Hepatic Encephalopathy - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

HEPATIC ENCEPHALOPATHY A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENC...

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HEPATIC

ENCEPHALOPATHY A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES

J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1

Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Hepatic Encephalopathy: 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: 0-497-00533-6 1. Hepatic Encephalopathy-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.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International, Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

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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 hepatic encephalopathy. 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 HEPATIC ENCEPHALOPATHY ................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Hepatic Encephalopathy................................................................ 5 E-Journals: PubMed Central ....................................................................................................... 13 The National Library of Medicine: PubMed ................................................................................ 13 CHAPTER 2. NUTRITION AND HEPATIC ENCEPHALOPATHY ......................................................... 59 Overview...................................................................................................................................... 59 Finding Nutrition Studies on Hepatic Encephalopathy .............................................................. 59 Federal Resources on Nutrition ................................................................................................... 60 Additional Web Resources ........................................................................................................... 61 CHAPTER 3. ALTERNATIVE MEDICINE AND HEPATIC ENCEPHALOPATHY ................................... 63 Overview...................................................................................................................................... 63 National Center for Complementary and Alternative Medicine.................................................. 63 Additional Web Resources ........................................................................................................... 66 General References ....................................................................................................................... 67 CHAPTER 4. PATENTS ON HEPATIC ENCEPHALOPATHY ................................................................ 69 Overview...................................................................................................................................... 69 Patents on Hepatic Encephalopathy............................................................................................. 69 Patent Applications on Hepatic Encephalopathy......................................................................... 70 Keeping Current .......................................................................................................................... 73 CHAPTER 5. BOOKS ON HEPATIC ENCEPHALOPATHY ................................................................... 75 Overview...................................................................................................................................... 75 Book Summaries: Federal Agencies.............................................................................................. 75 Book Summaries: Online Booksellers........................................................................................... 80 Chapters on Hepatic Encephalopathy .......................................................................................... 81 CHAPTER 6. MULTIMEDIA ON HEPATIC ENCEPHALOPATHY......................................................... 85 Overview...................................................................................................................................... 85 Video Recordings ......................................................................................................................... 85 CHAPTER 7. PERIODICALS AND NEWS ON HEPATIC ENCEPHALOPATHY...................................... 87 Overview...................................................................................................................................... 87 News Services and Press Releases................................................................................................ 87 Academic Periodicals covering Hepatic Encephalopathy............................................................. 89 CHAPTER 8. RESEARCHING MEDICATIONS .................................................................................... 91 Overview...................................................................................................................................... 91 U.S. Pharmacopeia....................................................................................................................... 91 Commercial Databases ................................................................................................................. 94 Researching Orphan Drugs ......................................................................................................... 94 APPENDIX A. PHYSICIAN RESOURCES ............................................................................................ 99 Overview...................................................................................................................................... 99 NIH Guidelines............................................................................................................................ 99 NIH Databases........................................................................................................................... 101 Other Commercial Databases..................................................................................................... 103 APPENDIX B. PATIENT RESOURCES ............................................................................................... 105 Overview.................................................................................................................................... 105 Patient Guideline Sources.......................................................................................................... 105 Finding Associations.................................................................................................................. 107 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 109 Overview.................................................................................................................................... 109 Preparation................................................................................................................................. 109

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Finding a Local Medical Library................................................................................................ 109 Medical Libraries in the U.S. and Canada ................................................................................. 109 ONLINE GLOSSARIES................................................................................................................ 115 Online Dictionary Directories ................................................................................................... 119 HEPATIC ENCEPHALOPATHY DICTIONARY .................................................................... 121 INDEX .............................................................................................................................................. 169

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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 hepatic encephalopathy 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 hepatic encephalopathy, 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 hepatic encephalopathy, 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 hepatic encephalopathy. 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 hepatic encephalopathy, 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 hepatic encephalopathy. 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 HEPATIC ENCEPHALOPATHY Overview In this chapter, we will show you how to locate peer-reviewed references and studies on hepatic encephalopathy.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and hepatic encephalopathy, 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 “hepatic encephalopathy” (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: •

Hepatic Encephalopathy: Metabolic Consequence of Cirrhosis Often is Reversible Source: Postgraduate Medicine. 109(2): 52-54, 57-60, 63-65, 69-70. February 2001. Contact: Available from McGraw-Hill, Inc. 1221 Avenue of the Americas, New York, NY 10020. (612) 832-7869. Summary: This article discusses hepatic encephalopathy, a condition characterized by neuropsychiatric manifestations ranging from a slightly altered mental status to coma, and neuromuscular symptoms may be present. This complication of chronic or acute liver disease is a result of the failure of the liver to detoxify toxins originating in the intestine. The pathogenesis (how it occurs) probably is multifactorial, although the predominant causative agent appears to be ammonia. About 30 percent of patients with

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Hepatic Encephalopathy

cirrhosis (scarring of the liver) die in hepatic coma. The molecular basis of neurotoxicity of ammonia or other agents implicated in the condition is poorly understood. Therapy includes timely recognition and correction of precipitating factors. Once the condition is manifested, standard therapy is acute administration of lactulose, a disaccharide that is undigested in the small intestine. The beneficial action of lactulose is not fully understood. The use of oral antibiotics and BCAAs (branched chain amino acids) is of some benefit in patients who do not respond to lactulose. Limitation of protein in the diet may be useful for short periods but is not recommended for long term use because of potential worsening of already poor nutrition. The ultimate therapy for hepatic encephalopathy is orthotopic liver transplantation. Future research will likely focus on the correction of alterations in neurotransmission. 2 figures. 4 tables. 20 references. •

Hepatic Encephalopathy: Current Approaches Source: Contemporary Gastroenterology. 4(3): 51-56. May-June 1991. Summary: This article discusses the current approaches to treating hepatic encephalopathy, focusing on portal-systemic encephalopathy, a reversible metabolic disorder seen almost exclusively in patients with cirrhosis and portal hypertension. The authors suggest limiting protein intake and administering lactulose, once other causes of altered mental status have been eliminated and the precipitating factors have been identified and treated. Liver transplantation may be necessary if this therapy is not helpful and the syndrome recurs. 3 tables. 41 references. (AA-M).

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Complications of Cirrhosis: Ascites and Hepatic Encephalopathy Source: Current Opinion in Gastroenterology. 6(3): 365-369. June 1990. Summary: This article discusses two of the complications of cirrhosis: ascites and hepatic encephalopathy. Ascites is the most common complication of cirrhosis. It is associated with about 50 percent of deaths in these patients. Hepatic encephalopathy (HE) is the metabolic effect of liver failure on the central nervous system. Permanent structural changes in the central nervous system do not occur and the syndrome is completely reversible. The clinical course and treatment for both of these conditions is considered in detail, with numerous citations to current research. 23 annotated references.

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Hepatic Encephalopathy, Revisited