cold. Normally, the kidneys send out a signal (erythropoietin) that tells the body when to make new red blood cells. But in people with kidney disease, the kidneys may not be able to send this signal. A medication called epoetin alfa (EPO), a synthetic version of erythropoietin, can be given. EPO controls anemia by signaling the body to make red blood cells. Most often, EPO is used to treat people on dialysis. The handout also discusses the role of iron in making blood cells. Most people who take EPO need extra iron. The handout offers a list of strategies for people who are taking iron (particularly suggestions for avoiding the constipation that can accompany iron intake). The handout is written in nontechnical language and is illustrated with colorful drawings.
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Anemia in Hemodialysis and CAPD Source: McGaw Park, IL: Baxter Healthcare Corporation, Renal Division. 1995. 4 p. Contact: Available from Baxter Healthcare Corporation, Renal Division. 1620 Waukegan Road, McGaw Park, IL 60085. (800) 284-4060. PRICE: Single copy free. Summary: This physician fact sheet discusses anemia in hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD). Topics include the incidence of anemia in patients with end-stage renal disease (ESRD); the effects of HD versus CAPD on anemia in chronic renal failure; the use of erythropoietin (EPO) to manage anemia in the dialysis population, including dosage and administration and quality of life issues; the adverse side effects of EPO, including hypertension and seizures, access clotting, and dialysis efficiency; and the cost implications of EPO. The fact sheet includes reports from research studies in this area. The author concludes that the degree of anemia in patients on CAPD is less severe than for patients on chronic hemodialysis; this may become an important consideration in the selection of dialysis modality as the cost of health care continues to be scrutinized. The fact sheet is printed on cardstock, with 3color charts. 2 figures. 2 tables. 15 references.
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Thalassemia Among Asians Source: Oakland, CA: Association of Asian Pacific Community Health Organizations. 1992. 2 p. Contact: National Maternal and Child Health Clearinghouse. 2070 Chain Bridge Road, Suite 450, Vienna, VA 22182-2536. (703) 821-8955. Fax (703) 821-2098. PRICE: Single copy free. Summary: This brochure provides readers with information about thalassemia, an inherited blood disorder that has a high prevalence in Asians, particularly Southeast Asians. The brochure discusses how thalassemia is inherited, the two main types of thalassemia disease (alpha and beta), the thalassemia trait, screening tests, how to minimize concerns about thalassemia, and where to get more information. The brochure emphasizes the importance of early diagnosis of thalassemia in infants. Culturally appropriate line drawings illustrate the brochure.
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Questions about thalassemia Source: Providence, RI: Providence Ambulatory Health Care Foundation, and Rhode Island Department of Health. 1991. 4 pp. Contact: Available from Providence Ambulatory Health Care Foundation, 469 Angell Street, Providence, RI 02906-4490. Telephone: (401) 444-0400 / fax: (401) 444-0421. Summary: This pamphlet simply explains the genetic basis for thalassemia. It is available in English, Cambodian, and Laotian. It augments the information in a related videotape 'HBG E, Anemia, and Basic Genetics.' [Funded by the Maternal and Child Health Bureau].
The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “anemia” (or synonyms). The following was recently posted: ·
NKF-K/DOQI clinical practice guidelines for anemia of chronic kidney disease: update 2000 Source: National Kidney Foundation - Disease Specific Society; 1997 (updated 2000); 67 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2784&nbr=2010&a mp;string=anemia
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:
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Anemia in Kidney Disease and Dialysis Summary: Describes when anemia begins, its diagnosis, treatment, and causes other than kidney disease. Source: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6490
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Dialysis Facility Compare Summary: Locate and compare dialysis services available in your area by looking at dialysis facility location, shifts that start or continue after 5 PM, adequacy of hemodialysis, anemia management and patient Source: Centers for Medicare and Medicaid Services (CMS), formerly the Health Care Financing Administration http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6015
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Facts About Sickle Cell Anemia Summary: Also available In: Source: National Heart, Lung, and Blood Institute, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=1214
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FAQ - About Sickle Cell Anemia Summary: This site contains online answers to questions from patients and the general public regarding this blood disorder. Also available, are links to additional information about this disease. Source: Sickle Cell Information Center http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2892
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FAQ - About Thalassemia Summary: This online document answers questions consumers frequently have about this group of genetic blood disorders. Topics covered include symptoms, treatment and management of the disorder. Source: Cooley's Anemia Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5143
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FAQ: Aplastic Anemia, Myelodysplastic Syndromes, and Paroxysmal Nocturnal Hemoglobinuria (PNH) Summary: Answers questions about causes, symptoms, and therapies for aplastic anemia, myelodysplastic syndromes, and paroxysmal nocturnal hemoglobinuria. Source: Aplastic Anemia & MDS International Foundation, Inc. http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7378
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How is Fanconi Anemia Related to Leukemia and Other Cancers Summary: This document discusses Fanconi anemia patients' risks of developing leukemia and other related cancers. Source: Fanconi Anemia Research Fund, Inc. http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4636
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How Is Fanconi Anemia Treated? Summary: A discussion of the types of therapies used in the treatment of Fanconi anemia and who benefits from which, and the risks involved. Source: Fanconi Anemia Research Fund, Inc. http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4635
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Thalassemia Summary: Also available In: Source: March of Dimes Birth Defects Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3272
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What Is Fanconi Anemia And How Is It Diagnosed? Summary: This consumer health information fact sheet contains basic information about Fanconi anemia including history, description of the disease and its symptoms and treatment. Source: Fanconi Anemia Research Fund, Inc. http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4634
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What is Thalassemia? Summary: A description of thalassemia -- a fatal blood disease that is found predominantly among people of Mediterranean and Asian Indian, South Asian and Chinese ancestry. Source: Cooley's Anemia Foundation http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2567 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 anemia. 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
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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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WebMDÒHealth: http://my.webmd.com/health_topics
Associations and Anemia The following is a list of associations that provide information on and resources relating to anemia: ·
Children's Blood Foundation Address: Telephone: (212) 297-4336 Toll-free: Fax: (212) 297-4340 Email:
[email protected] Background: The Children s Blood Foundation (CBF) is a nonprofit organization dedicated to promoting and/or supporting research, medical training of physicians, and care of children with leukemia, thalassemia, hemophilia, anemia, cancer, immune disorders, and AIDS. Established in 1952, the CBF has the largest hemophilia center in the New York area and the largest thalassemia center in North America, receiving more than 5,000 patient visits every year. All affected children are served, regardless of the family s ability to pay. Educational materials include a self-titled brochure, a regular newsletter entitled 'The Key to Life for a Child,' and a booklet entitled 'What s It Called Again? - Answers to the Most Commonly Asked Questions About Idiopathic Thrombocytopenic Purpura (ITP) In Children.' CBF has support groups, offers networking services, and engages in educational activities.
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Cochrane Cystic Fibrosis and Genetic Disorders Review Group Address: Telephone: (151) 252-5696 Toll-free: Fax: (151) 252-5456 Email:
[email protected] Patient Resources 451
Web Site: www.liv.ac.uk/cfgd Background: Cochrane Cystic Fibrosis and Genetic Disorders Review Group is an international network of health care professionals, researchers and consumers preparing, maintaining, and disseminating systematic reviews of randomized control trials in the treatment of cystic fibrosis and other genetic disorders. The group's aim is to help people make well-informed decisions about healthcare with the aid of these reviews. Abstracts (summaries) of these reviews are available free of charge on the group's website. The Chochrane Collaboration is a non-profit organization, established as a company, limited by guarantee, and registered as a charity in the UK. ·
Cooley's Anemia Foundation, Inc Address: Telephone: (718) 321-2873 Toll-free: (800) 522-7222 Fax: (718) 321-3340 Email:
[email protected] Web Site: http://www.cooleysanemia.org Background: The Cooley's Anemia Foundation, Inc. is a national not-for-profit organization dedicated to advancing the treatment and cure of Cooley's Anemia, an inherited blood disorder. Established in 1954, the Foundation conducts national programs that promote medical research and provides a variety of patient services and educational programs. The Foundation has more than 15 chapters throughout the United States and supports the Thalassemia Action Group (TAG), a support group for affected individuals and their families. Services provided by the Cooley's Anemia Foundation include: information on thalassemia, referrals to local medical sources and emergency medical supplies to people in need. Informational materials available from the Foundation including video tapes, brochures, and regular newsletters.
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Iron Overload Diseases Association, Inc Address: Telephone: (561) 840-8512 Toll-free: Fax: (561) 842-9881 Email:
[email protected] Web Site: http://www.ironoverload.org Background: Iron Overload Diseases Association, Inc. is a voluntary not-for-profit organization dedicated to leading the search for individuals who have undiagnosed Hemochromatosis and preventing the health problems that may result. Hereditary Hemochromatosis is a metabolic disorder characterized by increased absorption of dietary iron. Without appropriate treatment, excessive iron may accumulate in the liver, heart, pancreas, and other organs, causing organ dysfunction and tissue damage. Established in 1981, the Association is also committed to providing information and support to affected individuals and their families; educating the general public; promoting and supporting research; and pressing for earlier diagnosis and more effective treatment for Hemochromatosis. The Association acts as an international clearinghouse for affected individuals, family members, and physicians; provides telephone consultations; offers referrals to genetic counseling and support groups; promotes patient advocacy; and conducts an annual medical symposium as well as
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conference meetings between patients and health care professionals. The Iron Overload Diseases Association also provides a variety of educational and support materials including books, brochures, fact sheets, and a bimonthly newsletter entitled 'Ironic Blood.'. ·
March of Dimes Birth Defects Foundation Address: Telephone: (914) 428-7100 Toll-free: (888) 663-4637 Fax: (914) 997-4763 Email:
[email protected] Web Site: http://www.marchofdimes.com Background: The March of Dimes Birth Defects Foundation is a national not-for-profit organization that was established in 1938. The mission of the Foundation is to improve the health of babies by preventing birth defects and infant mortality. The March of Dimes funds programs of research, community services, education, and advocacy. Educational programs that seek to prevent birth defects are important to the Foundation and to that end it also produces a wide variety of printed informational materials and videos. The Pregnancy and Newborn Health Education Center staffs trained health information specialists who provide researched information on pregnancy issues, complications and risks, newborn care, birth defects, genetic diseases and related topics as well as referrals to relevant organizations and support groups.
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Sickle Cell Disease Association of America, Inc Address: Telephone: (310) 216-6363 Toll-free: (800) 421-8453 Fax: (310) 215-3722 Email:
[email protected] Web Site: www.sicklecelldisease.org Background: The Sickle Cell Disease Association of America (SCDAA) is a voluntary service organization dedicated to educating the public and providing support to people affected by Sickle Cell Disease. The Association was founded in 1971 as the umbrella organization for community-based groups providing support and services to persons affected by sickle cell conditions. The Association seeks to educate the public about sickle cell disease and the sickle cell trait and develop educational materials on these conditions for extensive circulation. It also educates legislators on issues regarding sickle cell disease and other genetic disorders and fosters ongoing medical research to improve the well-being of those affected by sickle cell disease. In addition, the Association supports research, advocates on behalf of all individuals affected by sickle cell diseases, and provides appropriate referrals to medical professionals. The Association is the only national community-based voluntary health agency working full-time to resolve issues surrounding sickle cell conditions. The Sickle Cell Disease Association provides an extensive supply of resources. These include guidebooks, brochures, pamphlets, audio and visual tapes, fact sheets, and a periodic newsletter entitled 'Sickle Cell News.'.
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Finding Associations There are a number of Internet directories that provide lists of medical associations with information on or resources relating to anemia. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with anemia.
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 anemia. 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 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 “anemia” (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 “anemia”. 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 “anemia” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months.
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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 “anemia” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. 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 anemia. 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 DIÒ Advice for the PatientÒ 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 anemia. 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 anemia: Albendazole ·
Systemic - U.S. Brands: Albenza; Eskazole; Zentel http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202668.html
Anabolic Steroids ·
Systemic - U.S. Brands: Anadrol-50; Deca-Durabolin; Durabolin; Durabolin-50; Hybolin Decanoate; Hybolin-Improved; Kabolin; Oxandrin; Winstrol http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202035.html
Androgens ·
Systemic - U.S. Brands: Andro L.A. 200; Androderm; AndroGel 1%; Android; Android-F; Andronate 100; Andronate 200; Andropository 200; Andryl 200; Delatest; Delatestryl; Depotest; Depo-Testosterone; Everone 200; Halotestin; ORETON Methyl; T-Cypionate; Testamone 100; Testaqua; Te http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202036.html
Copper Supplements ·
Systemic - U.S. Brands: Note: http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202164.html
Deferoxamine ·
Systemic - U.S. Brands: Desferal http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203185.html
Epoetin ·
Systemic - U.S. Brands: Epogen; Procrit http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202214.html
Folic Acid (Vitamin B 9 ) ·
Systemic - U.S. Brands: Folvite http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202250.html
Furazolidone ·
Oral - U.S. Brands: Furoxone http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202252.html
Ganciclovir ·
Systemic - U.S. Brands: Cytovene; Cytovene-IV http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202255.html
Hydroxyurea ·
Systemic - U.S. Brands: Droxia; Hydrea http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202291.html
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Iron Supplements ·
Systemic - U.S. Brands: DexFerrum; Femiron; Feosol; Feostat; Feostat Drops; Feratab; Fer-gen-sol; Fergon; Fer-In-Sol Capsules; Fer-In-Sol Drops; Fer-In-Sol Syrup; Fer-Iron Drops; Fero-Gradumet; Ferospace; Ferralet; Ferralet Slow Release; Ferralyn Lanacaps; Ferra-TD; Ferretts; http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202305.html
Leucovorin ·
Systemic - U.S. Brands: Wellcovorin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202321.html
Leuprolide ·
Systemic - U.S. Brands: Lupron; Viadur http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202322.html
Niacin (Vitamin B 3 ) ·
Systemic - U.S. Brands: Endur-Acin; Nia-Bid; Niac; Niacels; Niacor; Nico-400; Nicobid Tempules; Nicolar; Nicotinex Elixir; Slo-Niacin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202405.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
Pyrantel ·
Oral - U.S. Brands: Pin-X http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202490.html
Pyridoxine (Vitamin B 6 ) ·
Systemic - U.S. Brands: Beesix; Doxine; Nestrex; Pyri; Rodex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202493.html
Valganciclovir ·
Systemic - U.S. Brands: Valcyte http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500289.html
Vitamin B 12 ·
Systemic - U.S. Brands: Alphamin; Cobex; Cobolin-M; Crystamine; Crysti-12; Cyanoject; Cyomin; Hydrobexan; Hydro-Cobex; Hydro-Crysti-12; HydroxyCobal; LA-12; Nascobal; Neuroforte-R; Primabalt; Rubramin PC; Shovite; Vibal; Vibal LA; Vitabee 12 http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202596.html
Zinc Supplements ·
Systemic - U.S. Brands: Orazinc; Verazinc; Zinc 15; Zinc-220; Zinca-Pak; Zincate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202622.html
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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 ConsultÔ Mosby’s Drug ConsultÔ 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.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to anemia by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “anemia” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for
Researching Medications 459
marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for anemia: ·
Epoetin alfa (trade name: Epogen) http://www.rarediseases.org/nord/search/nodd_full?code=364
·
decutabine http://www.rarediseases.org/nord/search/nodd_full?code=1301
·
Isobutyramide (trade name: Isobutyramide oral solution) http://www.rarediseases.org/nord/search/nodd_full?code=157
·
Isobutyramide http://www.rarediseases.org/nord/search/nodd_full?code=161
·
Sodium phenylbutyrate http://www.rarediseases.org/nord/search/nodd_full?code=191
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Epoetin alfa (trade name: Epogen) http://www.rarediseases.org/nord/search/nodd_full?code=370
·
Epoetin Alpha (trade name: Procrit) http://www.rarediseases.org/nord/search/nodd_full?code=381
·
Epoetin alpha (trade name: Procrit) http://www.rarediseases.org/nord/search/nodd_full?code=387
·
Epoetin alpha (trade name: Procrit) http://www.rarediseases.org/nord/search/nodd_full?code=394
·
Epoetin beta (trade name: Marogen) http://www.rarediseases.org/nord/search/nodd_full?code=400
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Polymeric oxygen http://www.rarediseases.org/nord/search/nodd_full?code=409
·
Erythropoietin (recombinant human) http://www.rarediseases.org/nord/search/nodd_full?code=447
·
Etiocholanedione http://www.rarediseases.org/nord/search/nodd_full?code=476
·
Arginine butyrate http://www.rarediseases.org/nord/search/nodd_full?code=673
·
Arginine Butyrate http://www.rarediseases.org/nord/search/nodd_full?code=674
·
Hydroxyurea (trade name: Droxia) http://www.rarediseases.org/nord/search/nodd_full?code=771
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·
40SD02 http://www.rarediseases.org/nord/search/nodd_full?code=959
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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APPENDIX D. 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.27
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. 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 libraries recommended by the National
27
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)28: ·
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
·
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
·
Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
·
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
·
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
·
California: Gateway Health Library (Sutter Gould Medical Foundation)
·
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
·
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
·
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
·
California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
·
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
·
California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
·
California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
·
California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
·
Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
·
Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
·
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
28
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
Finding Medical Libraries 463
·
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
·
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
·
Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
·
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
·
Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
·
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
·
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
·
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
·
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
·
Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
·
Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
·
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
·
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
·
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
·
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
·
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
·
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
·
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
464 Anemia
·
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
·
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
·
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
·
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
·
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
·
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
·
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
·
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
·
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
·
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
·
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
·
Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
·
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
·
Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
·
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
·
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
·
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/
·
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
Finding Medical Libraries 465
·
Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
·
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
·
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
·
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
·
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
·
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
·
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
·
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
·
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/
·
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
·
Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
·
Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
·
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/
·
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 anemia: ·
Basic Guidelines for Anemia Anemia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000560.htm Anemia - B12 deficiency Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000574.htm Anemia- chronic disease Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000565.htm Anemia- folate deficiency Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000551.htm
·
Signs & Symptoms for Anemia Anemia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000560.htm
468 Anemia
Babinski Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003294.htm Diarrhea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003126.htm Dizziness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003093.htm Fatigue Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Headache Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003024.htm Jaundice Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003243.htm Lethargy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Loss of appetite Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003121.htm Numbness and tingling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003206.htm Paleness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003244.htm Pallor Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003244.htm Shortness of breath Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm Tiredness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003088.htm Weakness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003174.htm ·
Diagnostics and Tests for Anemia Bone marrow examination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003658.htm CBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm
Online Glossaries 469
Erythropoietin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003683.htm Folate - test Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003686.htm Hematocrit Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm Hemoglobin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003645.htm LDH Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003471.htm Pap smear Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003911.htm Reticulocyte count Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003637.htm Schilling test Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003572.htm Serum ferritin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003490.htm Serum iron Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003488.htm TIBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003489.htm Total iron binding capacity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003489.htm ·
Nutrition for Anemia Balanced diet Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002449.htm Folate Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002408.htm Folic acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002408.htm Vitamin B12 Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002403.htm
470 Anemia
Well-balanced diet Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002449.htm ·
Background Topics for Anemia Central nervous system Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002311.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Epithelial cells Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002358.htm Incidence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002387.htm Intrinsic factor Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002381.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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ANEMIA DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 5-Methoxytryptamine: sedatives. [NIH]
Serotonin derivative proposed as potentiator for hypnotics and
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 Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Ablation: The removal of an organ by surgery. [NIH] Abscess: Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection. [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] Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [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] Aclarubicin: An anthracycline antibiotic produced by Streptomyces galilaeus. It has potent antineoplastic activity, especially in the treatment of leukemias, with reduced cardiac toxicity in comparison to daunorubicin or doxorubicin. [NIH] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [NIH] Acremonium: A mitosporic fungal genus with many reported ascomycetous teleomorphs. Cephalosporin antibiotics are derived from this genus. [NIH] Acute leukemia: A rapidly progressing cancer of the blood-forming tissue (bone marrow). [NIH]
Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow.
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Also called acute lymphoblastic leukemia. [NIH] Acute myelogenous leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute nonlymphocytic leukemia. [NIH] Acute myeloid leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myelogenous leukemia or acute nonlymphocytic leukemia. [NIH] Acute nonlymphocytic leukemia: A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute myelogenous leukemia. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] 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 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] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenoma: A benign epithelial tumor with a glandular organization. [NIH] 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] Adenylate Kinase: An enzyme that catalyzes the phosphorylation of AMP to ADP in the presence of ATP or inorganic triphosphate. EC 2.7.4.3. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [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] Adjuvant therapy: Treatment given after the primary treatment to increase the chances of a cure. Adjuvant therapy may include chemotherapy, radiation therapy, or hormone therapy. [NIH]
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] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH]
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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] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [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 metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, oxidative metabolism, or cell respiration. [NIH] Aerobic respiration: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as oxidative metabolism, cell respiration, or aerobic metabolism. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
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 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] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Age Distribution: The frequency of different ages or age groups in a given population. The distribution may refer to either how many or what proportion of the group. The population is usually patients with a specific disease but the concept is not restricted to humans and is not restricted to medicine. [NIH] Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Aged, 80 and over: A person 80 years of age and older. [NIH] Agenesis: Lack of complete or normal development; congenital absence of an organ or part. [NIH]
Agglutinins:
Substances, usually of biological origin, that cause cells or other organic
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particles to aggregate and stick to each other. They also include those antibodies which cause aggregation or agglutination of a particulate or insoluble antigen. [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] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [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] Allo: A female hormone. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allogeneic bone marrow transplantation: A procedure in which a person receives stem cells, the cells from which all blood cells develop, from a compatible, though not genetically identical, donor. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha Cell: A type of cell in the pancreas (in areas called the islets of Langerhans). Alpha cells make and release a hormone called glucagon, which raises the level of glucose (sugar) in the blood. [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-Thalassemia: A disorder characterized by reduced synthesis of the alpha chains of hemoglobin. The severity of this condition can vary from mild anemia to death, depending on the number of genes deleted. [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] Alternative Splicing: A process whereby multiple protein isoforms are generated from a single gene. Alternative splicing involves the splicing together of nonconsecutive exons during the processing of some, but not all, transcripts of the gene. Thus a particular exon
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may be connected to any one of several alternative exons to form messenger RNA. The alternative forms produce proteins in which one part is common while the other part is different. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Ameliorated: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amifostine: A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia. [NIH] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] 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] Amlodipine: 2-((2-Aminoethoxy)methyl)-4-(2-chlorophenyl)-1,4-dihydro-6-methyl-3,5pyridinedicarboxylic acid 3-ethyl 5-methyl ester. A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of angina pectoris and hypertension. [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] Amnion: The extraembryonic membrane which contains the embryo and amniotic fluid. [NIH]
Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amputation: Surgery to remove part or all of a limb or appendage. [NIH] Amyl Nitrite: A vasodilator that is administered by inhalation. It is also used recreationally due to its supposed ability to induce euphoria and act as an aphrodisiac. [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] 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
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occurs when the equilibrium between blood loss (through bleeding or destruction) and blood production is disturbed. [EU] Anaerobic: 1. lacking molecular oxygen. 2. growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaerobic Threshold: The oxygen consumption level above which aerobic energy production is supplemented by anaerobic mechanisms during exercise, resulting in a sustained increase in lactate concentration and metabolic acidosis. The anaerobic threshold is affected by factors that modify oxygen delivery to the tissues; it is low in patients with heart disease. Methods of measurement include direct measure of lactate concentration, direct measurement of bicarbonate concentration, and gas exchange measurements. [NIH] 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] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [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] 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] Anemia, Sickle Cell: A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S. [NIH] Anemic: Hypoxia due to reduction of the oxygen-carrying capacity of the blood as a result of a decrease in the total hemoglobin or an alteration of the hemoglobin constituents. [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]
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Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiography: Radiography of blood vessels after injection of a contrast medium. [NIH] Angiosarcoma: A type of cancer that begins in the lining of 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] 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] Anisotropy: A physical property showing different values in relation to the direction in or along which the measurement is made. The physical property may be with regard to thermal or electric conductivity or light refraction. In crystallography, it describes crystals whose index of refraction varies with the direction of the incident light. It is also called acolotropy and colotropy. The opposite of anisotropy is isotropy wherein the same values characterize the object when measured along axes in all directions. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anomalies: Birth defects; abnormalities. [NIH] Anorexia: Clinical manifestation consisting of a physiopathological lack or loss of appetite accompanied by an aversion to food and the inability to eat. [NIH] Anterior Cerebral Artery: Artery formed by the bifurcation of the internal carotid artery. Branches of the anterior cerebral artery supply the caudate nucleus, internal capsule, putamen, septal nuclei, gyrus cinguli, and surfaces of the frontal lobe and parietal lobe. [NIH] Anthracycline: A member of a family of anticancer drugs that are also antibiotics. [NIH] Anthrax: An acute bacterial infection caused by ingestion of bacillus organisms. Carnivores may become infected from ingestion of infected carcasses. It is transmitted to humans by contact with infected animals or contaminated animal products. The most common form in humans is cutaneous anthrax. [NIH] Antiallergic: Counteracting allergy or allergic conditions. [EU] 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] Antibodies, Anticardiolipin: Antiphospholipid antibodies found in association with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase immunoassay employing the purified phospholipid
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antigen cardiolipin. [NIH] Antibodies, Antiphospholipid: Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC), ANTIPHOSPHOLIPID SYNDROME, related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals. [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] Antibody therapy: Treatment with an antibody, a substance that can directly kill specific tumor cells or stimulate the immune system to kill tumor cells. [NIH] 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] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [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] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Antihypertensive: An agent that reduces high blood pressure. [EU] Antihypertensive Agents: Drugs used in the treatment of acute or chronic hypertension regardless of pharmacological mechanism. Among the antihypertensive agents are diuretics (especially diuretics, thiazide), adrenergic beta-antagonists, adrenergic alpha-antagonists, angiotensin-converting enzyme inhibitors, calcium channel blockers, ganglionic blockers, and vasodilator agents. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimycotic: Suppressing the growth of fungi. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU]
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Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [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] Antiphospholipid Syndrome: The presence of antibodies directed against phospholipids (antibodies, antiphospholipid). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (antibodies, anticardiolipin). Present also are high levels of lupus anticoagulant (lupus coagulation inhibitor). [NIH] Antipruritic: Relieving or preventing itching. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antisickling Agents: Agents used to prevent or reverse the pathological events leading to sickling of erythrocytes in sickle cell conditions. [NIH] Antithymocyte globulin: A protein used to reduce the risk of or to treat graft-versus-host disease. [NIH] Antituberculosis: Refers to a drug used to treat tuberculosis. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Antrectomy: An operation to remove the upper portion of the stomach, called the antrum. This operation helps reduce the amount of stomach acid. It is used when a person has complications from ulcers. [NIH] Anuria: Inability to form or excrete urine. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Apheresis: Components being separated out, as leukapheresis, plasmapheresis, plateletpheresis. [NIH] Aplasia: Lack of development of an organ or tissue, or of the cellular products from an organ or tissue. [EU] Aplastic anemia: A condition in which the bone marrow is unable to produce blood cells. [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] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Aqueous: Having to do with water. [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
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the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arginine butyrate: A substance that is being studied as a treatment for cancer. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Arteriovenous: Both arterial and venous; pertaining to or affecting an artery and a vein. [EU] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Arthralgia: Pain in the joint. [NIH] 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] Aseptic: Free from infection or septic material; sterile. [EU] Aspergillosis: Infections with fungi of the genus Aspergillus. [NIH] Asphyxia: A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life. [NIH] Aspiration: The act of inhaling. [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] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atrial: Pertaining to an atrium. [EU] Atrial Fibrillation:
Disorder of cardiac rhythm characterized by rapid, irregular atrial
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impulses and ineffective atrial contractions. [NIH] 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] 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] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autologous bone marrow transplantation: A procedure in which bone marrow is removed from a person, stored, and then given back to the person after intensive treatment. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autosuggestion: Suggestion coming from the subject himself. [NIH] Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent. [NIH] Bacillus: A genus of Bacillaceae that are spore-forming, rod-shaped cells. Most species are saprophytic soil forms with only a few species being pathogenic. [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] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary
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movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [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] Basophils: Granular leukocytes characterized by a relatively pale-staining, lobate nucleus and cytoplasm containing coarse dark-staining granules of variable size and stainable by basic dyes. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Beta-Lactamases: Enzymes found in many bacteria which catalyze the hydrolysis of the amide bond in the beta-lactam ring. Well known antibiotics destroyed by these enzymes are penicillins and cephalosporins. EC 3.5.2.6. [NIH] Beta-Thalassemia: A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent. [NIH] Bifida: A defect in development of the vertebral column in which there is a central deficiency of the vertebral lamina. [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 duct: A tube through which bile passes in and out of the liver. [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 Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of HEME. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biochemical reactions: In living cells, chemical reactions that help sustain life and allow cells to grow. [NIH] 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] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH]
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Biopterin: A natural product that has been considered as a growth factor for some insects. [NIH]
Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] 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] Biotinylation: Incorporation of biotinyl groups into molecules. [NIH] Bladder: The organ that stores urine. [NIH] Blasts: Immature blood cells. [NIH] Bleeding Time: Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function. [NIH] Bleomycin: A complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors. [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 Viscosity: The internal resistance of the blood to shear forces. The in vitro measure of whole blood viscosity is of limited clinical utility because it bears little relationship to the actual viscosity within the circulation, but an increase in the viscosity of circulating blood can contribute to morbidity in patients suffering from disorders such as sickle cell anemia and polycythemia. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bolus: A single dose of drug usually injected into a blood vessel over a short period of time.
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Also called bolus infusion. [NIH] Bolus infusion: A single dose of drug usually injected into a blood vessel over a short period of time. Also called bolus. [NIH] 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] Bone marrow aspiration: The removal of a small sample of bone marrow (usually from the hip) through a needle for examination under a microscope. [NIH] Bone marrow biopsy: The removal of a sample of tissue from the bone marrow with a needle for examination under a microscope. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone Marrow Examination: picture. [NIH]
Removal of bone marrow and evaluation of its histologic
Bone Marrow Transplantation: animal to another. [NIH]
The transference of bone marrow from one human or
Bone metastases: Cancer that has spread from the original (primary) tumor to the bone. [NIH]
Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [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] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [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] 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] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU]
Bronchioles: The tiny branches of air tubes in the lungs. [NIH] Bronchiolitis: Inflammation of the bronchioles. [NIH]
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Bronchiseptica: A small, gram-negative, motile bacillus. A normal inhabitant of the respiratory tract in man, dogs, and pigs, but is also associated with canine infectious tracheobronchitis and atrophic rhinitis in pigs. [NIH] 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]
Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Busulfan: An anticancer drug that belongs to the family of drugs called alkylating agents. [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] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [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] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels. [NIH] Calorimeter: Measures the amounts of heat absorbed or given off by a solid, a liquid, or a gas. [NIH] Candidiasis: Infection with a fungus of the genus Candida. It is usually a superficial infection of the moist cutaneous areas of the body, and is generally caused by C. albicans; it most commonly involves the skin (dermatocandidiasis), oral mucous membranes (thrush, def. 1), respiratory tract (bronchocandidiasis), and vagina (vaginitis). Rarely there is a systemic infection or endocarditis. Called also moniliasis, candidosis, oidiomycosis, and formerly blastodendriosis. [EU] Candidosis: An infection caused by an opportunistic yeasts that tends to proliferate and
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become pathologic when the environment is favorable and the host resistance is weakened. [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] Capsid: The outer protein protective shell of a virus, which protects the viral nucleic acid. [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] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] 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] Cardiolipins: Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of the Wassermann-type antigen that is used in nontreponemal syphilis serodiagnosis. [NIH] Cardiomegaly: Hypertrophy or enlargement of the heart. [NIH] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiopulmonary Bypass: Diversion of the flow of blood from the entrance of the right atrium directly to the aorta (or femoral artery) via an oxygenator thus bypassing both the heart and lungs. [NIH] Cardiotoxic: Having a poisonous or deleterious effect upon the heart. [EU] 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] Carnitine: Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. [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] Carpal Tunnel Syndrome: A median nerve injury inside the carpal tunnel that results in
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symptoms of pain, numbness, tingling, clumsiness, and a lack of sweating, which can be caused by work with certain hand and wrist postures. [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] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Catalyse: To speed up a chemical reaction. [EU] Cataracts: In medicine, an opacity of the crystalline lens of the eye obstructing partially or totally its transmission of light. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [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] Causal: Pertaining to a cause; directed against a cause. [EU] Causality: The relating of causes to the effects they produce. Causes are termed necessary when they must always precede an effect and sufficient when they initiate or produce an effect. Any of several factors may be associated with the potential disease causation or outcome, including predisposing factors, enabling factors, precipitating factors, reinforcing factors, and risk factors. [NIH] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cavernous Sinus: An irregularly shaped venous space in the dura mater at either side of the sphenoid bone. [NIH] Cefotetan: A semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms. It has a high rate of efficacy in many types of infections and to date no severe side effects have been noted. [NIH] Ceftriaxone: Broad-spectrum cephalosporin antibiotic with a very long half-life and high penetrability to usually inaccessible infections, including those involving the meninges, eyes, inner ears, and urinary tract. [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]
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Cell Aging: The decrease in the cell's ability to proliferate with the passing of time. Each cell is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences cell death via the process of apoptosis. [NIH] Cell Count: A count of the number of cells of a specific kind, usually measured per unit volume of sample. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter 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 Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [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] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [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] Cephalosporins: A group of broad-spectrum antibiotics first isolated from the Mediterranean fungus Acremonium (Cephalosporium acremonium). They contain the betalactam moiety thia-azabicyclo-octenecarboxylic acid also called 7-aminocephalosporanic acid. [NIH]
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Cerebellar: Pertaining to the cerebellum. [EU] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Arteries: The arteries supplying the cerebral cortex. [NIH] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., infarction, anterior cerebral artery), and etiology (e.g., embolic infarction). [NIH]
Cerebral Palsy: Refers to a motor disability caused by a brain dysfunction. [NIH] 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] 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] Cheilitis: Inflammation of the lips. It is of various etiologies and degrees of pathology. [NIH] Chelation: Combination with a metal in complexes in which the metal is part of a ring. [EU] Chelation Therapy: Therapy of heavy metal poisoning using agents which sequester the metal from organs or tissues and bind it firmly within the ring structure of a new compound which can be eliminated from the body. [NIH] 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] Chemotherapeutic agent: A drug used to treat cancer. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [NIH] Chicken Anemia Virus: The type species of Circovirus, a small, non-enveloped DNA virus originally isolated from contaminated vaccines in Japan. It causes chicken infectious anemia and may possibly play a key role in hemorrhagic anemia syndrome, anemia dermatitis, and blue wing disease. [NIH] Child Care: Care of children in the home or institution. [NIH] Chimeras: Organism that contains a mixture of genetically different cells. [NIH]
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Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for the passage of blood vessels and a nerve. [NIH] Chiropractic: A system of treating bodily disorders by manipulation of the spine and other parts, based on the belief that the cause is the abnormal functioning of a nerve. [NIH] Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholelithiasis: Presence or formation of gallstones. [NIH] 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] Cholestyramine: Strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium as Cl(-) anion. It exchanges chloride ions with bile salts, thus decreasing their concentration and that of cholesterol. It is used as a hypocholesteremic in diarrhea and biliary obstruction and as an antipruritic. [NIH] Choroid: The thin, highly vascular membrane covering most of the posterior of the eye between the retina and sclera. [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] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chromosome Breakage: A type of chromosomal aberration which may result from spontaneous or induced breakage. Alkylating agents, various types of irradiation, and chemical mutagens have been found to cause induced chromosomal breakage. Breakage can induce base pair translocations, deletions, or chromatid breakage. [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 granulocytic leukemia: A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myelogenous leukemia or chronic myeloid leukemia. [NIH] Chronic leukemia: A slowly progressing cancer of the blood-forming tissues. [NIH] Chronic lymphocytic leukemia: A slowly progressing disease in which too many white blood cells (called lymphocytes) are found in the body. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic renal:
Slow and progressive loss of kidney function over several years, often
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resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Cisplatin: An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH] C-kit receptor: A protein on the surface of some cells that binds to stem cell factor (a substance that causes certain types of cells to grow). Altered forms of this receptor may be associated with some types of cancer. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [NIH] Cleave: A double-stranded cut in DNA with a restriction endonuclease. [NIH] Cleft Palate: Congenital fissure of the soft and/or hard palate, due to faulty fusion. [NIH] 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] Clodronate: A drug used as treatment for hypercalcemia (abnormally high levels of calcium in the blood) and for cancer that has spread to the bone (bone metastases). It may decrease pain, the risk of fractures, and the development of new bone metastases. [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] Clotrimazole: An imidazole derivative with a broad spectrum of antimycotic activity. It inhibits biosynthesis of the sterol ergostol, an important component of fungal cell membranes. Its action leads to increased membrane permeability and apparent disruption of enzyme systems bound to the membrane. [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] Codon: A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (codon, terminator). Most codons are universal, but
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some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [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 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] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colon Polyps: Small, fleshy, mushroom-shaped growths in the colon. [NIH] Colony-Stimulating Factors: Glycoproteins found in a subfraction of normal mammalian plasma and urine. They stimulate the proliferation of bone marrow cells in agar cultures and the formation of colonies of granulocytes and/or macrophages. The factors include interleukin-3 (IL-3), granulocyte colony-stimulating factor (G-CSF), macrophage colonystimulating factor (M-CSF), and granulocyte-macrophage colony-stimulating factor (GMCSF). [NIH] 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] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Common Variable Immunodeficiency: Heterogeneous group of immunodeficiency syndromes characterized by hypogammaglobulinemia of most isotypes, variable B-cell defects, and the presence of recurrent bacterial infections. [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
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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] Complement 3: The fourth component to attach in the complement reaction sequence. It is a beta-globulin with a sedimentation coefficient of 5.5, a molecular weight of 185,000 and a serum concentration of 1.3 micrograms/ml. Its fragments have anaphylatoxic, chemotactic, and histaminic action and affect smooth muscle. [NIH] Complement Activation: The sequential activation of serum components C1 through C9, initiated by an erythrocyte-antibody complex or by microbial polysaccharides and properdin, and producing an inflammatory response. [NIH] Complement Factor D: A serum protein which during the alternate pathway of complement activation converts the inactive factor B to complement 3 convertase. EC 3.4.21.46. [NIH] 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 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] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [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] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized
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tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [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] Cone: One of the special retinal receptor elements which are presumed to be primarily concerned with perception of light and color stimuli when the eye is adapted to light. [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] Conjugation: 1. the act of joining together or the state of being conjugated. 2. a sexual process seen in bacteria, ciliate protozoa, and certain fungi in which nuclear material is exchanged during the temporary fusion of two cells (conjugants). In bacterial genetics a form of sexual reproduction in which a donor bacterium (male) contributes some, or all, of its DNA (in the form of a replicated set) to a recipient (female) which then incorporates differing genetic information into its own chromosome by recombination and passes the recombined set on to its progeny by replication. In ciliate protozoa, two conjugants of separate mating types exchange micronuclear material and then separate, each now being a fertilized cell. In certain fungi, the process involves fusion of two gametes, resulting in union of their nuclei and formation of a zygote. 3. in chemistry, the joining together of two compounds to produce another compound, such as the combination of a toxic product with some substance in the body to form a detoxified product, which is then eliminated. [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] Connective Tissue Diseases: A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constriction: The act of constricting. [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] Contraception: Use of agents, devices, methods, or procedures which diminish the likelihood of or prevent conception. [NIH] 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
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treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contrast medium: A substance that is introduced into or around a structure and, because of the difference in absorption of x-rays by the contrast medium and the surrounding tissues, allows radiographic visualization of the structure. [EU] 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: group. [NIH]
An experiment or clinical trial that includes a comparison (control)
Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] 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 Arteriosclerosis: Thickening and loss of elasticity of the coronary arteries. [NIH] 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] 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] 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] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to
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stress. [NIH] Cost Savings: Reductions in all or any portion of the costs of providing goods or services. Savings may be incurred by the provider or the consumer. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Critical Care: Health care provided to a critically ill patient during a medical emergency or crisis. [NIH] Critical Illness: A disease or state in which death is possible or imminent. [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] Cyanide: An extremely toxic class of compounds that can be lethal on inhaling of ingesting in minute quantities. [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] Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] 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] Cytarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Cytidine: A pyrimidine nucleoside that is composed of the base cytosine linked to the five-
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carbon sugar D-ribose. [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] Cytogenetics: A branch of genetics which deals with the cytological and molecular behavior of genes and chromosomes during cell division. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B 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] Cytomegalovirus Retinitis: Infection of the retina by cytomegalovirus characterized by retinal necrosis, hemorrhage, vessel sheathing, and retinal edema. Cytomegalovirus retinitis is a major opportunistic infection in AIDS patients and can cause blindness. [NIH] Cytopenia: A reduction in the number of blood cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a 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] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxic chemotherapy: Anticancer drugs that kill cells, especially cancer cells. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Daclizumab: A monoclonal antibody that is being studied for treatment of adult T-cell leukemia. Also called dacliximab. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [NIH] Danazol: A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders. [NIH] Daunorubicin: Very toxic anthracycline aminoglycoside antibiotic isolated from Streptomyces peucetius and others, used in treatment of leukemias and other neoplasms. [NIH]
De novo: In cancer, the first occurrence of cancer in the body. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decitabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
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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]
Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the form of its mesylate. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydration: The condition that results from excessive loss of body water. [NIH] 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 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] 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] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. branched like a tree. 2. pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [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] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
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]
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Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Dermatitis: Any inflammation of the skin. [NIH] Dermatology: A medical specialty concerned with the skin, its structure, functions, diseases, and treatment. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Detoxification: Treatment designed to free an addict from his drug habit. [EU] 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 of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [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] Diaphragm: The musculofibrous partition that separates the thoracic cavity from the abdominal cavity. Contraction of the diaphragm increases the volume of the thoracic cavity aiding inspiration. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastole: Period of relaxation of the heart, especially the ventricles. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt, diclofenac sodium. [NIH] Diclofenac Sodium: The sodium form of diclofenac. It is used for its analgesic and antiinflammatory properties. [NIH] Diethylstilbestrol: DES. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [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] Dihydrotestosterone: Anabolic agent. [NIH]
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Dilatation: The act of dilating. [NIH] Dilator: A device used to stretch or enlarge an opening. [NIH] Dilution: A diluted or attenuated medicine; in homeopathy, the diffusion of a given quantity of a medicinal agent in ten or one hundred times the same quantity of water. [NIH] Diphtheria: A localized infection of mucous membranes or skin caused by toxigenic strains of Corynebacterium diphtheriae. It is characterized by the presence of a pseudomembrane at the site of infection. Diphtheria toxin, produced by C. diphtheriae, can cause myocarditis, polyneuritis, and other systemic toxic effects. [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] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] 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] Dissociative Disorders: Sudden temporary alterations in the normally integrative functions of consciousness. [NIH] 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] Diuretics, Thiazide: Diuretics characterized as analogs of 1,2,4-benzothiadiazine-1,1dioxide. All have a common mechanism of action and differ primarily in the dose required to produce a given effect. They act directly on the kidney to increase the excretion of sodium chloride and water and also increase excretion of potassium ions. [NIH] Diverticulosis: A condition marked by small sacs or pouches (diverticula) in the walls of an organ such as the stomach or colon. These sacs can become inflamed and cause a condition called diverticulitis, which may be a risk factor for certain types of cancer. [NIH] Diverticulum: A pathological condition manifested as a pouch or sac opening from a tubular or sacular organ. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [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
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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] 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] 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] Doxycycline: A synthetic tetracycline derivative with a range of antimicrobial activity and mode of action similar to that of tetracycline, but more effective against many species. Animal studies suggest that it may cause less tooth staining than other tetracyclines. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration. [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] Dumping Syndrome: Gastrointestinal symptoms resulting from an absent or nonfunctioning pylorus. [NIH] Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dyspepsia: Impaired digestion, especially after eating. [NIH] Dysphagia: Difficulty in swallowing. [EU] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [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] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [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
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based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [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] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]
Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Emboli: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embolism: Blocking of a blood vessel by a blood clot or foreign matter that has been transported from a distant site by the blood stream. [NIH] Embolization: The blocking of an artery by a clot or foreign material. Embolization can be done as treatment to block the flow of blood to a tumor. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid 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] Embryogenesis: The process of embryo or embryoid formation, whether by sexual (zygotic) or asexual means. In asexual embryogenesis embryoids arise directly from the explant or on intermediary callus tissue. In some cases they arise from individual cells (somatic cell embryoge). [NIH]
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Emesis: Vomiting; an act of vomiting. Also used as a word termination, as in haematemesis. [EU]
Emollient: Softening or soothing; called also malactic. [EU] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH] Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Encephalomyelitis: A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature. [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] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]
Endometriosis: A condition in which tissue more or less perfectly resembling the uterine mucous membrane (the endometrium) and containing typical endometrial granular and stromal elements occurs aberrantly in various locations in the pelvic cavity. [NIH] Endometrium: The layer of tissue that lines the uterus. [NIH] Endoscope: A thin, lighted tube used to look at tissues inside the body. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum for visualization of the ampulla of Vater. [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, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood
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capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [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] 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] Enhancer: Transcriptional element in the virus genome. [NIH] Enteroscopy: An examination of the small intestine with an endoscope. The endoscope is inserted through the mouth and stomach into the small intestine. [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] 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] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its cytoplasm, which plays a role in hypersensitivity reactions. [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] 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] Epidermoid carcinoma: A type of cancer in which the cells are flat and look like fish scales. Also called squamous cell carcinoma. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epiphyseal: Pertaining to or of the nature of an epiphysis. [EU] Epiphyses: The head of a long bone that is separated from the shaft by the epiphyseal plate until bone growth stops. At that time, the plate disappears and the head and shaft are united. [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] Epitopes: Sites on an antigen that interact with specific antibodies. [NIH] Epoetin alfa: A colony-stimulating factor that is made in the laboratory. It increases the production of red blood cells. [NIH] Equine Infectious Anemia: Viral disease of horses caused by the equine infectious anemia
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virus (EIAV). It is characterized by intermittent fever, weakness, and anemia. Chronic infection consists of acute episodes with remissions. [NIH] Erectile: The inability to get or maintain an erection for satisfactory sexual intercourse. Also called impotence. [NIH] Erection: The condition of being made rigid and elevated; as erectile tissue when filled with blood. [EU] ERV: The expiratory reserve volume is the largest volume of gas that can be expired from the end-expiratory level. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythema Infectiosum: Contagious infection with human B19 Parvovirus most commonly seen in school age children and characterized by fever, headache, and rashes of the face, trunk, and extremities. It is often confused with rubella. [NIH] Erythroblasts: Immature, nucleated erythrocytes occupying the stage of erythropoiesis that follows formation of erythroid progenitor cells and precedes formation of reticulocytes. Popularly called normoblasts. [NIH] Erythrocyte Count: A count of the number of red blood cells per unit volume in a sample of venous blood. [NIH] Erythrocyte Indices: Quantification of size and cell hemoglobin content or concentration of the erythrocyte, usually derived from erythrocyte count, blood hemoglobin concentration, and hematocrit. Includes the mean cell volume (MCV), mean cell hemoglobin (MCH), and mean cell hemoglobin concentration (MCHC). Use also for cell diameter and thickness. [NIH] Erythrocyte Transfusion: The transfer of erythrocytes from a donor to a recipient or reinfusion to the donor. [NIH] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by radioisotope dilution technique. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythroid Progenitor Cells: Committed, erythroid stem cells derived from myeloid stem cells. The progenitor cells develop in two phases: erythroid burst-forming units (BFU-E) followed by erythroid colony-forming units (CFU-E). BFU-E differentiate into CFU-E on stimulation by erythropoietin, and then further differentiate into erythroblasts when stimulated by other factors. [NIH] Erythroleukemia: Cancer of the blood-forming tissues in which large numbers of immature, abnormal red blood cells are found in the blood and bone marrow. [NIH] Erythropoiesis: The production of erythrocytes. [EU] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophageal Varices: Stretched veins in the esophagus that occur when the liver is not working properly. If the veins burst, the bleeding can cause death. [NIH] Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach.
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[NIH]
Estrogen: One of the two female sex hormones. [NIH] Ethidium: A trypanocidal agent and possible antiviral agent that is widely used in experimental cell biology and biochemistry. Ethidium has several experimentally useful properties including binding to nucleic acids, noncompetitive inhibition of nicotinic acetylcholine receptors, and fluorescence among others. It is most commonly used as the bromide. [NIH] Etodolac: A nonsteroidal anti-inflammatory agent with potent analgesic and antiarthritic properties. It has been shown to be effective in the treatment of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and in the alleviation of postoperative pain. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Euphoria: An exaggerated feeling of physical and emotional well-being not consonant with apparent stimuli or events; usually of psychologic origin, but also seen in organic brain disease and toxic states. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evaluable patients: Patients whose response to a treatment can be measured because enough information has been collected. [NIH] Evoked Potentials: The electric response evoked in the central nervous system by stimulation of sensory receptors or some point on the sensory pathway leading from the receptor to the cortex. The evoked stimulus can be auditory, somatosensory, or visual, although other modalities have been reported. Event-related potentials is sometimes used synonymously with evoked potentials but is often associated with the execution of a motor, cognitive, or psychophysiological task, as well as with the response to a stimulus. [NIH] Excisional: The surgical procedure of removing a tumor by cutting it out. The biopsy is then examined under a microscope. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [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]
Exfoliation: A falling off in scales or layers. [EU] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: 1. secreting outwardly, via a duct;. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU]
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Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Expiratory: The volume of air which leaves the breathing organs in each expiration. [NIH] Expiratory Reserve Volume: The extra volume of air that can be expired with maximum effort beyond the level reached at the end of a normal, quiet expiration. Common abbreviation is ERV. [NIH] External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] 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] Extravascular: Situated or occurring outside a vessel or the vessels. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fanconi anemia: A rare and often fatal inherited disease in which the bone marrow fails to produce red blood cells, white blood cells, platelets, or a combination of these cells. The disease may transform into myelodysplastic syndrome or leukemia. Also called Fanconi's syndrome. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The feeling of weariness of mind and body. [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] Ferric Compounds: Inorganic or organic compounds containing trivalent iron. [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 Blood: Blood of the fetus. Exchange of nutrients and waste between the fetal and maternal blood occurs via the placenta. The cord blood is blood contained in the umbilical vessels at the time of delivery. [NIH] Fetal Death: Death of the young developing in utero. [NIH] Fetal Hemoglobin: The major component of hemoglobin in the fetus. This hemoglobin has two alpha and two gamma polypeptide subunits in comparison to normal adult hemoglobin, which has two alpha and two beta polypeptide subunits. Fetal hemoglobin concentrations can be elevated (usually above 0.5%) in children and adults affected by
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leukemia and several types of anemia. [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] Fibronectin: An adhesive glycoprotein. One form circulates in plasma, acting as an opsonin; another is a cell-surface protein which mediates cellular adhesive interactions. [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] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fludarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Flunarizine: Flunarizine is a selective calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity. It is effective in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescence Polarization: Measurement of the polarization of fluorescent light from solutions or microscopic specimens. It is used to provide information concerning molecular size, shape, and conformation, molecular anisotropy, electronic energy transfer, molecular interaction, including dye and coenzyme binding, and the antigen-antibody reaction. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH]
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Flushing: A transient reddening of the face that may be due to fever, certain drugs, exertion, stress, or a disease process. [NIH] 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] Forearm: The part between the elbow and the wrist. [NIH] Founder Effect: The principle that when a small subgroup of a larger population establishes itself as a separate and isolated entity, its gene pool carries only a fraction of the genetic diversity of the parental population. This may result in an increased frequency of certain diseases in the subgroup, especially those diseases known to be autosomal recessive. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH] Frontal Lobe: The anterior part of the cerebral hemisphere. [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] Fulminant Hepatic Failure: Liver failure that occurs suddenly in a previously healthy person. The most common causes of FHF are acute hepatitis, acetaminophen overdose, and liver damage from prescription drugs. [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] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallstones: The solid masses or stones made of cholesterol or bilirubin that form in the gallbladder or bile ducts. [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of
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shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglionic Blockers: Agents having as their major action the interruption of neural transmission at nicotinic receptors on postganglionic autonomic neurons. Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drugs. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery. [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 Antral Vascular Ectasia: A capillary ectasia of the gastric antrum mucosa characterized by thickened, red vascular folds radiating longitudinally from the pylorus to the antrum and resembling, upon endoscopic examination, the stripes on the skin of a ripened watermelon. Histological characteristics include dilated mucosal capillaries, focal thrombosis, and fibromuscular hypertrophy of the lamina propria. It is a cause of chronic upper gastrointestinal bleeding. [NIH] Gastric atrophy: A condition in which the stomach muscles shrink and become weak. The digestive (peptic) glands may also shrink, resulting in a lack of digestive juices. [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]
Gastritis: Inflammation of the stomach. [EU] 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] Gastroesophageal Reflux: Reflux of gastric juice and/or duodenal contents (bile acids, pancreatic juice) into the distal esophagus, commonly due to incompetence of the lower esophageal sphincter. Gastric regurgitation is an extension of this process with entry of fluid into the pharynx or mouth. [NIH] Gastroesophageal Reflux Disease: Flow of the stomach's contents back up into the esophagus. Happens when the muscle between the esophagus and the stomach (the lower esophageal sphincter) is weak or relaxes when it shouldn't. May cause esophagitis. Also called esophageal reflux or reflux esophagitis. [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal Hemorrhage: Bleeding in the gastrointestinal tract. [NIH] Gastrointestinal tract: The stomach and intestines. [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
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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 Deletion: A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus. [NIH] Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Frequency: The proportion of one particular allele in the total of all alleles for one genetic locus in a breeding population. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [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] 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 Techniques: Chromosomal, biochemical, intracellular, and other methods used in the study of genetics. [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] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geriatric: Pertaining to the treatment of the aged. [EU] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] 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]
Glomerular Filtration Rate: The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to inulin clearance. [NIH] Glomeruli: Plural of glomerulus. [NIH]
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Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH] Glomerulosclerosis: Scarring of the glomeruli. It may result from diabetes mellitus (diabetic glomerulosclerosis) or from deposits in parts of the glomerulus (focal segmental glomerulosclerosis). The most common signs of glomerulosclerosis are proteinuria and kidney failure. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glossitis: Inflammation of the tongue. [NIH] Glottis: The vocal apparatus of the larynx, consisting of the true vocal cords (plica vocalis) and the opening between them (rima glottidis). [NIH] Glucagonoma: Glucagon-secreting tumor of the pancreatic alpha cells characterized by a distinctive rash, weight loss, stomatitis, glossitis, diabetes, hypoaminoacidemia, and normochromic normocytic anemia. [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] Glucokinase: A group of enzymes that catalyzes the conversion of ATP and D-glucose to ADP and D-glucose 6-phosphate. They are found in invertebrates and microorganisms and are highly specific for glucose. (Enzyme Nomenclature, 1992) EC 2.7.1.2. [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] Glucuronosyltransferase: A family of enzymes accepting a wide range of substrates, including phenols, alcohols, amines, and fatty acids. They function as drug-metabolizing enzymes that catalyze the conjugation of UDPglucuronic acid to a variety of endogenous and exogenous compounds. EC 2.4.1.17. [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] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [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
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metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerol Kinase: An enzyme that catalyzes the formation of glycerol 3-phosphate from ATP and glycerol. Dihydroxyacetone and L-glyceraldehyde can also act as acceptors; UTP and, in the case of the yeast enzyme, ITP and GTP can act as donors. It provides a way for glycerol derived from fats or glycerides to enter the glycolytic pathway. EC 2.7.1.30. [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] Glycols: A generic grouping for dihydric alcohols with the hydroxy groups (-OH) located on different carbon atoms. They are viscous liquids with high boiling points for their molecular weights. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosylation: The chemical or biochemical addition of carbohydrate or glycosyl groups to other chemicals, especially peptides or proteins. Glycosyl transferases are used in this biochemical reaction. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonads: The gamete-producing glands, ovary or testis. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Government Agencies: Administrative units of government responsible for policy making and management of governmental activities in the U.S. and abroad. [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] 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 Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Graft vs Host Disease: The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the graft vs host reaction. [NIH] Graft vs Host Reaction: An immunological attack mounted by a graft against the host because of tissue incompatibility when immunologically competent cells are transplanted to an immunologically incompetent host; the resulting clinical picture is that of graft vs host disease. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Graft-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU]
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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] Granulocyte: A type of white blood cell that fights bacterial infection. Neutrophils, eosinophils, and basophils are granulocytes. [NIH] Granulocyte Colony-Stimulating Factor: A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, G-CSF is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines. [NIH] Granulocyte-Macrophage Colony-Stimulating Factor: An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages. [NIH] Granulocytopenia: A deficiency in the number of granulocytes, a type of white blood cell. [NIH]
Granulomas: Small lumps in tissues caused by inflammation. [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] Gravidity: Pregnancy; the condition of being pregnant, without regard to the outcome. [EU] Groin: The external junctural region between the lower part of the abdomen and the thigh. [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 pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Haematemesis: The vomiting of blood. [EU] Hairy cell leukemia: A type of chronic leukemia in which the abnormal white blood cells appear to be covered with tiny hairs when viewed under a microscope. [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] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [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;
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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] Headache Disorders: Common conditions characterized by persistent or recurrent headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [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] Helminths: Commonly known as parasitic worms, this group includes the acanthocephala, nematoda, and platyhelminths. Some authors consider certain species of leeches that can become temporarily parasitic as helminths. [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] Hematologic Diseases: Disorders of the blood and blood forming tissues. [NIH] Hematologic malignancies: Cancers of the blood or bone marrow, including leukemia and lymphoma. Also called hematologic cancers. [NIH] Hematologist: A doctor who specializes in treating diseases of the blood. [NIH] Hematology: A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues. [NIH] Hematopoiesis: The development and formation of various types of blood cells. [NIH] Hematopoietic growth factors: A group of proteins that cause blood cells to grow and mature. [NIH] Hematopoietic Stem Cell Transplantation: The transference of stem cells from one animal or human to another (allogeneic), or within the same individual (autologous). The source for the stem cells may be the bone marrow or peripheral blood. Stem cell transplantation has been used as an alternative to autologous bone marrow transplantation in the treatment of a variety of neoplasms. [NIH] Hematopoietic Stem Cells: Progenitor cells from which all blood cells derive. [NIH] Hematopoietic tissue: Tissue in which new blood cells are formed. [NIH] Hematuria: Presence of blood in the urine. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemochromatosis: A disease that occurs when the body absorbs too much iron. The body stores the excess iron in the liver, pancreas, and other organs. May cause cirrhosis of the liver. Also called iron overload disease. [NIH] Hemodiafiltration:
The
combination of hemodialysis and hemofiltration either
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simultaneously or sequentially. Convective transport (hemofiltration) may be better for removal of larger molecular weight substances and diffusive transport (hemodialysis) for smaller molecular weight solutes. [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] Hemodilution: Reduction of blood viscosity usually by the addition of cell free solutions. Used clinically l) in states of impaired microcirculation, 2) for replacement of intraoperative blood loss without homologous blood transfusion, and 3) in cardiopulmonary bypass and hypothermia. [NIH] Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [NIH] Hemofiltration: Extracorporeal ultrafiltration technique without hemodialysis for treatment of fluid overload and electrolyte disturbances affecting renal, cardiac, or pulmonary function. [NIH] 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 A: Normal adult human hemoglobin. The globin moiety consists of two alpha and two beta chains. [NIH] Hemoglobin C: A commonly occurring abnormal hemoglobin in which lysine replaces a glutamic acid residue at the sixth position of the beta chains. It results in reduced plasticity of erythrocytes. [NIH] Hemoglobin H: An abnormal hemoglobin composed of four beta chains. It is caused by the reduced synthesis of the alpha chain. This abnormality results in alpha-thalassemia. [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] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemolysis: The destruction of erythrocytes by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemophilia: Refers to a group of hereditary disorders in which affected individuals fail to make enough of certain proteins needed to form blood clots. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH]
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Hemosiderin: Molecule which can bind large numbers of iron atoms. [NIH] Hemosiderosis: Conditions in which there is a generalized increase in the iron stores of body tissues, particularly of liver and the reticuloendothelial system, without demonstrable tissue damage. The name refers to the presence of stainable iron in the tissue in the form of hemosiderin. [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 A: Hepatitis caused by hepatovirus. It can be transmitted through fecal contamination of food or water. [NIH] Hepatobiliary: Pertaining to the liver and the bile or the biliary ducts. [EU] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hepatomegaly: Enlargement of the liver. [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] Heritability: The proportion of observed variation in a particular trait that can be attributed to inherited genetic factors in contrast to environmental ones. [NIH] Hernia: Protrusion of a loop or knuckle of an organ or tissue through an abnormal opening. [NIH]
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 virus: A member of the herpes family of viruses. [NIH] Heterodimers: Zippered pair of nonidentical proteins. [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] Heterozygote: An individual having different alleles at one or more loci in homologous chromosome segments. [NIH] Hexokinase: An enzyme that catalyzes the conversion of ATP and a D-hexose to ADP and a D-hexose 6-phosphate. D-Glucose, D-mannose, D-fructose, sorbitol, and D-glucosamine can act as acceptors; ITP and dATP can act as donors. The liver isoenzyme has sometimes been called glucokinase. (From Enzyme Nomenclature, 1992) EC 2.7.1.1. [NIH] Hiatal Hernia: A small opening in the diaphragm that allows the upper part of the stomach to move up into the chest. Causes heartburn from stomach acid flowing back up through the opening. [NIH] Histamine:
1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic
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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] Histone Deacetylase: Hydrolyzes N-acetyl groups on histones. [NIH] Histones: Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] 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] Homozygote: An individual in which both alleles at a given locus are identical. [NIH] Hookworm: A parasitic infection that may affect workers exposed to warm moist soil in which the larvae of the worm lives. [NIH] 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 therapy: Treatment of cancer by removing, blocking, or adding hormones. Also called endocrine therapy. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. a normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. a secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [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] Hydrocephalus: Excessive accumulation of cerebrospinal fluid within the cranium which may be associated with dilation of cerebral ventricles, intracranial hypertension; headache; lethargy; urinary incontinence; and ataxia (and in infants macrocephaly). This condition may be caused by obstruction of cerebrospinal fluid pathways due to neurologic abnormalities, intracranial hemorrhages; central nervous system infections; brain neoplasms; craniocerebral trauma; and other conditions. Impaired resorption of cerebrospinal fluid from the arachnoid villi results in a communicating form of
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hydrocephalus. Hydrocephalus ex-vacuo refers to ventricular dilation that occurs as a result of brain substance loss from cerebral infarction and other conditions. [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] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrops Fetalis: Edema of the entire body due to abnormal accumulation of serous fluid in the tissues, associated with severe anemia and occurring in fetal erythroblastosis. [NIH] Hydroxides: Inorganic compounds that contain the OH- group. [NIH] Hydroxyl Radical: The univalent radical OH that is present in hydroxides, alcohols, phenols, glycols. [NIH] 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] Hydroxyurea: An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase. [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] Hyperhomocysteinemia: An inborn error of methionone metabolism which produces an excess of homocysteine in the blood. It is often caused by a deficiency of cystathionine betasynthase and is a risk factor for coronary vascular disease. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hyperreflexia: Exaggeration of reflexes. [EU] 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] 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] Hypervitaminosis: A condition due to ingestion of an excess of one or more vitamins; called also supervitaminosis. [EU] Hypnotics and Sedatives: Drugs used to induce drowsiness or sleep or to reduce psychological excitement or anxiety. [NIH] Hypogammaglobulinemia: The most common primary immunodeficiency in which antibody production is deficient. [NIH]
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Hypoglycaemia: An abnormally diminished concentration of glucose in the blood, which may lead to tremulousness, cold sweat, piloerection, hypothermia, and headache, accompanied by irritability, confusion, hallucinations, bizarre behaviour, and ultimately, convulsions and coma. [EU] Hypoglycemia: Abnormally low blood sugar [NIH] Hypogonadism: Condition resulting from or characterized by abnormally decreased functional activity of the gonads, with retardation of growth and sexual development. [NIH] Hypotension: Abnormally low blood pressure. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [NIH] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Hypoxic: Having too little oxygen. [NIH] Iatrogenic: Resulting from the activity of physicians. Originally applied to disorders induced in the patient by autosuggestion based on the physician's examination, manner, or discussion, the term is now applied to any adverse condition in a patient occurring as the result of treatment by a physician or surgeon, especially to infections acquired by the patient during the course of treatment. [EU] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Ida: An alkylating agent. [NIH] Idarubicin: An orally administered anthracycline antibiotic. The compound has shown activity against breast cancer, lymphomas and leukemias, together with potential for reduced cardiac toxicity. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Idiopathic myelofibrosis: A progressive disease in which the bone marrow is replaced by fibrous tissue and is unable to produce red blood cells; the cause is unknown. [NIH] Ileum: The lower end of the small intestine. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: (antigens). [NIH]
The activity of the immune system against foreign substances
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immune Tolerance: The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic effects of foreign microorganisms or to the toxic effect of antigenic substances. [NIH] 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
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(thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunofluorescence: A technique for identifying molecules present on the surfaces of cells or in tissues using a highly fluorescent substance coupled to a specific antibody. [NIH] Immunoglobulin: A protein that acts as an antibody. [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] Immunophilins: Members of a family of highly conserved proteins which are all cis-trans peptidyl-prolyl isomerases (peptidylprolyl isomerase). They bind the immunosuppressant drugs cyclosporine; tacrolimus and sirolimus. They possess rotomase activity, which is inhibited by the immunosuppressant drugs that bind to them. EC 5.2.1.- [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] Impotence: The inability to perform sexual intercourse. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] 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] Incision: A cut made in the body during surgery. [NIH] Incompetence: Physical or mental inadequacy or insufficiency. [EU] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH]
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Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Incubation period: The period of time likely to elapse between exposure to the agent of the disease and the onset of clinical symptoms. [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU]
Indolent: A type of cancer that grows slowly. [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 Mortality: Perinatal, neonatal, and infant deaths in a given population. [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]
Infectious Mononucleosis: A common, acute infection usually caused by the Epstein-Barr virus (Human herpesvirus 4). There is an increase in mononuclear white blood cells and other atypical lymphocytes, generalized lymphadenopathy, splenomegaly, and occasionally hepatomegaly with hepatitis. [NIH] 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] Infestation: Parasitic attack or subsistence on the skin and/or its appendages, as by insects, mites, or ticks; sometimes used to denote parasitic invasion of the organs and tissues, as by helminths. [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] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called
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intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate 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] In-line: A sexually-reproducing population derived from a common parentage. [NIH] Inner ear: The labyrinth, comprising the vestibule, cochlea, and semicircular canals. [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] 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] 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-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] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [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 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
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and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-11: Lymphohematopoietic cytokine that has the ability to modulate antigenspecific antibody responses, potentiate megakaryocytes, and regulate bone marrow adipogenesis. [NIH] Interleukin-12: A heterodimeric cytokine that stimulates the production of interferon gamma from T-cells and natural killer cells, and also induces differentiation of Th1 helper cells. It is an initiator of cell-mediated immunity. [NIH] Interleukin-2: Soluble substances elaborated by antigen- or mitogen-stimulated Tlymphocytes which induce DNA synthesis in naive lymphocytes. [NIH] Interleukin-3: A multilineage cell growth factor secreted by lymphocytes, epithelial cells, and astrocytes which stimulates clonal proliferation and differentiation of various types of blood and tissue cells. Also called multi-CSF, it is considered one of the hematopoietic colony stimulating factors. [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] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [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] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interphase: The interval between two successive cell divisions during which the chromosomes are not individually distinguishable and DNA replication occurs. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intervertebral: Situated between two contiguous vertebrae. [EU] Intervertebral Disk Displacement: An intervertebral disk in which the nucleus pulposus has protruded through surrounding fibrocartilage. This occurs most frequently in the lower lumbar region. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [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]
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Intracellular: Inside a cell. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravascular: Within a vessel or vessels. [EU] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intrinsic Factor: A glycoprotein secreted by the cells of the gastric glands that is required for the absorption of vitamin B 12. Deficiency of intrinsic factor results in pernicious anemia. [NIH]
Inulin: A starch found in the tubers and roots of many plants. Since it is hydrolyzable to fructose, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function. [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]
Involuntary: Reaction occurring without intention or volition. [NIH] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [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] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a 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] Iron Compounds: molecule. [NIH]
Inorganic compounds that contain iron as an integral part of the
Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic Colitis: diarrhea. [NIH]
Decreased blood flow to the colon. Causes fever, pain, and bloody
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
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their properties. [NIH] Isozymes: The multiple forms of a single enzyme. [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]
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] Keratoconjunctivitis: Simultaneous inflammation of the cornea and conjunctiva. [NIH] Keratoconjunctivitis Sicca: Drying and inflammation of the conjunctiva as a result of insufficient lacrimal secretion. When found in association with xerostomia and polyarthritis, it is called Sjogren's syndrome. [NIH] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Ketoconazole: Broad spectrum antifungal agent used for long periods at high doses, especially in immunosuppressed patients. [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 Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [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: another. [NIH]
The transference of a kidney from one human or animal to
Kinetic: Pertaining to or producing motion. [EU] Labile: 1. gliding; moving from point to point over the surface; unstable; fluctuating. 2. chemically unstable. [EU]
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Laceration: 1. the act of tearing. 2. a torn, ragged, mangled wound. [EU] Lacrimal: Pertaining to the tears. [EU] Lactation: The period of the secretion of milk. [EU] Lamivudine: A reverse transcriptase inhibitor and zalcitabine analog in which a sulfur atom replaces the 3' carbon of the pentose ring. It is used to treat HIV disease. [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] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]
Leg Ulcer: Ulceration of the skin and underlying structures of the lower extremity. About 90% of the cases are due to venous insufficiency (varicose ulcer), 5% to arterial disease, and the remaining 5% to other causes. [NIH] Leiomyosarcoma: A tumor of the muscles in the uterus, abdomen, or pelvis. [NIH] Leishmaniasis: A disease caused by any of a number of species of protozoa in the genus Leishmania. There are four major clinical types of this infection: cutaneous (Old and New World), diffuse cutaneous, mucocutaneous, and visceral leishmaniasis. [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] Lentivirus: A genus of the family Retroviridae consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species. [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] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH]
Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leukapheresis: The preparation of leukocyte concentrates with the return of red cells and leukocyte-poor plasma to the donor. [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]
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Leukocytosis: A transient increase in the number of leukocytes in a body fluid. [NIH] Leukoencephalopathy: A condition with spongy holes in the brain's white matter. [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [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: circulation. [NIH]
Services offered to the library user. They include reference and
Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [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] Linkages: 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] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [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] 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] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver cancer: A disease in which malignant (cancer) cells are found in the tissues of the liver. [NIH] Liver Cirrhosis: Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules. [NIH] Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH]
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Living will: A health care directive that tells others how a person would like to be treated if they lose their capacity to make decisions about health care; it contains instructions about the person's choices of medical treatment and it is prepared in advance. [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] Longitudinal Studies: Studies in which variables relating to an individual or group of individuals are assessed over a period of time. [NIH] 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] 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 Back Pain: Acute or chronic pain in the lumbar or sacral regions, which may be associated with musculo-ligamentous sprains and strains; intervertebral disk displacement; and other conditions. [NIH] Lower Esophageal Sphincter: The muscle between the esophagus and stomach. When a person swallows, this muscle relaxes to let food pass from the esophagus to the stomach. It stays closed at other times to keep stomach contents from flowing back into the esophagus. [NIH]
Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [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]
Lymphadenopathy: Disease or swelling of the lymph nodes. [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] 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] Lymphoblastic: One of the most aggressive types of non-Hodgkin lymphoma. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH]
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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] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphocytosis: Excess of normal lymphocytes in the blood or in any effusion. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphopenia: Reduction in the number of lymphocytes. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphoproliferative Disorders: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [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] Macrolides: A group of organic compounds that contain a macrocyclic lactone ring linked glycosidically to one or more sugar moieties. [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] Macrophage Colony-Stimulating Factor: A mononuclear phagocyte colony-stimulating factor synthesized by mesenchymal cells. The compound stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series. M-CSF is a disulfide-bonded glycoprotein dimer with a MW of 70 kDa. It binds to a specific high affinity receptor (receptor, macrophage colony-stimulating factor). [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [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] 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
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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] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Malondialdehyde: The dialdehyde of malonic acid. [NIH] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Maternal Mortality: Maternal deaths resulting from complications of pregnancy and childbirth in a given population. [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]
Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Median Nerve: A major nerve of the upper extremity. In humans, the fibers of the median nerve originate in the lower cervical and upper thoracic spinal cord (usually C6 to T1), travel via the brachial plexus, and supply sensory and motor innervation to parts of the forearm and hand. [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 Oncology: neoplasms. [NIH]
A subspecialty of internal medicine concerned with the study of
Medicament: A medicinal substance or agent. [EU] Medication Errors: Errors in prescribing, dispensing, or administering medication with the result that the patient fails to receive the correct drug or the indicated proper drug dosage. [NIH]
MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Megaloblastic: anaemia. [EU]
A large abnormal red blood cell appearing in the blood in pernicious
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Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [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] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Menorrhagia: Excessive menstrual flow. [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] 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] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic acidosis: (met-ah-BOL-ik as-id-O-sis): A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). [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] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH]
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Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methotrexate: An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of dihydrofolate reductase and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA. [NIH] Methylene Blue: A compound consisting of dark green crystals or crystalline powder, having a bronze-like luster. Solutions in water or alcohol have a deep blue color. Methylene blue is used as a bacteriologic stain and as an indicator. It inhibits Guanylate cyclase, and has been used to treat cyanide poisoning and to lower levels of methemoglobin. [NIH] Methylprednisolone: (6 alpha,11 beta)-11,17,21-Trihydroxy-6-methylpregna-1,4-diene-3,2dione. A prednisolone derivative which has pharmacological actions similar to prednisolone. [NIH] Methyltransferase: A drug-metabolizing enzyme. [NIH] Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic. [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] Mice Minute Virus: The type species of parvovirus prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microcirculation: The vascular network lying between the arterioles and venules; includes capillaries, metarterioles and arteriovenous anastomoses. Also, the flow of blood through this network. [NIH] 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] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Middle Cerebral Artery: The largest and most complex of the cerebral arteries. Branches of the middle cerebral artery supply the insular region, motor and premotor areas, and large regions of the association cortex. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [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]
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Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It acts as a bi- or trifunctional alkylating agent causing cross-linking of DNA and inhibition of DNA synthesis. [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] Mitral Valve: The valve between the left atrium and left ventricle of the heart. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [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] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]
Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] 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] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monocyte: A type of white blood cell. [NIH] Monogenic: A human disease caused by a mutation in a single gene. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [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] Mosaicism: The occurrence in an individual of two or more cell populations of different chromosomal constitutions, derived from a single zygote, as opposed to chimerism in which the different cell populations are derived from more than one zygote. [NIH] Motilin:
A 22-amino acid polypeptide (molecular weight 2700) isolated from the
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duodenum. At low pH it inhibits gastric motor activity, whereas at high pH it has a stimulating effect. [NIH] Motility: The ability to move spontaneously. [EU] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [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 Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [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] Muscle relaxant: An agent that specifically aids in reducing muscle tension, as those acting at the polysynaptic neurons of motor nerves (e.g. meprobamate) or at the myoneural junction (curare and related compounds). [EU] Muscle Spindles: Mechanoreceptors found between skeletal muscle fibers. Muscle spindles are arranged in parallel with muscle fibers and respond to the passive stretch of the muscle, but cease to discharge if the muscle contracts isotonically, thus signaling muscle length. The muscle spindles are the receptors responsible for the stretch or myotactic reflex. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Musculoskeletal System: Themuscles, bones, and cartilage of the body. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagenic: Inducing genetic mutation. [EU] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Mycophenolate mofetil: A drug that is being studied for its effectiveness in preventing graft-versus-host disease and autoimmune disorders. [NIH] Mycoplasma: A genus of gram-negative, facultatively anaerobic bacteria bounded by a plasma membrane only. Its organisms are parasites and pathogens, found on the mucous membranes of humans, animals, and birds. [NIH] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelitis: Inflammation of the spinal cord. Relatively common etiologies include infections; autoimmune diseases; spinal cord; and ischemia (see also spinal cord vascular diseases). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction. [NIH] Myelodysplasia: Abnormal bone marrow cells that may lead to myelogenous leukemia. [NIH]
Myelodysplastic syndrome: Disease in which the bone marrow does not function normally. Also called preleukemia or smoldering leukemia. [NIH]
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Myelofibrosis: A disorder in which the bone marrow is replaced by fibrous tissue. [NIH] Myelogenous: Produced by, or originating in, the bone marrow. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [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] 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] Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myoglobin: A conjugated protein which is the oxygen-transporting pigment of muscle. It is made up of one globin polypeptide chain and one heme group. [NIH] Myopathy: Any disease of a muscle. [EU] Narcosis: A general and nonspecific reversible depression of neuronal excitability, produced by a number of physical and chemical aspects, usually resulting in stupor. [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] Natriuresis: The excretion of abnormal amounts of sodium in the urine. [EU] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH] Natural selection: A part of the evolutionary process resulting in the survival and reproduction of the best adapted individuals. [NIH] 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] Necrolysis: Separation or exfoliation of tissue due to necrosis. [EU] 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]
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Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Neoplastic Processes: The pathological mechanisms and forms taken by tissue during degeneration into a neoplasm and its subsequent activity. [NIH] Neopterin: A pteridine derivative present in body fluids; elevated levels result from immune system activation, malignant disease, allograft rejection, and viral infections. (From Stedman, 26th ed) Neopterin also serves as a precursor in the biosynthesis of biopterin. [NIH] Nephrectomy: Surgery to remove a kidney. Radical nephrectomy removes the kidney, the adrenal gland, nearby lymph nodes, and other surrounding tissue. Simple nephrectomy removes only the kidney. Partial nephrectomy removes the tumor but not the entire kidney. [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] Nephroblastoma: A malignant kidney tumor made up of three cell types: blastemal, stromal, and epithelial, but not all present in every case. [NIH] Nephrology: A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney. [NIH] 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] 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] Neuroblastoma: Cancer that arises in immature nerve cells and affects mostly infants and children. [NIH] Neurologic: Having to do with nerves or 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] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] 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,
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and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophil: A type of white blood cell. [NIH] Niceritrol: An ester of nicotinic acid that lowers cholesterol and triglycerides in total plasma and in the VLD- and LD-lipoprotein fractions. [NIH] Nil: Nothing, zero. [EU] 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] Nitroglycerin: A highly volatile organic nitrate that acts as a dilator of arterial and venous smooth muscle and is used in the treatment of angina. It provides relief through improvement of the balance between myocardial oxygen supply and demand. Although total coronary blood flow is not increased, there is redistribution of blood flow in the heart when partial occlusion of coronary circulation is effected. [NIH] Nitrous Oxide: Nitrogen oxide (N2O). A colorless, odorless gas that is used as an anesthetic and analgesic. High concentrations cause a narcotic effect and may replace oxygen, causing death by asphyxia. It is also used as a food aerosol in the preparation of whipping cream. [NIH]
Nonmalignant: Not cancerous. [NIH] Nonmalignant hematologic disorders: leukemia. [NIH]
Disorders of the blood, some of which lead to
Non-small cell lung cancer: A group of lung cancers that includes squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear Matrix: The fibrogranular network of residual structural elements within which are immersed both chromatin and ribonucleoproteins. It extends throughout the nuclear interior from the nucleolus to the nuclear pore complexes along the nuclear periphery. [NIH] Nuclear Pore: An opening through the nuclear envelope formed by the nuclear pore complex which transports nuclear proteins or RNA into or out of the cell nucleus and which, under some conditions, acts as an ion channel. [NIH] Nuclear Proteins: Proteins found in the nucleus of a cell. Do not confuse with nucleoproteins which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH]
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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] Nucleoli: A small dense body (sub organelle) within the nucleus of eukaryotic cells, visible by phase contrast and interference microscopy in live cells throughout interphase. Contains RNA and protein and is the site of synthesis of ribosomal RNA. [NIH] Nucleolus: A small dense body (sub organelle) within the nucleus of eukaryotic cells, visible by phase contrast and interference microscopy in live cells throughout interphase. Contains RNA and protein and is the site of synthesis of ribosomal RNA. [NIH] Nucleoproteins: Proteins conjugated with nucleic acids. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] Nutritive Value: An indication of the contribution of a food to the nutrient content of the diet. This value depends on the quantity of a food which is digested and absorbed and the amounts of the essential nutrients (protein, fat, carbohydrate, minerals, vitamins) which it contains. This value can be affected by soil and growing conditions, handling and storage, and processing. [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] Occult: Obscure; concealed from observation, difficult to understand. [EU] Occult Bleeding: Blood in stool that is not visible to the naked eye. May be a sign of disease such as diverticulosis or colorectal cancer. [NIH] Occult Blood: Chemical, spectroscopic, or microscopic detection of extremely small amounts of blood. [NIH] Oesophagitis: Inflammation of the esophagus. [EU] Oligoelement: A chemical substance, minute amounts of which can be found in living organisms. [EU] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Omeprazole: A highly effective inhibitor of gastric acid secretion used in the therapy of gastric ulcers and Zollinger-Ellison syndrome. The drug inhibits the H(+)-K(+)-ATPase (H(+)-K(+)-exchanging ATPase) in a pH-dependent manner. This ATPase is considered the proton pump in the secretory membrane of the parietal cell. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH]
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Oncologist: A doctor who specializes in treating cancer. Some oncologists specialize in a particular type of cancer treatment. For example, a radiation oncologist specializes in treating cancer with radiation. [NIH] Oncology: The study of cancer. [NIH] On-line: A sexually-reproducing population derived from a common parentage. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Ophthalmic: Pertaining to the eye. [EU] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Opsin: A visual pigment protein found in the retinal rods. It combines with retinaldehyde to form rhodopsin. [NIH] Optic Disk: The portion of the optic nerve seen in the fundus with the ophthalmoscope. It is 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] Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Oral Hygiene: The practice of personal hygiene of the mouth. It includes the maintenance of oral cleanliness, tissue tone, and general preservation of oral health. [NIH] Oral Manifestations: Disorders of the mouth attendant upon non-oral disease or injury. [NIH]
Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Orthodontics: A dental specialty concerned with the prevention and correction of dental and oral anomalies (malocclusion). [NIH] Orthopaedic: Pertaining to the correction of deformities of the musculoskeletal system; pertaining to orthopaedics. [EU] Orthostatic: Pertaining to or caused by standing erect. [EU]
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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] 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] Osteomyelitis: Inflammation of bone caused by a pyogenic organism. It may remain localized or may spread through the bone to involve the marrow, cortex, cancellous tissue, and periosteum. [EU] 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] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Otitis Media: Inflammation of the middle ear. [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] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxaliplatin: An anticancer drug that belongs to the family of drugs called platinum compounds. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [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]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative metabolism: A chemical process in which oxygen is used to make energy from
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carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oximetry: The determination of oxygen-hemoglobin saturation of blood either by withdrawing a sample and passing it through a classical photoelectric oximeter or by electrodes attached to some translucent part of the body like finger, earlobe, or skin fold. It includes non-invasive oxygen monitoring by pulse oximetry. [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [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] Pallor: A clinical manifestation consisting of an unnatural paleness of the skin. [NIH] 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] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Papilledema: Swelling around the optic disk. [NIH] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [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 parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] 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] Parenteral: Not through the alimentary canal but rather by injection through some other
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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] 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] Parity: The number of offspring a female has borne. It is contrasted with gravidity, which refers to the number of pregnancies, regardless of outcome. [NIH] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Particle: A tiny mass of material. [EU] Parturition: The act or process of given birth to a child. [EU] Parvovirus: A genus of the family Parvoviridae, subfamily Parvovirinae, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is mice minute virus. [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 Advocacy: Promotion and protection of the rights of patients, frequently through a legal process. [NIH] Patient Compliance: regimen. [NIH]
Voluntary cooperation of the patient in following a prescribed
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] Pediatrics: A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence. [NIH] Pelvic: Pertaining to the pelvis. [EU] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease. [NIH]
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Penicillin: An antibiotic drug used to treat infection. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pentoxifylline: A methylxanthine derivative that inhibits phosphodiesterase and affects blood rheology. It improves blood flow by increasing erythrocyte and leukocyte flexibility. It also inhibits platelet aggregation. Pentoxifylline modulates immunologic activity by stimulating cytokine production. [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] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Pericarditis: Inflammation of the pericardium. [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] Periodontitis: simplex. [NIH]
Inflammation of the periodontal membrane; also called periodontitis
Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral stem cells: Immature cells found circulating in the bloodstream. New blood cells develop from peripheral stem cells. [NIH] Peripheral Vascular Disease: Disease in the large blood vessels of the arms, legs, and feet. People who have had diabetes for a long time may get this because major blood vessels in their arms, legs, and feet are blocked and these limbs do not receive enough blood. The signs of PVD are aching pains in the arms, legs, and feet (especially when walking) and foot sores that heal slowly. Although people with diabetes cannot always avoid PVD, doctors say they have a better chance of avoiding it if they take good care of their feet, do not smoke, and keep both their blood pressure and diabetes under good control. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and 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
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layer of the bowel wall. [NIH] Pernicious: Tending to a fatal issue. [EU] Pernicious anemia: A type of anemia (low red blood cell count) caused by the body's inability to absorb vitamin B12. [NIH] Peroxidase: A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7. [NIH] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] Pertussis: An acute, highly contagious infection of the respiratory tract, most frequently affecting young children, usually caused by Bordetella pertussis; a similar illness has been associated with infection by B. parapertussis and B. bronchiseptica. It is characterized by a catarrhal stage, beginning after an incubation period of about two weeks, with slight fever, sneezing, running at the nose, and a dry cough. In a week or two the paroxysmal stage begins, with the characteristic paroxysmal cough, consisting of a deep inspiration, followed by a series of quick, short coughs, continuing until the air is expelled from the lungs; the close of the paroxysm is marked by a long-drawn, shrill, whooping inspiration, due to spasmodic closure of the glottis. This stage lasts three to four weeks, after which the convalescent stage begins, in which paroxysms grow less frequent and less violent, and finally cease. Called also whooping cough. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Pharmacist: A person trained to prepare and distribute medicines and to give information about them. [NIH] Pharmacodynamics: The study of the biochemical and physiological effects of drugs and the mechanisms of their actions, including the correlation of actions and effects of drugs with their chemical structure; also, such effects on the actions of a particular drug or drugs. [EU]
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] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [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] Phenylacetate: A drug being studied in the treatment of cancer. [NIH] Phenylbutyrate: An anticancer drug that belongs to the family of drugs called differentiating agents. [NIH] Phenytoin: An anticonvulsant that is used in a wide variety of seizures. It is also an antiarrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited
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by its many adverse effects and interactions with other drugs. [NIH] Phlebotomy: The letting of blood from a vein. Although it is one of the techniques used in drawing blood to be used in diagnostic procedures, in modern medicine, it is used commonly in the treatment of erythrocytosis, hemochromocytosis, polycythemia vera, and porphyria cutanea tarda. Its historical counterpart is bloodletting. (From Cecil Textbook of Medicine, 19th ed & Wintrobe's Clinical Hematology, 9th ed) Venipuncture is not only for the letting of blood from a vein but also for the injecting of a drug into the vein for diagnostic analysis. [NIH] Phosphodiesterase: Effector enzyme that regulates the levels of a second messenger, the cyclic GMP. [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] Phosphorylated: 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] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Photodynamic therapy: Treatment with drugs that become active when exposed to light. These drugs kill cancer cells. [NIH] Photosensitivity: An abnormal cutaneous response involving the interaction between photosensitizing substances and sunlight or filtered or artificial light at wavelengths of 280400 mm. There are two main types : photoallergy and photoxicity. [EU] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] Physical Therapy: The restoration of function and the prevention of disability following disease or injury with the use of light, heat, cold, water, electricity, ultrasound, and exercise. [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]
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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] 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] 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] Plasmapheresis: Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use. [NIH] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] 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] Platelet Count: A count of the number of platelets per unit volume in a sample of venous blood. [NIH] Platelet Transfusion: The transfer of blood platelets from a donor to a recipient or reinfusion to the donor. [NIH] Plateletpheresis: The preparation of platelet concentrates with the return of red cells and
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platelet-poor plasma to the donor. [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]
Platinum Compounds: Inorganic compounds which contain platinum as the central atom. [NIH]
Pleura: The thin serous membrane enveloping the lungs and lining the thoracic cavity. [NIH] Pleural: A circumscribed area of hyaline whorled fibrous tissue which appears on the surface of the parietal pleura, on the fibrous part of the diaphragm or on the pleura in the interlobar fissures. [NIH] Pleural cavity: A space enclosed by the pleura (thin tissue covering the lungs and lining the interior wall of the chest cavity). It is bound by thin membranes. [NIH] Pleural Effusion: Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces. It is a sign of disease and not a diagnosis in itself. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] Podiatry: A specialty concerned with the diagnosis and treatment of foot disorders and injuries and anatomic defects of the foot. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Policy Making: The decision process by which individuals, groups or institutions establish policies pertaining to plans, programs or procedures. [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] Polycythemia Vera: A myeloproliferative disorder of unknown etiology, characterized by abnormal proliferation of all hematopoietic bone marrow elements and an absolute increase in red cell mass and total blood volume, associated frequently with splenomegaly, leukocytosis, and thrombocythemia. Hematopoiesis is also reactive in extramedullary sites (liver and spleen). In time myelofibrosis occurs. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation
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analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] 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] Polyneuritis: Inflammation of several peripheral nerves at the same time. [NIH] Polyp: A growth that protrudes from a mucous membrane. [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] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Porphyria: A group of disorders characterized by the excessive production of porphyrins or their precursors that arises from abnormalities in the regulation of the porphyrin-heme pathway. The porphyrias are usually divided into three broad groups, erythropoietic, hepatic, and erythrohepatic, according to the major sites of abnormal porphyrin synthesis. [NIH]
Porphyria Cutanea Tarda: A form of hepatic porphyria (porphyria, hepatic) characterized by photosensitivity resulting in bullae that rupture easily to form shallow ulcers. This condition occurs in two forms: a sporadic, nonfamilial form that begins in middle age and has normal amounts of uroporphyrinogen decarboxylase with diminished activity in the liver; and a familial form in which there is an autosomal dominant inherited deficiency of uroporphyrinogen decarboxylase in the liver and red blood cells. [NIH] Porphyrins: A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin. [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] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postoperative: After surgery. [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] Potentiate: 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
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the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [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] Precipitating Factors: Factors associated with the definitive onset of a disease, illness, accident, behavioral response, or course of action. Usually one factor is more important or more obviously recognizable than others, if several are involved, and one may often be regarded as "necessary". Examples include exposure to specific disease; amount or level of an infectious organism, drug, or noxious agent, etc. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] 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] 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] Preleukemia: Conditions in which the abnormalities in the peripheral blood or bone marrow represent the early manifestations of acute leukemia, but in which the changes are not of sufficient magnitude or specificity to permit a diagnosis of acute leukemia by the usual clinical criteria. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prenatal Diagnosis: Determination of the nature of a pathological condition or disease in the postimplantation embryo, fetus, or pregnant female before birth. [NIH] Preoperative: Preceding an operation. [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] Priapism: Persistent abnormal erection of the penis, usually without sexual desire, and accompanied by pain and tenderness. It is seen in diseases and injuries of the spinal cord, and may be caused by vesical calculus and certain injuries to the penis. [EU] 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
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cirrhosis in later stages of the disease. [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] Primum: The first atrial septum to appear in the embryonic heart. [NIH] Private Sector: That distinct portion of the institutional, industrial, or economic structure of a country that is controlled or owned by non-governmental, private interests. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Proctocolectomy: An operation to remove the colon and rectum. Also called coloproctectomy. [NIH] Progeny: The offspring produced in any generation. [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 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 disease: Cancer that is increasing in scope or severity. [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] Prophylaxis: An attempt to prevent disease. [NIH] Propidium: Quaternary ammonium analog of ethidium; an intercalating dye with a specific affinity to certain forms of DNA and, used as diiodide, to separate them in density gradients; also forms fluorescent complexes with cholinesterase which it inhibits. [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] 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
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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). 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] 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] 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 Isoforms: Different forms of a protein that may be produced from different genes, or from the same gene by alternative splicing. [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] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [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] Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia. [NIH]
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] Proton Pump: Integral membrane proteins that transport protons across a membrane against a concentration gradient. This transport is driven by hydrolysis of ATP by H(+)-
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transporting ATP synthase. [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] Protozoan: 1. any individual of the protozoa; protozoon. 2. of or pertaining to the protozoa; protozoal. [EU] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Psoralen: A substance that binds to the DNA in cells and stops them from multiplying. It is being studied in the treatment of graft-versus-host disease and is used in the treatment of psoriasis and vitiligo. [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [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] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] 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] 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]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, 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]
Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [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]
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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] Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pyelonephritis: Inflammation of the kidney and its pelvis, beginning in the interstitium and rapidly extending to involve the tubules, glomeruli, and blood vessels; due to bacterial infection. [EU] Pylorus: The opening in a vertebrate from the stomach into the intestine. [EU] Pyrexia: A fever, or a febrile condition; abnormal elevation of the body temperature. [EU] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [NIH] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and uracil) and form the basic structure of the barbiturates. [NIH] Pyruvate Kinase: ATP:pyruvate 2-O-phosphotransferase. A phosphotransferase that catalyzes reversibly the phosphorylation of pyruvate to phosphoenolpyruvate in the presence of ATP. It has four isozymes (L, R, M1, and M2). Deficiency of the enzyme results in hemolytic anemia. EC 2.7.1.40. [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] Quiescent: Marked by a state of inactivity or repose. [EU] Quinolinic: It is produced by immune cells and slowly infiltrates the brain tissues after an injury. [NIH] Quinolinic Acid: 2,3-Pyridinedicarboxylic acid. A metabolite of tryptophan with a possible role in neurodegenerative disorders. Elevated CSF levels of quinolinic acid are significantly correlated with the severity of neuropsychological deficits in patients who have AIDS. [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] 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] Radiation oncologist: A doctor who specializes in using radiation to treat cancer. [NIH] Radiation Oncology: A subspecialty of medical oncology and radiology concerned with the radiotherapy of cancer. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH]
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Radioimmunotherapy: Radiotherapy where cytotoxic radionuclides are linked to antibodies in order to deliver toxins directly to tumor targets. Therapy with targeted radiation rather than antibody-targeted toxins (immunotoxins) has the advantage that adjacent tumor cells, which lack the appropriate antigenic determinants, can be destroyed by radiation cross-fire. Radioimmunotherapy is sometimes called targeted radiotherapy, but this latter term can also refer to radionuclides linked to non-immune molecules (radiotherapy). [NIH] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [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] Reactivation: The restoration of activity to something that has been inactivated. [EU] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] 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] Recombinant: 1. 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] Reconstitution: 1. a type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. the restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH]
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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] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [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] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [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] Rehabilitation Centers: Facilities which provide programs for rehabilitating the mentally or physically disabled individuals. [NIH] Relapse: The return of signs and symptoms of cancer after a period of improvement. [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 cell cancer: Cancer that develops in the lining of the renal tubules, which filter the blood and produce urine. [NIH] Renal cell carcinoma: A type of kidney cancer. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal pelvis: The area at the center of the kidney. Urine collects here and is funneled into the ureter, the tube that connects the kidney to the bladder. [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] Repopulation: The replacement of functional cells, usually by proliferation, following or during irradiation. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes,
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which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Reproduction Techniques: Methods pertaining to the generation of new individuals. [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] Resection: Removal of tissue or part or all of an organ by surgery. [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] 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] Restless legs: Legs characterized by or showing inability to remain at rest. [EU] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Reticulocyte Count: Determination of the number of reticulocytes in a measured volume of blood. Values for reticulocytes are expressed as a percentage of the erythrocyte count or in the form of a so-called "corrected" reticulocyte "index". An increase in circulating reticulocytes, often referred to as reticulocytosis, is among the simplest and most reliable signs of accelerated erythrocyte production. Reticulocytosis, or an increased reticulocyte count, occurs during active blood regeneration (stimulation of red bone marrow) and in certain anemias, particularly congenital hemolytic anemia. [NIH] Reticulocytes: Immature erythrocytes. In humans, these are erythroid cells that have just undergone extrusion of their cell nucleus. They still contain some organelles that gradually decrease in number as the cells mature. ribosomes are last to disappear. Certain staining techniques cause components of the ribosomes to precipitate into characteristic "reticulum" (not the same as the endoplasmic reticulum), hence the name reticulocytes. [NIH] 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] Retinal Vein: Central retinal vein and its tributaries. It runs a short course within the optic nerve and then leaves and empties into the superior ophthalmic vein or cavernous sinus. [NIH]
Retinal Vein Occlusion: Occlusion of the retinal vein. Those at high risk for this condition include patients with hypertension, diabetes mellitus, arteriosclerosis, and other
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cardiovascular diseases. [NIH] Retinitis: Inflammation of the retina. It is rarely limited to the retina, but is commonly associated with diseases of the choroid (chorioretinitis) and of the optic nerve (neuroretinitis). The disease may be confined to one eye, but since it is generally dependent on a constitutional factor, it is almost always bilateral. It may be acute in course, but as a rule it lasts many weeks or even several months. [NIH] 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] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. retinitis (= inflammation of the retina). 2. retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retinosis: Non-inflammatory degeneration of the retina. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Rheology: The study of the deformation and flow of matter, usually liquids or fluids, and of the plastic flow of solids. The concept covers consistency, dilatancy, liquefaction, resistance to flow, shearing, thixotrophy, and viscosity. [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] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribavirin: 1-beta-D-Ribofuranosyl-1H-1,2,4-triazole-3-carboxamide. A nucleoside antimetabolite antiviral agent that blocks nucleic acid synthesis and is used against both RNA and DNA viruses. [NIH] Ribonucleoproteins: Proteins conjugated with ribonucleic acids (RNA) or specific RNA. Many viruses are ribonucleoproteins. [NIH] Ribonucleoside Diphosphate Reductase: An enzyme of the oxidoreductase class that catalyzes the formation of 2'-deoxyribonucleotides from the corresponding ribonucleotides using NADPH as the ultimate electron donor. The deoxyribonucleoside diphosphates are used in DNA synthesis. (From Dorland, 27th ed) EC 1.17.4.1. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Rickets:
A condition caused by deficiency of vitamin D, especially in infancy and
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childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Rituximab: A type of monoclonal antibody used in cancer detection or therapy. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [NIH] Rod: A reception for vision, located in the retina. [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 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] 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] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, hallucinations, emotional disharmony, and regressive behavior. [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
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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] 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] Scurvy: A deficiency disease due to lack of vitamin C in the diet. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [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] Segmental: Describing or pertaining to a structure which is repeated in similar form in successive segments of an organism, or which is undergoing segmentation. [NIH] 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] 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] Sensory loss: A disease of the nerves whereby the myelin or insulating sheath of myelin on the nerves does not stay intact and the messages from the brain to the muscles through the nerves are not carried properly. [NIH] Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] 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] Sequela: Any lesion or affection following or caused by an attack of disease. [EU] Sequence Analysis: A multistage process that includes the determination of a sequence (protein, carbohydrate, etc.), its fragmentation and analysis, and the interpretation of the resulting sequence information. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Sequester: A portion of dead bone which has become detached from the healthy bone tissue, as occurs in necrosis. [NIH]
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Serial Passage: Inoculation of a series of animals or in vitro tissue with an infectious bacterium or virus, as in virulence studies and the development of vaccines. [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] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [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] Serous: Having to do with serum, the clear liquid part of blood. [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] Serum Sickness: Immune complex disease caused by the administration of foreign serum or serum proteins and characterized by fever, lymphadenopathy, arthralgia, and urticaria. When they are complexed to protein carriers, some drugs can also cause serum sickness when they act as haptens inducing antibody responses. [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] Sexually Transmitted Diseases: Diseases due to or propagated by sexual contact. [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]
Shunt: A surgically created diversion of fluid (e.g., blood or cerebrospinal fluid) from one area of the body to another area of the body. [NIH] Sicca: Failure of lacrimal secretion, keratoconjunctivitis sicca, failure of secretion of the salivary glands and mucous glands of the upper respiratory tract and polyarthritis. [NIH] Sickle Cell Trait: The condition of being heterozygous for hemoglobin S. [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 receptor-
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mediated 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] Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to immunophilins. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skin Pigmentation: Coloration of the skin. [NIH] Skin test: A test for an immune response to a compound by placing it on or under the skin. [NIH]
Small cell lung cancer: A type of lung cancer in which the cells appear small and round when viewed under the microscope. Also called oat cell lung cancer. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smoldering leukemia: Disease in which the bone marrow does not function normally. Also called preleukemia or myelodysplastic syndrome. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [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] 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] Solvent: 1. dissolving; effecting a solution. 2. a liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] 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] Sorbitol: A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several
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research applications. [NIH] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Spasmodic: Of the nature of a spasm. [EU] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [NIH] 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]
Spectroscopic: The recognition of elements through their emission spectra. [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] Spherocytes: Small, abnormal spherical red blood cells with more than the normal amount of hemoglobin. [NIH] Spherocytosis: A condition in which there are abnormally thick, almost spherical, red blood cells or spherocytes in the blood. [NIH] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] 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] Spinal Cord Vascular Diseases: Hypoxic-ischemic and hemorrhagic disorders of the spinal cord. Arteriosclerosis, emboli, and vascular malformations are potential causes of these conditions. [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] Splenectomy: An operation to remove the spleen. [NIH] Splenomegaly: Enlargement of the spleen. [NIH]
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Spondylitis: Inflammation of the vertebrae. [EU] 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] Sports Medicine: The field of medicine concerned with physical fitness and the diagnosis and treatment of injuries sustained in sports activities. [NIH] Sprains and Strains: A collective term for muscle and ligament injuries without dislocation or fracture. A sprain is a joint injury in which some of the fibers of a supporting ligament are ruptured but the continuity of the ligament remains intact. A strain is an overstretching or overexertion of some part of the musculature. [NIH] Squamous: Scaly, or platelike. [EU] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cells: Flat cells that look like fish scales under a microscope. These cells cover internal and external surfaces of the body. [NIH] Stabilization: The creation of a stable state. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Standardize: To compare with or conform to a standard; to establish standards. [EU] Stasis: A word termination indicating the maintenance of (or maintaining) a constant level; preventing increase or multiplication. [EU] Steady state: Dynamic equilibrium. [EU] Steatosis: Fatty degeneration. [EU] Stem Cell Factor: Hematopoietic growth factor and the ligand of the c-kit receptor CD117 (proto-oncogene protein C-kit). It is expressed during embryogenesis and provides a key signal in multiple aspects of mast-cell differentiation and function. [NIH] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] 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]
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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] Stomatitis: Inflammation of the oral mucosa, due to local or systemic factors which may involve the buccal and labial mucosa, palate, tongue, floor of the mouth, and the gingivae. [EU]
Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [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]
Stroma: The middle, thickest layer of tissue in the cornea. [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] 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] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [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] 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]
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Substrate: A substance upon which an enzyme acts. [EU] Sudden cardiac death: Cardiac arrest caused by an irregular heartbeat. [NIH] Sulfadoxine: A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections. [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] Superinfection: A frequent complication of drug therapy for microbial infection. It may result from opportunistic colonization following immunosuppression by the primary pathogen and can be influenced by the time interval between infections, microbial physiology, or host resistance. Experimental challenge and in vitro models are sometimes used in virulence and infectivity studies. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [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] Supportive care: Treatment given to prevent, control, or relieve complications and side effects and to improve the comfort and quality of life of people who have cancer. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress activity, function, symptoms. [EU] 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 response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatology: 1. that branch of medicine with treats of symptoms; the systematic discussion of symptoms. 2. the combined symptoms of a disease. [EU] 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] 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]
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Systemic therapy: Treatment that uses substances that travel through the bloodstream, reaching and affecting cells all over the body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] T cell: One type of white blood cell that attacks virus-infected cells, foreign cells, and cancer cells. T cells also produce a number of substances that regulate the immune response. [NIH] Tapeworm: A flatworm that is an endoparasite and belongs to the class Cestoda. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Telomere: A terminal section of a chromosome which has a specialized structure and which is involved in chromosomal replication and stability. Its length is believed to be a few hundred base pairs. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Terminator: A DNA sequence sited at the end of a transcriptional unit that signals the end of transcription. [NIH] Testicular: Pertaining to a testis. [EU] 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] Tetani: Causal agent of tetanus. [NIH] Tetanic: Having the characteristics of, or relating to tetanus. [NIH] Tetanus: A disease caused by tetanospasmin, a powerful protein toxin produced by Clostridium tetani. Tetanus usually occurs after an acute injury, such as a puncture wound or laceration. Generalized tetanus, the most common form, is characterized by tetanic muscular contractions and hyperreflexia. Localized tetanus presents itself as a mild condition with manifestations restricted to muscles near the wound. It may progress to the generalized form. [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] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalassemia: A group of hereditary hemolytic anemias in which there is decreased synthesis of one or more hemoglobin polypeptide chains. There are several genetic types
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with clinical pictures ranging from barely detectable hematologic abnormality to severe and fatal anemia. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thiamine: 3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2methylthiazolium chloride. [NIH]
hydroxyethyl)-4-
Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Thioredoxin: A hydrogen-carrying protein that participates in a variety of biochemical reactions including ribonucleotide reduction. Thioredoxin is oxidized from a dithiol to a disulfide during ribonucleotide reduction. The disulfide form is then reduced by NADPH in a reaction catalyzed by thioredoxin reductase. [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] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thrombocytosis: Increased numbers of platelets in the peripheral blood. [EU] Thrombolytic: 1. dissolving or splitting up a thrombus. 2. a thrombolytic agent. [EU] 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]
Thrombopenia: Reduction in the number of platelets in the blood. [NIH] Thrombophilia: A disorder of hemostasis in which there is a tendency for the occurrence of thrombosis. [NIH] Thrombopoietin: A humoral factor that controls blood platelet production through stimulation of megakaryocyte populations. Bone marrow megakaryocytes increase in both size and number in response to exposure to thrombopoietin. [NIH] Thromboses: The formation or presence of a blood clot within a blood vessel during life. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thrush: A disease due to infection with species of fungi of the genus Candida. [NIH] Thymoma: A tumor of the thymus, an organ that is part of the lymphatic system and is located in the chest, behind the breastbone. [NIH] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH]
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Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, 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] Thyroiditis: Inflammation of the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Ticks: Blood-sucking arachnids of the order Acarina. [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] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [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] Tone: 1. the normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. a particular quality of sound or of voice. 3. to make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonicity: The normal state of muscular tension. [NIH] Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA topoisomerase. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [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]
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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] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] 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] Transaminase: Aminotransferase (= a subclass of enzymes of the transferase class that catalyse the transfer of an amino group from a donor (generally an amino acid) to an acceptor (generally 2-keto acid). Most of these enzymes are pyridoxal-phosphate-proteins. [EU]
Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] 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] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Transferases: Transferases are enzymes transferring a group, for example, the methyl group or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2. [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] Transfusion-Transmitted Virus: An unclassified, non-enveloped DNA virus associated with transfusions and hepatitis. However, no etiological role has been found for TTV in hepatitis, and evidence suggests it is not a Hepatovirus. [NIH] Transient Ischemic Attacks: Focal neurologic abnormalities of sudden onset and brief duration that reflect dysfunction in the distribution of the internal carotid-middle cerebral or the vertebrobasilar arterial system. [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] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH]
Dictionary 571
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] Transplantation Conditioning: Preparative treatment of transplant recipient with various conditioning regimens including radiation, immune sera, chemotherapy, and/or immunosuppressive agents, prior to transplantation. Transplantation conditioning is very common before bone marrow transplantation. [NIH] Transversion: A base-pair substitution mutation in which a purine-pyrimidine pair is replaced by the equivalent pyrimidine-purine pair, i. e. A-T becomes T-A. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]
Tricuspid Valve: The valve consisting of three cusps situated between the right atrium and right ventricle of the heart. [NIH] Trimetrexate: A nonclassical folic acid inhibitor through its inhibition of the enzyme dihydrofolate reductase. It is being tested for efficacy as an antineoplastic agent and as an antiparasitic agent against Pneumocystis carinii pneumonia in AIDS patients. Myelosuppression is its dose-limiting toxic effect. [NIH] Trisomy: The possession of a third chromosome of any one type in an otherwise diploid cell. [NIH] Trivalent: Having a valence of three. [EU] Trophic: Of or pertaining to nutrition. [EU] Tropical Medicine: The branch of medicine concerned with diseases, mainly of parasitic origin, common in tropical and subtropical regions. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [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] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] TYPHI: The bacterium that gives rise to typhoid fever. [NIH] Typhoid Fever: An acute systemic febrile infection caused by Salmonella typhi. [NIH] Typhoid Fever: An acute systemic febrile infection caused by Salmonella typhi. [NIH] Ulcer: A lesion on the surface of the skin or a mucous surface, produced by the sloughing of
572 Anemia
inflammatory necrotic tissue. [NIH] Ulceration: 1. the formation or development of an ulcer. 2. an ulcer. [EU] 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] Ultrasound test: A test that bounces sound waves off tissues and internal organs and changes the echoes into pictures (sonograms). [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] Umbilical cord blood: Blood from the placenta (afterbirth) that contains high concentrations of stem cells needed to produce new blood cells. [NIH] Umbilical cord blood transplantation: The injection of umbilical cord blood to restore an individual's own blood production system suppressed by anticancer drugs, radiation therapy, or both. It is being studied in the treatment of cancer and severe blood disorders such as aplastic anemia. Cord blood contains high concentrations of stem cells needed to produce new blood cells. [NIH] Univalent: Pertaining to an unpaired chromosome during the zygotene stage of prophase to first metaphase in meiosis. [NIH] Uracil: An anticancer drug that belongs to the family of drugs called alkylating agents. [NIH] Uraemia: 1. an excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. in current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]
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]
Uridine Diphosphate: A uracil nucleotide containing a pyrophosphate group esterified to C5 of the sugar moiety. [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
Dictionary 573
kidneys, ureters, bladder, and urethra. [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] 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] 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] 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] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginitis: Inflammation of the vagina characterized by pain and a purulent discharge. [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]
Valves: Flap-like structures that control the direction of blood flow through the heart. [NIH] Varicose: The common ulcer in the lower third of the leg or near the ankle. [NIH] Varicose Ulcer: Ulcer due to varicose veins. Chronic venous insufficiency in the deep veins of the legs leads to shunting the venous return into the superficial veins, in which pressure and flow rate, as well as oxygen content, are increased. [NIH] Varix: An enlarged, dilated, and tortuous venous channel. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoactive: Exerting an effect upon the calibre of blood vessels. [EU] 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] 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] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Venous Thrombosis: The formation or presence of a thrombus within a vein. [NIH] 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
574 Anemia
one's emotional problems. [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] Ventricular Dysfunction: A condition in which the ventricles of the heart exhibit a decreased functionality. [NIH] Ventricular Function: The hemodynamic and electrophysiological action of the ventricles. [NIH]
Ventricular Pressure: The pressure within a cardiac ventricle. Ventricular pressure waveforms can be measured in the beating heart by catheterization or estimated using imaging techniques (e.g., Doppler echocardiography). The information is useful in evaluating the function of the myocardium, cardiac valves, and pericardium, particularly with simultaneous measurement of other (e.g., aortic or atrial) pressures. [NIH] 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] Vertebral: Of or pertaining to a vertebra. [EU] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] Vesicular: 1. composed of or relating to small, saclike bodies. 2. pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Video Recording: The storing or preserving of video signals for television to be played back later via a transmitter or receiver. Recordings may be made on magnetic tape or discs (videodisc recording). [NIH] Videodisc Recording: The storing of visual and usually sound signals on discs for later reproduction on a television screen or monitor. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Hepatitis: Hepatitis caused by a virus. Five different viruses (A, B, C, D, and E) most commonly cause this form of hepatitis. Other rare viruses may also cause hepatitis. [NIH] Viremia: The presence of viruses in the blood. [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 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 Replication: The process of intracellular viral multiplication, consisting of the synthesis of proteins, nucleic acids, and sometimes lipids, and their assembly into a new
Dictionary 575
infectious particle. [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] Vitamin D: The vitamin that mediates intestinal calcium absorption, bone calcium metabolism, and probably muscle activity. It usually acts as a hormone precursor, requiring 2 stages of metabolism before reaching actual hormonal form. It is isolated from fish liver oils and used in the treatment and prevention of rickets. [NIH] Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached. [NIH] Vitreous: Glasslike or hyaline; often used alone to designate the vitreous body of the eye (corpus vitreum). [EU] 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] Wakefulness: A state in which there is an enhanced potential for sensitivity and an efficient responsiveness to external stimuli. [NIH] Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide. [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]
Whooping Cough: A respiratory infection caused by Bordetella pertussis and characterized by paroxysmal coughing ending in a prolonged crowing intake of breath. [NIH] Whooping Cough: A respiratory infection caused by Bordetella pertussis and characterized by paroxysmal coughing ending in a prolonged crowing intake of breath. [NIH] 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]
576 Anemia
Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] Xeroderma Pigmentosum: A rare, pigmentary, and atrophic autosomal recessive disease affecting all races. It is manifested as an extreme photosensitivity to ultraviolet light as the result of a deficiency in the enzyme that permits excisional repair of ultraviolet-damaged DNA. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [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] Zalcitabine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chainterminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy. [NIH] Zebrafish: A species of North American fishes of the family Cyprinidae. They are used in embryological studies and to study the effects of certain chemicals on development. [NIH] Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIVinduced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia. [NIH] Zoster: A virus infection of the Gasserian ganglion and its nerve branches, characterized by discrete areas of vesiculation of the epithelium of the forehead, the nose, the eyelids, and the cornea together with subepithelial infiltration. [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]
577
INDEX 5 5-Methoxytryptamine, 471 A Abdomen, 444, 471, 484, 504, 514, 524, 527, 528, 542, 543, 544, 563, 565, 568, 575 Abdominal, 471, 472, 499, 528, 542, 544, 572 Abdominal Pain, 471, 572 Aberrant, 19, 471 Ablation, 346, 471 Abscess, 471, 560 Acceptor, 471, 528, 541, 570 Acetaminophen, 471, 509 Acetylcholine, 471, 506, 537, 538 Aclarubicin, 471 Acquired Immunodeficiency Syndrome, 25, 471 Acremonium, 471, 488 Acute leukemia, 335, 341, 471, 550 Acute lymphoblastic leukemia, 471, 472 Acute lymphocytic leukemia, 471 Acute myelogenous leukemia, 22, 472 Acute myeloid leukemia, 472 Acute nonlymphocytic leukemia, 12, 472 Acute renal, 472, 516 Adaptability, 472, 488 Adaptation, 472, 547 Adenine, 472, 554 Adenocarcinoma, 472, 538 Adenoma, 29, 472 Adenosine, 54, 472, 546 Adenylate Kinase, 472 Adipocytes, 472, 527 Adjustment, 323, 442, 472 Adjuvant, 303, 472, 508, 510 Adjuvant therapy, 303, 472 Adolescence, 472, 543 Adrenal Cortex, 472, 495, 551, 556 Adrenal Glands, 472, 475 Adrenergic, 473, 478, 501 Adsorption, 473 Adsorptive, 473 Adverse effect, 39, 342, 397, 406, 473, 546, 561 Aerobic, 11, 473, 476, 487, 506, 534, 542 Aerobic metabolism, 473, 542 Aerobic respiration, 473, 542 Aerosol, 473, 538 Afferent, 473, 527 Affinity, 20, 41, 473, 480, 530, 551, 562 Agar, 473, 492 Age Distribution, 473 Age Groups, 44, 473
Aged, 80 and over, 473 Agenesis, 473 Agglutinins, 473 Albumin, 474, 547 Aldehydes, 474 Alimentary, 474, 542, 543 Alkylating Agents, 50, 474, 485, 572 Alleles, 18, 474, 511, 517, 518 Allo, 474 Allogeneic bone marrow transplantation, 341, 474 Allograft, 13, 474, 537 Alopecia, 407, 474, 496 Alpha Cell, 474, 512 Alpha Particles, 474, 554 Alpha-fetoprotein, 474, 508 Alpha-Thalassemia, 474, 516 Alternative medicine, 416, 474 Alternative Splicing, 55, 57, 474, 552 Alveoli, 475, 573 Ameliorated, 475 Ameliorating, 54, 475 Amifostine, 336, 475 Amino Acid Sequence, 475, 477, 507, 511 Amino Acid Substitution, 56, 475, 516 Amlodipine, 475 Ammonia, 475, 512, 572 Amnion, 475 Amniotic Fluid, 475 Ampulla, 475, 503 Amputation, 15, 475 Amyl Nitrite, 475 Amyloidosis, 475 Anaemia, 290, 291, 475, 531 Anaerobic, 334, 476, 487, 535 Anaerobic Threshold, 334, 476 Anaesthesia, 476, 522 Anal, 476, 529 Analgesic, 404, 471, 476, 499, 506, 534, 538 Analog, 37, 293, 476, 527, 551 Analytes, 436, 476 Anaphylatoxins, 476, 493 Anatomical, 476, 481, 490, 503, 521, 560 Androgenic, 476, 497 Androgens, 456, 472, 476, 495 Anemia, Sickle Cell, 334, 340, 476 Anesthesia, 328, 476 Angina, 15, 475, 476, 538 Angina Pectoris, 475, 476 Angiogenesis, 53, 477 Angiography, 405, 477 Angiosarcoma, 477
578 Anemia
Angiotensin-Converting Enzyme Inhibitors, 477, 478 Animal model, 16, 41, 44, 51, 477 Anions, 474, 477, 525, 561, 566 Anisotropy, 477, 508 Annealing, 477, 548 Anomalies, 18, 50, 477, 540, 567 Anorexia, 477, 513, 572 Anterior Cerebral Artery, 477, 489 Anthracycline, 471, 477, 497, 520 Anthrax, 477 Antiallergic, 477, 495, 496 Antibacterial, 477, 563 Antibiotic, 315, 410, 471, 477, 484, 487, 497, 501, 520, 534, 544, 563, 567 Antibodies, Anticardiolipin, 477, 479 Antibodies, Antiphospholipid, 478, 479 Antibody therapy, 478 Anticoagulant, 50, 478, 479, 552, 575 Anticonvulsant, 478, 545 Antiemetic, 478, 533 Antifungal, 478, 526, 562 Antigen-Antibody Complex, 478, 493 Antigen-presenting cell, 478, 498 Antihypertensive, 406, 478 Antihypertensive Agents, 406, 478 Anti-infective, 478, 519, 525 Anti-inflammatory, 318, 471, 478, 495, 499, 506, 512, 550 Anti-Inflammatory Agents, 478, 495 Antimetabolite, 478, 481, 533, 558 Antimycotic, 478, 491 Antineoplastic, 471, 474, 478, 479, 481, 483, 495, 496, 501, 519, 533, 534, 562, 569, 571 Antineoplastic Agents, 474, 479 Antioxidant, 293, 304, 479, 480, 541, 542 Antiphospholipid Syndrome, 477, 479 Antipruritic, 479, 490, 496 Antipyretic, 471, 479, 499 Antisickling Agents, 479 Antithymocyte globulin, 332, 335, 338, 344, 479 Antituberculosis, 315, 479 Antiviral, 479, 506, 524, 558 Antrectomy, 479 Anuria, 479, 526 Aorta, 479, 486, 515, 574 Apheresis, 332, 479 Aplasia, 33, 305, 326, 341, 350, 479 Applicability, 32, 479 Aqueous, 479, 482, 497, 519, 527, 528 Arachidonic Acid, 479, 551 Arginine, 330, 337, 459, 476, 480, 518, 538, 571 Arginine butyrate, 337, 459, 480
Arterial, 8, 10, 334, 406, 479, 480, 489, 519, 527, 538, 552, 567, 570 Arteries, 479, 480, 483, 489, 495, 515, 533, 536, 553, 572 Arterioles, 480, 483, 486, 533, 536 Arteriosclerosis, 480, 557, 563 Arteriovenous, 480, 533 Artery, 54, 334, 340, 405, 477, 480, 483, 486, 495, 502, 533, 553, 572, 574 Arthralgia, 480, 561 Ascorbic Acid, 303, 480, 519 Aseptic, 345, 480, 540, 564 Aspergillosis, 480 Asphyxia, 480, 538 Aspiration, 326, 480, 508 Assay, 17, 21, 32, 37, 46, 57, 480, 521 Astrocytes, 480, 524 Asymptomatic, 8, 62, 480, 482, 542 Ataxia, 32, 51, 480, 518, 567 Atrial, 480, 551, 574, 575 Atrial Fibrillation, 480, 575 Atrium, 480, 481, 486, 534, 571, 574 Atrophy, 481, 528 Atypical, 481, 522 Auditory, 481, 506 Autoantibodies, 478, 481 Autoantigens, 481 Autodigestion, 481, 542 Autoimmune disease, 332, 478, 481, 535 Autoimmunity, 481 Autologous, 16, 24, 28, 36, 331, 346, 481, 515 Autologous bone marrow transplantation, 481, 515 Autonomic, 471, 475, 481, 510, 535, 566 Autosuggestion, 481, 520 Azacitidine, 338, 481 B Bacillus, 477, 481, 485 Bacteria, 326, 473, 477, 478, 481, 482, 494, 498, 502, 504, 505, 507, 513, 514, 516, 532, 533, 535, 547, 555, 563, 570, 573 Bacterial Infections, 481, 488, 492 Bacterial Physiology, 472, 481 Bacteriophage, 481, 570, 574 Bacterium, 481, 494, 516, 561, 571 Basal Ganglia, 480, 481 Basal Ganglia Diseases, 480, 481 Base, 37, 46, 57, 472, 482, 490, 496, 498, 511, 526, 567, 571, 572 Basophils, 482, 514, 527 Benign, 472, 482, 497, 514, 537, 555, 559 Beta-Lactamases, 482, 487 Bifida, 482 Bile, 316, 482, 490, 509, 510, 517, 518, 526, 528, 550, 565 Bile Acids, 482, 510, 565
Index 579
Bile duct, 482, 490, 509, 550 Bile Pigments, 482, 526 Biliary, 482, 490, 517, 542 Biliary Tract, 482, 542 Bilirubin, 27, 474, 482, 509, 519 Bioavailability, 4, 291, 482 Biochemical reactions, 482, 568 Biological response modifier, 482, 523 Biological therapy, 482, 514 Biopsy, 326, 336, 346, 351, 482, 506 Biopterin, 483, 537 Biosynthesis, 40, 480, 483, 491, 537, 561 Biotechnology, 22, 33, 52, 54, 62, 404, 416, 425, 483 Biotinylation, 36, 483 Bladder, 483, 493, 521, 535, 552, 556, 572, 573 Blasts, 343, 483 Bleeding Time, 483 Bleomycin, 21, 483 Blood Cell Count, 27, 440, 441, 444, 483, 515, 545 Blood Coagulation, 483, 485, 568 Blood Glucose, 5, 483, 516, 523 Blood Platelets, 483, 531, 547, 561, 568 Blood Viscosity, 483, 516 Blood Volume, 483, 548 Blot, 23, 483 Body Fluids, 483, 485, 537, 562, 571 Body Mass Index, 483, 541 Bolus, 483, 484 Bolus infusion, 484 Bone marrow aspiration, 326, 329, 336, 350, 484 Bone marrow biopsy, 331, 339, 346, 440, 484 Bone Marrow Cells, 21, 37, 484, 492, 514, 531, 535 Bone Marrow Examination, 329, 484 Bone metastases, 484, 491 Bone scan, 19, 484, 559 Bowel, 4, 476, 484, 499, 522, 524, 527, 544, 565, 572 Bowel Movement, 484, 499, 565 Brachytherapy, 484, 524, 525, 554, 576 Bradykinin, 484, 538, 547 Branch, 418, 465, 484, 497, 502, 529, 543, 553, 563, 566, 568, 571 Breakdown, 484, 499 Breast Feeding, 417, 418, 484 Breeding, 18, 484, 511 Broad-spectrum, 484, 487, 488 Bronchioles, 475, 484 Bronchiolitis, 484 Bronchiseptica, 485, 545 Buffers, 485, 563 Bulimia, 485
Busulfan, 337, 485 Bypass, 485 C Cachexia, 485 Cadmium, 485 Cadmium Poisoning, 485 Calcium, 297, 475, 478, 485, 491, 492, 508, 519, 542, 552, 561, 567, 575 Calcium channel blocker, 475, 478, 485 Calcium Channel Blockers, 478, 485 Callus, 485, 502 Calmodulin, 485, 508 Calorimeter, 34, 485 Candidiasis, 485 Candidosis, 485 Capillary, 483, 484, 486, 510, 511, 574 Capsid, 486 Capsules, 457, 486, 511 Carbohydrate, 486, 495, 512, 513, 539, 549, 560 Carbon Dioxide, 334, 486, 510, 547, 557, 573 Carcinogenesis, 50, 486 Carcinogenic, 474, 486, 523, 539, 551, 565 Carcinogens, 486, 490, 539, 541 Carcinoma, 486, 538 Cardiolipins, 479, 486 Cardiomegaly, 486 Cardiopulmonary, 486, 516 Cardiopulmonary Bypass, 486, 516 Cardiotoxic, 486 Cardiovascular, 9, 10, 11, 13, 14, 15, 407, 486, 506, 558, 561 Cardiovascular disease, 10, 12, 14, 15, 486, 558 Carnitine, 11, 298, 303, 486 Carotene, 316, 486, 557 Carpal Tunnel Syndrome, 302, 486 Case series, 487, 491 Caspase, 487 Catabolism, 34, 487, 572 Catalase, 40, 487 Catalyse, 487, 570 Cataracts, 487 Catheter, 330, 334, 336, 346, 487 Catheterization, 487, 574 Causal, 487, 516, 567 Causality, 16, 487 Cause of Death, 344, 487 Cavernous Sinus, 487, 557 Cefotetan, 487 Ceftriaxone, 487 Cell Adhesion, 487, 523 Cell Aging, 60, 488 Cell Count, 332, 336, 349, 440, 488 Cell Cycle, 22, 32, 488, 491 Cell Death, 41, 479, 488, 536
580 Anemia
Cell Differentiation, 488, 561, 564 Cell Division, 481, 488, 497, 514, 524, 534, 547, 560 Cell Lineage, 488 Cell membrane, 485, 488, 491, 498, 546 Cell proliferation, 22, 336, 480, 488, 524, 561 Cell Respiration, 473, 488, 534, 542, 557 Cell Size, 488, 508 Cell Survival, 22, 488, 514 Cell Transplantation, 18, 309, 331, 332, 340, 341, 346, 350, 351, 437, 488, 515, 564 Central Nervous System, 471, 488, 506, 510, 512, 515, 518, 534, 535, 540, 561 Central Nervous System Infections, 488, 515, 518 Centrifugation, 488, 515 Cephalosporins, 317, 482, 488 Cerebellar, 480, 489, 556 Cerebral Arteries, 489, 533 Cerebral Cortex, 480, 489, 508 Cerebral Infarction, 42, 49, 489, 519 Cerebral Palsy, 407, 489 Cerebrospinal, 489, 518, 561 Cerebrospinal fluid, 489, 518, 561 Cerebrovascular, 27, 42, 44, 482, 485, 486, 489, 567 Cerebrum, 489 Cervical, 330, 339, 489, 531, 559 Cervix, 489 Character, 476, 489, 498, 512 Cheilitis, 489 Chelation, 308, 313, 347, 349, 489 Chelation Therapy, 347, 349, 489 Chemotactic Factors, 489, 493 Chemotherapeutic agent, 38, 489 Chest Pain, 301, 327, 338, 348, 419, 489 Chicken Anemia Virus, 60, 61, 489 Child Care, 290, 291, 489 Chimeras, 28, 489 Chin, 294, 309, 490, 532 Chiropractic, 407, 490 Chloroquine, 45, 62, 490 Cholangitis, 490 Cholelithiasis, 490 Cholesterol, 323, 490, 495, 509, 528, 532, 538, 565 Cholestyramine, 490 Choroid, 44, 490, 557, 558 Chromatin, 32, 479, 490, 538 Chromium, 297, 490 Chromosomal, 22, 32, 35, 37, 490, 511, 518, 534, 547, 558, 567 Chromosome, 18, 33, 35, 37, 55, 57, 62, 490, 494, 517, 526, 528, 560, 567, 571, 572 Chromosome Breakage, 35, 490 Chronic granulocytic leukemia, 490
Chronic leukemia, 490, 514 Chronic lymphocytic leukemia, 338, 490 Chronic myelogenous leukemia, 490 Cirrhosis, 491, 515, 551 CIS, 491, 521, 557 Cisplatin, 55, 330, 339, 491 Citrus, 480, 491 C-kit receptor, 491, 564 Clear cell carcinoma, 491, 499 Cleave, 491 Cleft Palate, 491 Clinical study, 327, 491, 495 Clinical trial, 15, 17, 24, 27, 42, 325, 342, 351, 425, 491, 495, 496, 543, 552, 555 Clodronate, 491 Clone, 22, 32, 37, 56, 491 Cloning, 16, 23, 35, 37, 56, 483, 491 Clotrimazole, 336, 337, 491 Coagulation, 50, 479, 483, 491, 517, 547, 568, 575 Codon, 37, 491, 511 Coenzyme, 304, 480, 492, 508 Cofactor, 46, 492, 552, 568 Colitis, 312, 492 Collagen, 50, 475, 492, 494, 508, 510, 547, 551 Colloidal, 474, 492, 502, 561 Colon, 313, 410, 492, 500, 522, 525, 527, 551, 572 Colon Polyps, 410, 492 Colony-Stimulating Factors, 492, 514 Colorectal, 492, 539 Colorectal Cancer, 492, 539 Combination Therapy, 329, 331, 492 Common Variable Immunodeficiency, 492 Complement, 26, 36, 44, 47, 290, 476, 492, 493, 511, 523, 526, 530, 547 Complement 3, 493 Complement Activation, 476, 493 Complement Factor D, 26, 493 Complementary and alternative medicine, 301, 302, 320, 493 Complementary medicine, 302, 493 Complementation, 17, 18, 20, 21, 22, 23, 32, 35, 37, 50, 346, 493 Complete remission, 493, 556 Compliance, 493 Computational Biology, 425, 493 Computed tomography, 334, 493, 494, 559 Computerized axial tomography, 493, 494, 559 Computerized tomography, 493, 494 Conception, 494, 508, 550, 564 Concomitant, 494 Cone, 494 Confusion, 494, 500, 520, 572
Index 581
Congestion, 494, 505 Congestive heart failure, 291, 494 Conjugated, 494, 497, 536, 538, 539, 558 Conjugation, 494, 512 Connective Tissue, 479, 480, 484, 492, 494, 508, 510, 529, 532, 558, 559, 565, 566 Connective Tissue Diseases, 479, 494 Consciousness, 476, 494, 498, 500, 553 Constipation, 446, 494 Constriction, 494, 525 Consumption, 306, 308, 334, 407, 494, 499, 539, 542 Contamination, 494, 517 Contraception, 345, 494 Contractility, 477, 494 Contraindications, ii, 494 Contrast medium, 477, 495 Control group, 44, 48, 495 Controlled clinical trial, 31, 495 Controlled study, 495 Coordination, 495, 535 Cornea, 495, 526, 560, 565, 576 Coronary, 15, 53, 405, 476, 486, 495, 519, 533, 536, 538 Coronary Arteriosclerosis, 495, 536 Coronary Disease, 495 Coronary heart disease, 486, 495 Coronary Thrombosis, 495, 533, 536 Coronary Vessels, 495 Cortex, 495, 506, 533, 541, 556 Cortical, 495, 506, 560, 567 Corticosteroid, 329, 495, 550, 565 Cortisol, 474, 495 Cost Savings, 33, 496 Cranial, 496, 514, 525, 540 Craniocerebral Trauma, 482, 496, 515, 518, 567, 569 Creatinine, 6, 8, 9, 15, 48, 345, 496, 526, 572 Critical Illness, 496 Crossing-over, 496, 555 Cross-Sectional Studies, 47, 496 Cultured cells, 59, 293, 496 Curative, 17, 496, 559, 568 Cutaneous, 477, 485, 496, 527, 529, 546 Cyanide, 496, 533 Cyanosis, 496, 516 Cyclic, 485, 496, 514, 538, 546, 549, 552 Cyclophosphamide, 307, 332, 341, 344, 496 Cyclosporine, 13, 329, 332, 335, 338, 349, 496, 521 Cyproheptadine, 496 Cyst, 496 Cysteine, 57, 496, 566 Cytarabine, 496 Cytidine, 481, 496 Cytochrome, 34, 497
Cytogenetics, 35, 408, 497 Cytokine, 35, 47, 497, 524, 544, 562 Cytomegalovirus, 339, 497 Cytomegalovirus Retinitis, 497 Cytopenia, 293, 497 Cytoplasm, 59, 61, 479, 482, 488, 497, 504 Cytoskeleton, 26, 40, 497, 523 Cytotoxic, 56, 58, 321, 497, 521, 555, 562 Cytotoxic chemotherapy, 497 Cytotoxicity, 491, 497 D Daclizumab, 326, 497 Danazol, 497 Daunorubicin, 471, 497, 501 De novo, 342, 343, 497 Deamination, 497, 572 Decitabine, 413, 497 Defense Mechanisms, 498, 523 Deferoxamine, 304, 340, 351, 456, 498 Degenerative, 498, 517, 541, 558 Dehydration, 347, 498 Deletion, 16, 37, 58, 60, 479, 498, 511 Delirium, 498 Dementia, 471, 498 Denaturation, 498, 548 Dendrites, 498 Dendritic, 24, 498 Dendritic cell, 24, 498 Density, 43, 483, 488, 498, 508, 528, 540, 551, 563 Dental Care, 407, 498 Dental Caries, 498 Depolarization, 498, 561 Deprivation, 41, 499 Dermatitis, 489, 499 Dermatology, 407, 499 Desensitization, 499, 521 Detoxification, 34, 499 Developing Countries, 50, 290, 309, 499 Dexamethasone, 348, 499 Diabetes Mellitus, 499, 512, 516, 557 Diabetic Retinopathy, 5, 499, 546 Diagnostic procedure, 35, 353, 416, 499, 546 Diaphragm, 499, 517, 548 Diarrhea, 468, 490, 499, 513, 525 Diastole, 499 Diastolic, 8, 406, 499, 519 Diclofenac, 499 Diclofenac Sodium, 499 Diethylstilbestrol, 499 Digestion, 4, 474, 484, 499, 501, 524, 528, 565 Digestive system, 352, 499, 510 Digestive tract, 444, 499, 562, 564 Dihydrotestosterone, 499, 556 Dilatation, 10, 500, 551, 573
582 Anemia
Dilator, 500, 538 Dilution, 500, 505 Diphtheria, 500 Diploid, 493, 500, 547, 571 Direct, iii, 9, 10, 16, 23, 27, 28, 29, 32, 37, 40, 45, 50, 401, 455, 476, 500, 501, 556 Discrimination, 324, 500 Disease Progression, 10, 31, 46, 322, 500 Disorientation, 494, 498, 500 Dissociation, 473, 500, 525 Dissociative Disorders, 500 Distal, 500, 510, 553 Diuretics, Thiazide, 478, 500 Diverticulosis, 500, 539 Diverticulum, 500 Dizziness, 327, 444, 468, 500, 574 Dopamine, 500, 533, 537 Dose-dependent, 53, 501, 576 Doxorubicin, 471, 501 Doxycycline, 53, 501 Drug Interactions, 458, 501 Drug Resistance, 28, 501 Drug Tolerance, 501, 569 Dumping Syndrome, 496, 501 Duodenum, 482, 501, 503, 526, 535, 542, 565 Dura mater, 487, 501, 532, 542 Dyspepsia, 410, 501 Dysphagia, 410, 501 Dysplasia, 501 Dystrophy, 408, 501 E Eating Disorders, 407, 501 Echocardiography, 501, 574 Ectopic, 25, 501 Edema, 497, 499, 501, 519, 525, 572 Effector, 24, 471, 492, 501, 546 Effector cell, 24, 501 Effusion, 502, 530 Elastic, 502, 512, 563 Elastin, 492, 494, 502 Elective, 60, 502 Electrocardiogram, 334, 346, 502 Electrocoagulation, 491, 502 Electrolyte, 495, 498, 502, 516, 526, 533, 549, 562, 572 Electrons, 479, 482, 502, 525, 541, 554, 555 Electrophoresis, 502 Electrophysiological, 502, 574 Emaciation, 471, 502 Emboli, 502, 563, 575 Embolism, 502, 553, 575 Embolization, 502, 575 Embolus, 502, 522 Embryo, 475, 488, 502, 522, 550, 564, 572 Embryo Transfer, 502, 550 Embryogenesis, 35, 502, 564
Emesis, 503 Emollient, 503, 513 Enamel, 498, 503 Encapsulated, 503, 528 Encephalitis, 503 Encephalomyelitis, 503 Endemic, 43, 503, 530, 564 Endocarditis, 485, 503 Endocardium, 503 Endocrine Glands, 19, 503, 542 Endogenous, 22, 481, 500, 503, 512, 541 Endometrial, 400, 503 Endometriosis, 400, 401, 497, 503 Endometrium, 503 Endoscope, 503, 504 Endoscopic, 405, 503, 510 Endothelial cell, 503, 568 Endothelium, 39, 503, 504, 538, 547 Endothelium, Lymphatic, 503 Endothelium, Vascular, 503 Endothelium-derived, 504, 538 Endotoxin, 504, 571 End-stage renal, 14, 406, 446, 491, 504, 548 Energy balance, 34, 504, 527 Enhancer, 55, 504 Enteroscopy, 405, 504 Environmental Health, 424, 426, 504 Enzyme Inhibitors, 504, 547 Eosinophil, 504, 514 Epidemic, 504, 564 Epidermal, 504 Epidermis, 504, 554 Epidermoid carcinoma, 504, 564 Epigastric, 504, 542 Epiphyseal, 504 Epiphyses, 504 Epithelial, 470, 472, 504, 517, 524, 537 Epithelial Cells, 504, 517, 524 Epithelium, 503, 504, 510, 576 Epitopes, 30, 58, 504 Erectile, 446, 505, 544 Erection, 505, 550 ERV, 445, 505, 507 Erythema, 46, 312, 505, 573 Erythema Infectiosum, 46, 505 Erythroblasts, 338, 505 Erythrocyte Count, 505, 557 Erythrocyte Indices, 483, 505 Erythrocyte Transfusion, 505 Erythrocyte Volume, 44, 483, 505 Erythroid Progenitor Cells, 10, 18, 505 Erythroleukemia, 505 Erythropoiesis, 4, 9, 29, 31, 33, 36, 43, 47, 49, 505 Esophageal, 410, 505, 510 Esophageal Varices, 410, 505
Index 583
Esophagitis, 505, 510 Esophagus, 499, 505, 510, 529, 539, 545, 556, 565 Estrogen, 506, 551 Ethidium, 506, 551 Etodolac, 506 Eukaryotic Cells, 506, 539, 540 Euphoria, 475, 506 Evacuation, 494, 506, 527 Evaluable patients, 6, 506 Evoked Potentials, 52, 506 Excisional, 506, 576 Excitation, 506, 508, 537 Excitatory, 506, 512 Excrete, 479, 506, 526 Exercise Test, 506 Exercise Tolerance, 46, 506 Exfoliation, 506, 536 Exhaustion, 419, 506, 530 Exocrine, 506, 542 Exogenous, 473, 503, 506, 512 Exon, 55, 474, 507 Expiratory, 505, 507 Expiratory Reserve Volume, 505, 507 External-beam radiation, 507, 525, 554, 576 Extracellular, 480, 494, 507, 508, 523, 562, 567 Extracellular Matrix, 494, 507, 508, 523 Extravascular, 507 Extremity, 507, 527, 531 F Family Planning, 408, 425, 507 Fat, 472, 479, 484, 486, 495, 502, 507, 527, 528, 535, 539, 541, 558, 562 Fatty acids, 24, 474, 507, 512, 513, 551 Fatty Liver, 507 Febrile, 507, 531, 554, 571 Feces, 494, 507, 565 Ferric Compounds, 507 Fertilization in Vitro, 507, 550 Fetal Blood, 507 Fetal Death, 46, 507 Fetal Hemoglobin, 16, 24, 39, 330, 346, 507 Fetoprotein, 508 Fetus, 53, 349, 474, 505, 507, 508, 520, 547, 550, 564, 565, 572, 573 Fibrin, 483, 508, 547, 568 Fibrinogen, 50, 508, 547, 568 Fibroblasts, 41, 322, 508, 524 Fibronectin, 25, 508 Fibrosis, 407, 450, 451, 508, 560 Fissure, 491, 508 Flow Cytometry, 508 Fludarabine, 337, 508 Flunarizine, 508 Fluorescence, 57, 506, 508
Fluorescence Polarization, 57, 508 Fluorescent Dyes, 508 Flushing, 509 Fold, 508, 509, 542 Folic Acid, 291, 295, 297, 306, 444, 445, 456, 509, 571 Forearm, 483, 509, 531 Founder Effect, 60, 509 Frameshift Mutation, 509 Free Radicals, 479, 500, 509 Frontal Lobe, 477, 489, 509 Fructose, 509, 517, 525 Fulminant Hepatic Failure, 509 Fungi, 478, 480, 494, 509, 514, 533, 564, 568, 576 Fungus, 485, 488, 509 G Gallbladder, 410, 471, 482, 499, 509, 510 Gallstones, 410, 490, 509 Gamma Rays, 509, 554, 555 Ganglia, 471, 475, 481, 510, 537, 566 Ganglionic Blockers, 478, 510 Gas exchange, 476, 510, 557, 573 Gastrectomy, 306, 496, 510 Gastric Acid, 319, 510, 539 Gastric Antral Vascular Ectasia, 510 Gastric atrophy, 510 Gastric Mucosa, 510 Gastrin, 510, 518 Gastritis, 510 Gastroesophageal Reflux, 410, 510 Gastroesophageal Reflux Disease, 410, 510 Gastrointestinal, 4, 5, 50, 51, 52, 405, 407, 410, 484, 485, 501, 510, 531, 561, 565, 571 Gastrointestinal Hemorrhage, 50, 510 Gastrointestinal tract, 510, 561, 571 Gelatin, 510, 513, 568 Gene Deletion, 511 Gene Expression, 20, 28, 41, 53, 55, 56, 511 Gene Frequency, 511 Gene Therapy, 17, 18, 21, 25, 32, 35, 37, 344, 345, 511 Genetic Code, 511, 539 Genetic Counseling, 32, 451, 511 Genetic Engineering, 483, 491, 511 Genetic Techniques, 511 Genetic testing, 511, 549 Genotype, 22, 330, 511, 545 Geriatric, 511 Gestation, 290, 511, 544, 547, 564 Gland, 472, 511, 529, 537, 542, 547, 552, 560, 565, 569 Glomerular, 8, 9, 511, 512, 525, 526, 556 Glomerular Filtration Rate, 8, 9, 511, 526 Glomeruli, 511, 512, 554 Glomerulonephritis, 512
584 Anemia
Glomerulosclerosis, 512 Glomerulus, 511, 512, 537 Glossitis, 512 Glottis, 512, 545 Glucagonoma, 512 Glucocorticoid, 499, 512, 550 Glucokinase, 512, 517 Glucose Intolerance, 499, 512 Glucuronosyltransferase, 27, 512 Glutamate, 512 Glutamic Acid, 509, 512, 516, 537, 551 Glutamine, 39, 334, 512 Glutathione Peroxidase, 294, 512 Gluten, 512 Glycerol, 486, 512, 513, 546 Glycerol Kinase, 513 Glycerophospholipids, 513, 546 Glycine, 475, 513, 537, 561 Glycols, 513, 519 Glycoprotein, 27, 33, 50, 322, 505, 508, 513, 514, 525, 530, 568, 571 Glycosylation, 513 Gonadal, 513, 565 Gonads, 19, 513, 520 Governing Board, 513, 550 Government Agencies, 407, 513, 550 Grade, 302, 337, 513 Graft, 325, 337, 342, 479, 513, 518, 535, 553 Graft Rejection, 325, 513 Graft vs Host Disease, 337, 513 Graft vs Host Reaction, 513 Grafting, 513 Graft-versus-host disease, 479, 513, 535, 553 Gram-negative, 485, 487, 513, 535 Gram-positive, 487, 514 Granulocyte, 492, 514 Granulocyte Colony-Stimulating Factor, 492, 514 Granulocyte-Macrophage Colony-Stimulating Factor, 492, 514 Granulocytopenia, 514 Granulomas, 514 Grasses, 509, 514 Gravidity, 514, 543 Groin, 336, 514 Growth factors, 33, 514 Guanylate Cyclase, 514, 538 H Haematemesis, 503, 514 Hairy cell leukemia, 514 Half-Life, 487, 514 Haplotypes, 514 Haptens, 473, 514, 561 Headache, 327, 468, 505, 514, 515, 518, 520 Headache Disorders, 515 Health Status, 417, 515
Heart attack, 486, 515 Heart failure, 14, 15, 331, 406, 414, 415, 477, 515 Heart Valves, 515 Heartbeat, 446, 515, 566 Helminths, 515, 522 Hematocrit, 6, 7, 9, 10, 11, 13, 39, 43, 397, 406, 407, 417, 418, 419, 436, 440, 445, 469, 483, 505, 515 Hematologic Diseases, 515 Hematologic malignancies, 24, 515 Hematologist, 17, 326, 515 Hematopoiesis, 32, 35, 41, 50, 402, 515, 548 Hematopoietic growth factors, 28, 515 Hematopoietic Stem Cell Transplantation, 25, 337, 515 Hematopoietic Stem Cells, 28, 60, 515 Hematopoietic tissue, 40, 484, 515 Hematuria, 515 Heme, 40, 404, 406, 497, 515, 516, 536, 549 Hemochromatosis, 27, 58, 451, 515 Hemodiafiltration, 515 Hemodilution, 52, 516 Hemodynamics, 516 Hemofiltration, 515, 516 Hemoglobin, 5, 6, 7, 8, 9, 11, 12, 13, 15, 16, 19, 20, 26, 31, 37, 39, 40, 47, 48, 49, 52, 62, 327, 330, 340, 346, 348, 349, 397, 406, 409, 417, 418, 419, 436, 440, 442, 444, 469, 474, 476, 482, 483, 496, 505, 507, 515, 516, 527, 542, 549, 561, 563, 567 Hemoglobin A, 16, 330, 346, 349, 406, 444, 516, 549 Hemoglobin C, 13, 15, 348, 407, 440, 442, 476, 505, 507, 516 Hemoglobin H, 507, 516 Hemoglobin M, 348, 496, 516 Hemoglobinopathies, 28, 31, 42, 327, 340, 403, 511, 516 Hemoglobinuria, 448, 516 Hemolysis, 337, 516 Hemophilia, 310, 450, 516 Hemorrhage, 50, 496, 497, 502, 514, 516, 554, 565, 575 Hemosiderin, 517 Hemosiderosis, 517 Hemostasis, 517, 523, 561, 568 Hepatic, 29, 57, 292, 308, 345, 474, 498, 517, 528, 549 Hepatitis A, 517 Hepatobiliary, 27, 517 Hepatocellular, 308, 517 Hepatocytes, 45, 517 Hepatomegaly, 517, 522 Heredity, 511, 517 Heritability, 44, 517
Index 585
Hernia, 517 Herpes, 302, 339, 517 Herpes virus, 339, 517 Heterodimers, 517, 523 Heterogeneity, 26, 473, 517 Heterozygote, 51, 517 Hexokinase, 39, 517 Hiatal Hernia, 517 Histamine, 317, 476, 496, 508, 517, 518 Histidine, 294, 518 Histone Deacetylase, 23, 518 Histones, 490, 518 Homeostasis, 22, 29, 40, 518 Homogeneous, 518 Homologous, 21, 34, 58, 474, 496, 511, 516, 517, 518, 560, 566 Homozygote, 518 Hookworm, 50, 518 Hormonal, 400, 481, 495, 518, 575 Hormone therapy, 348, 472, 518 Humoral, 53, 513, 518, 568 Humour, 518 Hybrid, 23, 491, 518 Hybridization, 23, 518 Hybridomas, 518, 524 Hydrocephalus, 518, 525 Hydrogen, 471, 482, 485, 486, 487, 498, 512, 519, 528, 534, 537, 541, 566, 568, 576 Hydrogen Peroxide, 487, 512, 519, 528, 566 Hydrolysis, 482, 491, 519, 546, 549, 552, 571 Hydrops Fetalis, 519 Hydroxides, 519 Hydroxyl Radical, 519 Hydroxylysine, 492, 519 Hydroxyproline, 475, 492, 519 Hyperbilirubinemia, 519, 526 Hypercalcemia, 491, 519 Hyperhomocysteinemia, 48, 519 Hyperplasia, 519 Hyperreflexia, 519, 567 Hypersensitivity, 18, 23, 32, 50, 499, 504, 519, 558 Hypertrophy, 10, 14, 405, 486, 510, 519 Hypervitaminosis, 519 Hypnotics and Sedatives, 471, 519 Hypogammaglobulinemia, 492, 519 Hypoglycaemia, 498, 520 Hypoglycemia, 520 Hypogonadism, 520 Hypotension, 510, 520 Hypothermia, 516, 520 Hypoxia, 5, 19, 61, 476, 498, 520, 567 Hypoxic, 54, 520, 563 I Iatrogenic, 520
Id, 295, 309, 436, 437, 447, 450, 464, 466, 520, 532 Ida, 438, 520 Idarubicin, 520 Idiopathic, 60, 450, 520 Idiopathic myelofibrosis, 520 Ileum, 520, 526 Imidazole, 491, 517, 520 Immune function, 11, 46, 328, 520, 521 Immune Tolerance, 520 Immunity, 44, 62, 326, 471, 520, 524, 570 Immunization, 51, 520, 551 Immunoassay, 477, 521 Immunodeficiency syndrome, 440, 492, 521 Immunofluorescence, 21, 521 Immunoglobulin, 58, 477, 521, 534 Immunologic, 4, 36, 489, 520, 521, 544, 555, 576 Immunology, 31, 43, 53, 472, 473, 508, 521 Immunophilins, 521, 562 Immunosuppressant, 474, 521, 533, 562 Immunosuppression, 326, 331, 344, 439, 521, 530, 540, 566 Immunosuppressive Agents, 521, 571 Immunosuppressive therapy, 415, 521 Impairment, 8, 52, 59, 306, 321, 480, 498, 521, 532 Implant radiation, 521, 524, 525, 554, 576 Impotence, 446, 505, 521 In situ, 35, 521 In vivo, 18, 19, 24, 28, 33, 37, 53, 511, 521, 530, 541 Incision, 521, 525 Incompetence, 510, 521 Incontinence, 518, 521, 535 Incubation, 522, 527, 545 Incubation period, 522, 527, 545 Indicative, 398, 522, 543, 573 Indolent, 522 Induction, 10, 43, 56, 57, 61, 406, 476, 510, 522, 551 Infancy, 33, 291, 346, 522, 558 Infant Mortality, 452, 522 Infantile, 522, 528 Infarction, 15, 42, 489, 522 Infectious Mononucleosis, 522 Infertility, 522 Infestation, 522 Infiltration, 512, 522, 576 Inflammatory bowel disease, 4, 29, 410, 522 Informed Consent, 27, 522 Infusion, 6, 54, 326, 332, 334, 347, 522, 570 Ingestion, 47, 49, 59, 306, 477, 485, 519, 523, 548, 567 Inhalation, 473, 475, 523, 548 Initiation, 7, 334, 523
586 Anemia
Initiator, 523, 524 Inlay, 523, 557 In-line, 45, 523 Inner ear, 487, 523 Inoculum, 46, 523 Inorganic, 472, 491, 507, 519, 523, 525, 535, 548 Insight, 13, 18, 37, 523 Insulator, 28, 523, 535 Insulin, 523 Insulin-dependent diabetes mellitus, 523 Insulin-like, 523 Integrins, 50, 523 Intensive Care, 294, 334, 523 Interferon-alpha, 523 Interleukin-1, 55, 524 Interleukin-10, 55, 524 Interleukin-11, 524 Interleukin-12, 524 Interleukin-2, 326, 524 Interleukin-3, 492, 524 Interleukin-6, 524 Interleukins, 521, 524 Intermittent, 308, 505, 524, 544 Internal radiation, 524, 525, 554, 576 Interphase, 524, 539 Interstitial, 484, 524, 525, 537, 556, 576 Intervertebral, 524, 529 Intervertebral Disk Displacement, 524, 529 Intestinal, 50, 408, 486, 524, 530, 575 Intestinal Mucosa, 50, 524 Intestine, 484, 492, 504, 524, 527, 554 Intoxication, 498, 524, 575 Intracellular, 26, 37, 41, 45, 485, 511, 522, 523, 525, 532, 538, 549, 552, 561, 574 Intracranial Hypertension, 515, 518, 525, 569 Intramuscular, 525, 543 Intravascular, 25, 36, 525 Intrinsic, 470, 473, 525 Intrinsic Factor, 525 Inulin, 511, 525 Invasive, 3, 59, 351, 520, 525, 530, 542 Involuntary, 481, 525, 536, 562 Iodine, 298, 525 Ionization, 525 Ionizing, 21, 22, 474, 525, 555 Ions, 482, 485, 490, 500, 502, 519, 525, 552 Iron Compounds, 525 Irradiation, 333, 490, 525, 556, 576 Ischemia, 19, 481, 525, 535 Ischemic Colitis, 525 Isoenzyme, 517, 525 Isozymes, 526, 554 J Jaundice, 468, 519, 526 Jejunum, 526
Joint, 30, 302, 400, 480, 526, 541, 564, 566 K Karyotype, 526 Kb, 62, 424, 526 Keratoconjunctivitis, 526, 561 Keratoconjunctivitis Sicca, 526, 561 Keto, 526, 570 Ketoconazole, 526 Kidney Failure, 442, 504, 512, 526 Kidney Failure, Acute, 526 Kidney Failure, Chronic, 526 Kidney stone, 302, 526 Kidney Transplantation, 526 Kinetic, 525, 526 L Labile, 492, 526 Laceration, 527, 567 Lacrimal, 526, 527, 561 Lactation, 527, 551 Lamivudine, 527 Large Intestine, 492, 499, 524, 527, 555, 562 Larynx, 512, 527, 570 Latent, 527, 550 Laxative, 473, 527, 562 Leg Ulcer, 345, 527 Leiomyosarcoma, 527 Leishmaniasis, 527 Lens, 487, 527, 575 Lentivirus, 18, 28, 56, 527 Leptin, 527 Lesion, 527, 529, 560, 571 Lethal, 58, 59, 496, 527 Leucine, 527 Leucocyte, 504, 527, 529 Leukapheresis, 335, 479, 527 Leukocytes, 482, 483, 484, 489, 523, 524, 527, 528, 545, 571 Leukocytosis, 528, 548 Leukoencephalopathy, 528 Leukopenia, 513, 528, 576 Libido, 476, 528 Library Services, 464, 528 Life Expectancy, 51, 528 Ligament, 528, 552, 564 Ligands, 523, 528 Linkages, 516, 518, 528, 576 Lipid, 45, 480, 512, 523, 526, 528, 535, 542 Lipid Peroxidation, 45, 528, 542 Lipodystrophy, 528 Lipoprotein, 513, 528, 538 Liposomal, 528 Liposome, 528 Liver cancer, 474, 528 Liver Cirrhosis, 528 Liver scan, 528, 559 Liver Transplantation, 528
Index 587
Living will, 408, 529 Lobe, 477, 489, 529, 543 Localization, 22, 32, 58, 59, 529 Localized, 61, 475, 498, 500, 503, 522, 528, 529, 535, 541, 547, 567, 573 Longitudinal Studies, 496, 529 Longitudinal study, 34, 529 Loop, 318, 517, 529 Low Back Pain, 529 Lower Esophageal Sphincter, 510, 529 Lumbar, 524, 529 Lupus, 334, 408, 477, 479, 529, 566 Lutein Cells, 529, 551 Lymph, 53, 414, 489, 503, 518, 522, 529, 537, 559, 561 Lymph node, 489, 529, 537, 559 Lymphadenopathy, 522, 529, 561 Lymphatic, 54, 311, 439, 503, 522, 529, 532, 559, 562, 563, 568 Lymphatic system, 529, 559, 562, 563, 568 Lymphoblastic, 529 Lymphoblasts, 22, 471, 529 Lymphocyte, 30, 40, 47, 49, 56, 321, 471, 478, 521, 530, 531 Lymphocyte Count, 471, 530 Lymphocyte Depletion, 521, 530 Lymphocytic, 341, 530 Lymphocytosis, 530 Lymphoid, 341, 477, 527, 530 Lymphoma, 302, 305, 306, 437, 515, 529, 530 Lymphopenia, 530 Lymphoproliferative, 342, 530 Lymphoproliferative Disorders, 530 Lysine, 516, 518, 519, 530, 571 Lytic, 530, 561, 574 M Macrolides, 318, 410, 530 Macrophage, 47, 59, 492, 514, 524, 530 Macrophage Colony-Stimulating Factor, 492, 530 Magnetic Resonance Imaging, 19, 334, 346, 530, 559 Major Histocompatibility Complex, 514, 530 Malabsorption, 306, 530 Malaria, Falciparum, 530, 531 Malaria, Vivax, 530, 531 Malignancy, 22, 25, 51, 326, 415, 531 Malignant, 302, 343, 471, 472, 478, 528, 531, 535, 537, 555, 559 Malignant tumor, 531, 535 Malnutrition, 474, 481, 485, 531 Malondialdehyde, 531 Manifest, 45, 531 Maternal Mortality, 406, 531 Meat, 406, 531 Medial, 480, 531
Median Nerve, 486, 531 Mediate, 18, 24, 50, 501, 531 Mediator, 29, 531, 561 Medical Oncology, 293, 531, 554 Medicament, 531 Medication Errors, 531 MEDLINE, 425, 531 Megakaryocytes, 484, 524, 531, 568 Membrane Lipids, 532, 546 Membrane Proteins, 532, 552, 563 Memory, 30, 498, 532 Meninges, 487, 488, 496, 501, 532 Meningitis, 311, 532 Menorrhagia, 5, 311, 532 Menstruation, 5, 401, 407, 532 Mental Disorders, 352, 532, 551, 553 Mental Health, v, 14, 328, 352, 408, 424, 427, 532, 551, 553 Mental Processes, 500, 532, 553 Mercury, 508, 532 Mesenchymal, 514, 530, 532 Meta-Analysis, 7, 532 Metabolic acidosis, 476, 532 Metabolic disorder, 26, 451, 532 Metabolite, 45, 323, 532, 554 Metastasis, 532, 533 Metastatic, 533, 560 Methionine, 533, 566 Methotrexate, 28, 533 Methylene Blue, 533 Methylprednisolone, 533 Methyltransferase, 481, 533 Metoclopramide, 533 MI, 470, 533 Mice Minute Virus, 533, 543 Microbe, 533, 569 Microbiology, 30, 32, 52, 472, 481, 533 Microcirculation, 19, 37, 516, 528, 533, 547 Micronutrients, 4, 533 Microorganism, 492, 533, 543, 575 Micro-organism, 498, 533 Microscopy, 533, 539 Middle Cerebral Artery, 533 Migration, 47, 59, 533 Mineralocorticoids, 472, 495, 533 Mitochondria, 40, 59, 293, 534, 540 Mitochondrial Swelling, 534, 536 Mitomycin, 18, 50, 534 Mitosis, 479, 534 Mitral Valve, 534 Mobility, 534 Mobilization, 25, 335, 534 Modeling, 24, 534 Modification, 16, 475, 511, 534, 554, 576 Modulator, 47, 49, 534 Monitor, 45, 330, 418, 496, 534, 538, 574
588 Anemia
Monoclonal, 325, 497, 518, 525, 534, 554, 559, 576 Monocyte, 334, 530, 534 Monogenic, 44, 534 Mononuclear, 336, 522, 530, 534, 571 Morphine, 534, 536 Morphological, 406, 411, 502, 509, 534 Morphology, 350, 515, 534 Mosaicism, 50, 61, 534 Motilin, 410, 534 Motility, 410, 535, 561 Motor Activity, 535 Mucosa, 510, 529, 535, 551, 565 Mucus, 535, 572 Multiple Myeloma, 535 Multiple sclerosis, 408, 535 Muscle relaxant, 535, 545 Muscle Spindles, 535, 545 Muscular Dystrophies, 501, 535 Musculoskeletal System, 535, 540 Mutagenesis, 37, 50, 535 Mutagenic, 37, 474, 535 Mutagens, 490, 509, 535 Mycophenolate mofetil, 293, 329, 349, 535 Mycoplasma, 488, 535 Myelin, 535, 560 Myelitis, 535 Myelodysplasia, 12, 343, 535 Myelofibrosis, 311, 536, 548 Myelogenous, 535, 536 Myeloma, 536 Myocardial infarction, 15, 495, 533, 536, 575 Myocardial Ischemia, 405, 476, 495, 536 Myocarditis, 500, 536 Myocardium, 476, 533, 536, 574 Myoglobin, 406, 536, 549 Myopathy, 40, 303, 536 N Narcosis, 536 Narcotic, 39, 534, 536, 538 Natriuresis, 477, 536 Natural killer cells, 524, 536 Natural selection, 26, 40, 536 Nausea, 478, 536, 572 NCI, 1, 329, 339, 343, 344, 348, 352, 423, 491, 536 Necrolysis, 536 Necrosis, 345, 479, 489, 497, 522, 533, 536, 560 Neonatal, 36, 40, 292, 522, 536 Neoplasia, 537 Neoplasm, 537, 559 Neoplastic, 5, 518, 530, 537 Neoplastic Processes, 5, 537 Neopterin, 48, 537 Nephrectomy, 537
Nephritis, 537 Nephroblastoma, 537 Nephropathy, 15, 526, 537 Nephrosis, 537 Nephrotic, 537 Nervous System, 52, 470, 473, 488, 531, 537, 565, 566 Neural, 473, 508, 510, 518, 537 Neuroblastoma, 537 Neurologic, 518, 537, 570 Neuropathy, 40, 537, 576 Neurophysiology, 290, 498, 537 Neurotransmitter, 471, 472, 475, 484, 500, 512, 513, 518, 537, 561, 565 Neutrons, 474, 525, 537, 554 Neutropenia, 341, 538 Neutrophil, 334, 538 Niceritrol, 538 Nil, 538 Nitric Oxide, 47, 54, 55, 292, 330, 333, 348, 538 Nitrogen, 323, 476, 496, 512, 526, 538, 571 Nitroglycerin, 348, 538 Nitrous Oxide, 20, 538 Nonmalignant, 341, 342, 538 Nonmalignant hematologic disorders, 342, 538 Non-small cell lung cancer, 305, 307, 538 Nuclear Matrix, 32, 538 Nuclear Pore, 538 Nuclear Proteins, 21, 538 Nuclei, 16, 20, 474, 477, 494, 502, 511, 518, 530, 534, 537, 538, 540, 559 Nucleic acid, 486, 506, 511, 518, 535, 538, 539, 554, 558, 574, 576 Nucleoli, 539 Nucleolus, 538, 539 Nucleoproteins, 538, 539 Nutritional Status, 8, 49, 290, 539 Nutritive Value, 290, 539 O Observational study, 6, 539 Occult, 405, 539 Occult Bleeding, 405, 539 Occult Blood, 539 Oesophagitis, 539 Oligoelement, 290, 539 Oliguria, 526, 539 Omeprazole, 318, 539 Oncogene, 539, 564 Oncogenic, 523, 527, 539 Oncologist, 17, 540 On-line, 467, 540 Opacity, 487, 498, 540 Open Reading Frames, 527, 540 Operon, 540, 557
Index 589
Ophthalmic, 540, 557 Opportunistic Infections, 471, 540 Opsin, 540, 557, 558 Optic Disk, 499, 540, 542 Optic Nerve, 540, 542, 557, 558, 560 Oral Health, 540 Oral Hygiene, 540 Oral Manifestations, 540 Organ Culture, 540, 569 Organ Transplantation, 338, 540 Organelles, 488, 497, 540, 557 Orthodontics, 408, 540 Orthopaedic, 540 Orthostatic, 540 Osmotic, 474, 534, 541, 561 Osteoarthritis, 506, 541 Osteomyelitis, 541 Osteoporosis, 335, 342, 347, 541 Otitis, 541 Otitis Media, 541 Outpatient, 329, 347, 541 Ovary, 513, 541, 565 Overdose, 509, 541 Overweight, 294, 418, 541 Ovum, 511, 541, 551, 575, 576 Oxaliplatin, 541 Oxidants, 40, 541 Oxidation, 40, 45, 471, 479, 497, 512, 516, 528, 541, 542 Oxidation-Reduction, 541 Oxidative metabolism, 45, 473, 541 Oxidative Stress, 40, 542 Oximetry, 542 Oxygen Consumption, 476, 506, 542, 557 Oxygenation, 19, 52, 542 P Pachymeningitis, 532, 542 Palate, 491, 542, 565 Palliative, 542, 568 Pallor, 468, 542 Pancreas, 451, 471, 474, 499, 510, 515, 523, 542, 571 Pancreatic, 414, 486, 510, 512, 542 Pancreatic cancer, 414, 542 Pancreatic Juice, 510, 542 Pancreatitis, 410, 542 Papilledema, 542 Parasite, 43, 45, 50, 542 Parasitic, 45, 49, 311, 407, 515, 518, 522, 542, 571 Parathyroid, 542, 559, 567 Parathyroid Glands, 542, 559 Parenteral, 16, 293, 294, 307, 542, 543 Parenteral Nutrition, 543 Parietal, 477, 539, 543, 544, 548 Parity, 418, 543
Paroxysmal, 448, 476, 515, 543, 545, 575 Partial remission, 543, 556 Particle, 528, 543, 563, 570, 575 Parturition, 543, 551 Parvovirus, 46, 505, 533, 543 Pathogen, 522, 523, 543, 566 Pathogenesis, 14, 23, 24, 29, 30, 35, 40, 42, 47, 49, 50, 53, 59, 294, 400, 410, 411, 543 Pathologic, 29, 40, 476, 479, 482, 486, 495, 519, 543, 553, 573 Pathologic Processes, 479, 543 Pathophysiology, 4, 14, 20, 24, 27, 29, 31, 36, 37, 39, 41, 44, 291, 399, 543 Patient Advocacy, 451, 543 Patient Compliance, 9, 33, 543 Patient Education, 9, 322, 418, 439, 441, 445, 446, 462, 464, 470, 543 Patient Selection, 5, 543 Pelvic, 503, 543, 552 Pelvis, 471, 527, 529, 543, 554, 573 Penicillamine, 543 Penicillin, 319, 543, 544, 573 Penis, 544, 550 Pentoxifylline, 544 Peptide, 29, 61, 475, 527, 544, 549, 552 Perception, 301, 494, 544, 559 Perennial, 306, 544 Perfusion, 19, 308, 334, 520, 544 Pericarditis, 544 Pericardium, 544, 566, 574 Perinatal, 522, 544 Periodontitis, 544 Peripheral stem cells, 513, 544 Peripheral Vascular Disease, 508, 544 Peritoneal, 12, 397, 406, 446, 544 Peritoneal Cavity, 544 Peritoneal Dialysis, 12, 397, 406, 446, 544 Peritoneum, 544 Peroxidase, 35, 528, 545 Peroxide, 545 Pertussis, 545, 575 Phagocyte, 530, 541, 545 Phagocytosis, 45, 545 Pharmacist, 545 Pharmacodynamics, 36, 545 Pharmacokinetic, 33, 545 Pharmacologic, 41, 476, 514, 545, 570 Pharynx, 510, 545 Phenotype, 22, 23, 34, 37, 40, 41, 44, 346, 493, 511, 545 Phenylacetate, 545 Phenylbutyrate, 24, 39, 338, 346, 459, 545 Phenytoin, 545 Phlebotomy, 44, 45, 546 Phosphodiesterase, 544, 546 Phospholipases, 546, 561
590 Anemia
Phospholipids, 478, 479, 486, 507, 528, 532, 546 Phosphorus, 485, 542, 546 Phosphorylated, 23, 492, 546 Phosphorylation, 61, 472, 546, 554 Photocoagulation, 491, 546 Photodynamic therapy, 546 Photosensitivity, 546, 549, 576 Physical Examination, 326, 330, 331, 334, 336, 339, 340, 345, 346, 546 Physical Fitness, 546, 564 Physical Therapy, 408, 546 Physiologic, 406, 483, 514, 525, 532, 533, 546, 551, 555 Physiology, 36, 293, 502, 510, 515, 537, 546, 566 Pigment, 349, 482, 536, 540, 546 Pilot study, 39, 46, 546 Pituitary Gland, 495, 547 Placenta, 507, 547, 551, 572 Plants, 484, 486, 491, 512, 525, 534, 547, 559, 564, 570 Plasma cells, 477, 535, 536, 547 Plasma protein, 474, 503, 547, 552, 561 Plasmapheresis, 479, 547 Plasmid, 25, 547, 573 Plasmin, 547 Plasminogen, 27, 547 Plasminogen Activators, 547 Plasticity, 516, 547 Platelet Activation, 547, 562 Platelet Aggregation, 293, 476, 538, 544, 547 Platelet Count, 349, 547 Platelet Transfusion, 52, 350, 547 Plateletpheresis, 479, 547 Platelets, 326, 331, 335, 336, 338, 343, 345, 507, 538, 547, 548, 568 Platinum, 491, 529, 541, 548 Platinum Compounds, 541, 548 Pleura, 548 Pleural, 548 Pleural cavity, 548 Pleural Effusion, 548 Pneumonia, 45, 339, 495, 548, 571 Pneumonitis, 46, 485, 548 Podiatry, 408, 548 Poisoning, 485, 489, 498, 524, 532, 533, 536, 548 Policy Making, 513, 548 Polyarthritis, 526, 548, 561 Polycystic, 419, 548 Polycythemia Vera, 311, 546, 548 Polymerase, 61, 548, 557 Polymerase Chain Reaction, 548 Polymers, 39, 549, 552 Polymorphic, 33, 549
Polymorphism, 33, 44, 549 Polyneuritis, 500, 549 Polyp, 549 Polypeptide, 61, 475, 492, 507, 508, 518, 534, 536, 547, 549, 551, 552, 567, 576 Polyposis, 492, 549 Polysaccharide, 478, 549 Porphyria, 546, 549 Porphyria Cutanea Tarda, 546, 549 Porphyrins, 549 Posterior, 476, 480, 490, 542, 549, 560 Postmenopausal, 406, 541, 549 Postnatal, 549, 564 Postoperative, 5, 506, 549 Postsynaptic, 549, 561 Potassium, 298, 500, 533, 549 Potentiate, 524, 549 Potentiation, 549, 562 Practicability, 550, 571 Practice Guidelines, 11, 15, 397, 427, 447, 550 Precipitating Factors, 487, 515, 550 Preclinical, 18, 24, 550 Precursor, 479, 496, 500, 501, 514, 537, 547, 550, 552, 571, 573, 575 Predisposition, 22, 25, 50, 51, 550 Prednisolone, 533, 550 Prednisone, 329, 335, 550 Pregnancy Outcome, 406, 418, 439, 550 Preleukemia, 535, 550, 562 Prenatal, 23, 502, 550 Prenatal Diagnosis, 23, 550 Preoperative, 307, 550 Priapism, 442, 550 Primary Biliary Cirrhosis, 291, 550 Primary Prevention, 38, 551 Primum, 551 Private Sector, 305, 551 Probe, 551 Proctocolectomy, 551 Progeny, 24, 28, 494, 551 Progesterone, 551, 565 Prognostic factor, 551 Progression, 10, 12, 19, 22, 31, 291, 477, 551 Progressive disease, 520, 551 Prolactin, 551 Proline, 492, 519, 551 Promoter, 551 Prone, 19, 22, 551 Prophylaxis, 302, 508, 551, 558, 573, 575 Propidium, 551 Proportional, 15, 337, 551 Prospective study, 529, 551 Prostaglandin, 477, 551 Prostate, 311, 348, 408, 552, 571 Protease, 50, 492, 552
Index 591
Protein Conformation, 475, 552 Protein Isoforms, 474, 552 Protein S, 404, 483, 511, 552, 567 Proteinuria, 512, 535, 552 Proteolytic, 492, 508, 547, 552 Prothrombin, 27, 552, 568 Protocol, 18, 25, 27, 29, 328, 329, 333, 336, 344, 552 Proton Pump, 319, 539, 552 Protozoa, 494, 527, 533, 553, 564 Protozoan, 488, 530, 553 Proximal, 54, 500, 553, 560 Psoralen, 553 Psoriasis, 553, 558 Psychiatric, 532, 553 Psychiatry, 553, 565, 573 Psychic, 528, 532, 553, 560 Psychoactive, 553, 575 Psychology, 500, 553 Psychomotor, 498, 553 Public Policy, 322, 425, 553 Publishing, 4, 5, 54, 553 Pulmonary Edema, 526, 553 Pulmonary Embolism, 553, 575 Pulmonary hypertension, 333, 340, 553 Pulmonary Ventilation, 334, 553 Pulse, 534, 542, 553 Purines, 554, 561 Purpura, 326, 450, 554 Purulent, 471, 554, 573 Pyelonephritis, 404, 554 Pylorus, 501, 510, 554 Pyrexia, 554 Pyridoxal, 554, 570 Pyrimidines, 554, 561 Pyruvate Kinase, 55, 56, 554 Q Quiescent, 488, 554, 575 Quinolinic, 554 Quinolinic Acid, 554 R Race, 34, 328, 400, 401, 526, 533, 554 Radiation oncologist, 540, 554 Radiation Oncology, 554 Radiation therapy, 330, 339, 343, 472, 507, 524, 525, 554, 572, 576 Radioactive, 484, 514, 519, 521, 524, 525, 528, 538, 539, 554, 555, 559, 576 Radioimmunotherapy, 555 Radioisotope, 505, 555 Radiolabeled, 525, 554, 555, 576 Radiological, 27, 555 Radiology, 554, 555 Radiotherapy, 337, 341, 484, 525, 554, 555, 576
Randomized, 31, 302, 305, 307, 308, 329, 330, 336, 339, 343, 344, 348, 451, 502, 555 Randomized clinical trial, 555 Reactivation, 555 Reactive Oxygen Species, 22, 555 Reagent, 555 Recombination, 21, 61, 494, 511, 555 Reconstitution, 555 Rectum, 484, 492, 499, 521, 522, 527, 551, 552, 555 Recurrence, 329, 556 Red Nucleus, 480, 556 Reductase, 27, 29, 34, 533, 556, 568, 571 Refer, 1, 473, 492, 500, 509, 517, 529, 538, 555, 556, 560, 570 Reflux, 510, 556 Refraction, 477, 556, 563 Regeneration, 555, 556, 557 Regimen, 28, 313, 325, 329, 333, 336, 337, 342, 346, 501, 543, 556 Regurgitation, 510, 515, 556 Rehabilitation Centers, 408, 556 Relapse, 325, 329, 331, 332, 335, 338, 344, 556 Remission, 29, 293, 331, 556 Renal cell cancer, 556 Renal cell carcinoma, 556 Renal failure, 10, 14, 33, 53, 291, 303, 327, 397, 404, 419, 441, 442, 446, 498, 548, 556, 572 Renal pelvis, 526, 556 Renin, 10, 477, 556 Renin-Angiotensin System, 477, 556 Repopulation, 21, 28, 556 Repressor, 23, 540, 556 Reproduction Techniques, 550, 557 Research Design, 17, 43, 557 Research Support, 36, 557 Resection, 557 Respiration, 486, 534, 557 Respiratory failure, 557 Respiratory Physiology, 557, 573 Restless legs, 415, 557 Restoration, 17, 546, 555, 557, 576 Reticulocyte Count, 39, 43, 48, 338, 557 Reticulocytes, 44, 46, 505, 557 Retina, 5, 44, 331, 490, 497, 499, 527, 540, 557, 558, 559, 575 Retinal, 5, 44, 494, 497, 499, 540, 557, 558 Retinal Vein, 557 Retinal Vein Occlusion, 557 Retinitis, 497, 558 Retinoids, 558 Retinol, 557, 558 Retinopathy, 5, 499, 558 Retinosis, 558
592 Anemia
Retrospective, 7, 9, 51, 304, 558 Retroviral vector, 20, 21, 28, 30, 511, 558 Retrovirus, 18, 57, 558 Reversion, 61, 558 Rheology, 544, 558 Rheumatism, 558 Rheumatoid arthritis, 3, 29, 404, 490, 506, 558 Rhodopsin, 540, 557, 558 Ribavirin, 558 Ribonucleoproteins, 538, 558 Ribonucleoside Diphosphate Reductase, 519, 558 Ribose, 472, 497, 558 Rickets, 558, 575 Risk patient, 38, 559 Rituximab, 559 Rod, 39, 481, 559 Rubella, 312, 505, 559 S Salivary, 497, 499, 542, 559, 561 Salivary glands, 497, 499, 559, 561 Saponins, 559, 565 Sarcoma, 559 Scans, 42, 334, 559 Scatter, 559 Schizoid, 559, 575 Schizophrenia, 559, 560, 575 Schizotypal Personality Disorder, 559, 575 Sclera, 490, 560 Sclerosis, 480, 535, 560 Screening, 5, 22, 323, 407, 417, 447, 491, 560 Scurvy, 291, 560 Secondary tumor, 532, 560 Secretion, 4, 319, 495, 518, 523, 524, 526, 527, 533, 535, 539, 560, 561 Secretory, 50, 539, 560 Segmental, 512, 560 Segregation, 555, 560 Seizures, 339, 446, 498, 543, 545, 560 Semen, 552, 560 Senile, 541, 560 Sensory loss, 535, 560, 567 Septal, 477, 560 Septic, 480, 560 Septum, 551, 560 Sequela, 560 Sequence Analysis, 18, 560 Sequencing, 33, 44, 549, 560 Sequester, 489, 560 Serial Passage, 561 Serine, 561, 571 Serologic, 521, 561 Serotonin, 471, 496, 537, 561, 571 Serous, 503, 519, 548, 561 Serum Albumin, 474, 561
Serum Sickness, 329, 338, 561 Sex Characteristics, 472, 476, 561, 567 Sexually Transmitted Diseases, 408, 561 Shock, 312, 561, 571 Shunt, 334, 561 Sicca, 561 Sickle Cell Trait, 442, 452, 561 Signal Transduction, 17, 21, 56, 561 Signs and Symptoms, 444, 445, 556, 562, 572 Sirolimus, 332, 333, 521, 562 Skeletal, 25, 35, 53, 476, 535, 562 Skin Pigmentation, 35, 562 Skin test, 329, 562 Small cell lung cancer, 562 Small intestine, 501, 504, 518, 520, 524, 526, 562, 571 Smoldering leukemia, 535, 562 Smooth muscle, 476, 485, 493, 518, 534, 538, 556, 562, 565 Sneezing, 545, 562 Social Environment, 554, 562 Sodium, 24, 39, 459, 499, 500, 533, 536, 562 Soft tissue, 484, 562 Solid tumor, 35, 329, 344, 477, 483, 501, 562 Solvent, 513, 541, 562 Soma, 562 Somatic, 29, 61, 472, 502, 518, 534, 562 Sorbitol, 517, 562 Sound wave, 563, 572 Spasmodic, 545, 563 Spatial disorientation, 500, 563 Specialist, 9, 453, 563 Specificity, 473, 550, 563 Spectrin, 563 Spectroscopic, 539, 563 Spectrum, 7, 23, 32, 487, 491, 526, 563 Sperm, 476, 490, 563 Spherocytes, 563 Spherocytosis, 563 Sphincter, 527, 563 Spina bifida, 563 Spinal cord, 480, 488, 489, 490, 501, 503, 531, 532, 535, 537, 542, 550, 563, 566 Spinal Cord Vascular Diseases, 535, 563 Spleen, 44, 56, 475, 497, 529, 548, 563 Splenectomy, 44, 415, 563 Splenomegaly, 522, 548, 563 Spondylitis, 506, 564 Spontaneous Abortion, 550, 564 Sporadic, 18, 33, 549, 564 Spores, 523, 564 Sports Medicine, 408, 462, 564 Sprains and Strains, 529, 564 Squamous, 504, 538, 564 Squamous cell carcinoma, 504, 538, 564 Squamous cells, 564
Index 593
Stabilization, 545, 564 Staging, 559, 564 Standardize, 342, 564 Stasis, 564 Steady state, 564 Steatosis, 507, 564 Stem Cell Factor, 350, 491, 564 Stem Cells, 16, 24, 28, 40, 60, 61, 325, 331, 333, 335, 338, 345, 474, 505, 515, 544, 564, 572 Sterile, 480, 542, 564 Sterility, 496, 522, 564 Steroid, 339, 348, 495, 497, 559, 565 Steroid therapy, 348, 565 Stillbirth, 550, 565 Stimulant, 496, 518, 565, 573 Stimulus, 494, 501, 506, 565, 568 Stomatitis, 512, 565 Stool, 328, 492, 521, 527, 539, 565 Strand, 322, 548, 565 Stress, 41, 302, 323, 408, 496, 509, 536, 542, 550, 558, 565, 573 Stroma, 565 Stromal, 484, 503, 537, 565 Stromal Cells, 484, 565 Stupor, 536, 565 Subacute, 522, 565 Subarachnoid, 514, 565 Subclinical, 522, 560, 565 Subcutaneous, 4, 7, 52, 57, 472, 501, 528, 543, 565 Substance P, 532, 555, 560, 565 Substrate, 504, 566 Sudden cardiac death, 15, 566 Sulfadoxine, 308, 566 Sulfur, 527, 533, 566 Superinfection, 46, 566 Superoxide, 40, 294, 566 Superoxide Dismutase, 40, 566 Support group, 398, 450, 451, 452, 566 Supportive care, 25, 566 Suppression, 495, 566, 576 Suppressive, 47, 49, 566 Sympathetic Nervous System, 477, 566 Symphysis, 490, 552, 566 Symptomatic, 10, 26, 542, 566 Symptomatology, 566 Synaptic, 537, 562, 566 Synergistic, 551, 566 Systemic lupus erythematosus, 57, 477, 478, 479, 490, 566 Systemic therapy, 490, 567 Systolic, 8, 519, 567 T T cell, 567 Tapeworm, 404, 567
Telangiectasia, 32, 51, 567 Telomere, 567 Teratogenic, 474, 567 Terminator, 491, 567, 576 Testicular, 408, 567 Testis, 513, 567 Testosterone, 456, 556, 567 Tetani, 567 Tetanic, 567 Tetanus, 567 Tetany, 542, 567 Tetracycline, 53, 319, 501, 567 Thalamic, 480, 567 Thalamic Diseases, 480, 567 Therapeutics, 304, 458, 568 Thermal, 477, 500, 537, 548, 568 Thiamine, 41, 59, 291, 293, 568 Thigh, 514, 568 Thioredoxin, 568 Thorax, 471, 529, 568 Threonine, 561, 568 Threshold, 476, 519, 568 Thrombin, 508, 547, 552, 568 Thrombocytosis, 312, 568 Thrombolytic, 547, 568 Thrombomodulin, 552, 568 Thrombopenia, 479, 568 Thrombophilia, 308, 568 Thrombopoietin, 568 Thromboses, 48, 479, 568 Thrombosis, 27, 50, 510, 523, 552, 565, 568 Thrombus, 495, 522, 536, 547, 568, 573 Thrush, 485, 568 Thymoma, 343, 568 Thymus, 521, 529, 568 Thyroid, 19, 319, 346, 402, 525, 542, 569 Thyroid Gland, 346, 542, 569 Thyroid Hormones, 319, 569 Thyroiditis, 569 Thyroxine, 474, 569 Ticks, 522, 569 Tin, 468, 487, 548, 569 Tinnitus, 541, 569 Tissue Culture, 41, 569 Tolerance, 24, 472, 512, 569 Tomography, 569 Tone, 20, 540, 569 Tonicity, 516, 569 Tonus, 569 Tooth Preparation, 472, 569 Topotecan, 569 Torsion, 522, 569 Toxicity, 24, 28, 36, 336, 337, 339, 471, 501, 520, 532, 569 Toxicology, 426, 570 Toxin, 500, 504, 567, 569, 570
594 Anemia
Trace element, 290, 291, 490, 569, 570 Trachea, 527, 545, 569, 570 Transaminase, 345, 570 Transcriptase, 319, 527, 558, 570, 576 Transduction, 21, 25, 53, 561, 570 Transfection, 483, 511, 570 Transfer Factor, 520, 570 Transferases, 513, 570 Transfusion-Transmitted Virus, 570 Transient Ischemic Attacks, 308, 570 Translation, 475, 570 Translational, 24, 35, 570 Translocation, 570 Transmitter, 471, 480, 500, 531, 570, 574 Transplantation Conditioning, 28, 571 Transversion, 37, 571 Trauma, 4, 52, 309, 401, 444, 498, 505, 536, 542, 571 Treatment Outcome, 571 Tricuspid Valve, 340, 571 Trimetrexate, 29, 571 Trisomy, 571 Trivalent, 507, 571 Trophic, 571 Tropical Medicine, 30, 39, 571 Trypsin, 571 Tryptophan, 492, 554, 561, 571 Tuberculosis, 479, 494, 529, 571 Tumor marker, 571 Tumor Necrosis Factor, 55, 571 TYPHI, 571 Typhoid Fever, 571 U Ulcer, 571, 572, 573 Ulceration, 527, 572 Ulcerative colitis, 522, 572 Ultrasonography, 572 Ultrasound test, 340, 572 Umbilical Arteries, 572 Umbilical Cord, 36, 343, 572 Umbilical cord blood, 343, 572 Umbilical cord blood transplantation, 343, 572 Univalent, 519, 541, 572 Uracil, 554, 572 Uraemia, 542, 572 Urea, 6, 8, 526, 572 Uremia, 9, 526, 556, 572 Ureters, 526, 572, 573 Urethra, 544, 552, 572, 573 Uridine Diphosphate, 572 Urinary, 302, 487, 518, 521, 539, 566, 572 Urinary tract, 487, 566, 572 Urine, 479, 483, 492, 496, 515, 516, 521, 526, 536, 539, 552, 556, 572, 573 Urticaria, 561, 573
Uterus, 444, 489, 503, 527, 532, 551, 573 V Vaccination, 42, 573 Vaccine, 42, 43, 51, 472, 552, 573 Vagina, 485, 489, 499, 532, 573 Vaginitis, 485, 573 Valine, 543, 573 Valves, 573, 574 Varicose, 527, 573 Varicose Ulcer, 527, 573 Varix, 573 Vascular, 7, 10, 15, 20, 25, 39, 42, 44, 53, 397, 485, 490, 503, 510, 515, 519, 522, 528, 533, 538, 547, 563, 568, 569, 573 Vascular endothelial growth factor, 54, 573 Vasculitis, 542, 573 Vasoactive, 573 Vasodilation, 475, 477, 573 Vasodilator, 475, 478, 484, 501, 518, 573 Vector, 17, 25, 28, 30, 53, 570, 573 Vein, 326, 328, 329, 330, 332, 334, 336, 339, 346, 480, 525, 538, 546, 557, 572, 573 Venous, 339, 479, 480, 483, 487, 489, 505, 527, 538, 547, 552, 573, 575 Venous blood, 483, 489, 505, 547, 573 Venous Thrombosis, 573, 575 Ventilation, 573 Ventricle, 534, 553, 567, 571, 574 Ventricular, 10, 14, 53, 405, 519, 574 Ventricular Dysfunction, 574 Ventricular Function, 54, 574 Ventricular Pressure, 54, 574 Venules, 483, 486, 503, 533, 574 Vertebrae, 524, 563, 564, 574 Vertebral, 482, 563, 574 Vertigo, 508, 541, 574 Vesicular, 574 Veterinary Medicine, 425, 574 Video Recording, 409, 574 Videodisc Recording, 574 Viral Hepatitis, 574 Viremia, 30, 46, 574 Virulence, 61, 561, 566, 569, 574 Virulent, 574 Virus Replication, 58, 324, 574 Viscera, 562, 575 Visceral, 312, 527, 544, 575 Vitamin D, 4, 437, 559, 575 Vitiligo, 312, 553, 575 Vitreous, 499, 527, 557, 575 Vitreous Body, 557, 575 Vitreous Hemorrhage, 499, 575 Vitro, 10, 16, 18, 28, 33, 37, 43, 45, 46, 50, 53, 62, 483, 502, 511, 521, 548, 561, 566, 569, 575 Vivo, 18, 28, 37, 45, 56, 530, 575
Index 595
W Wakefulness, 498, 575 Warfarin, 575 Weight Gain, 34, 290, 418, 575 Whooping Cough, 545, 575 Windpipe, 545, 569, 575 Withdrawal, 408, 498, 575 Womb, 349, 573, 575 Wound Healing, 523, 576 X Xenograft, 477, 576 Xeroderma Pigmentosum, 32, 51, 576
X-ray, 329, 333, 334, 339, 346, 347, 412, 493, 494, 495, 508, 510, 525, 538, 554, 555, 559, 576 X-ray therapy, 525, 576 Y Yeasts, 485, 509, 545, 576 Z Zalcitabine, 527, 576 Zebrafish, 37, 321, 576 Zidovudine, 576 Zoster, 517, 576 Zygote, 494, 534, 576 Zymogen, 552, 576
596 Anemia
Index 597
598 Anemia
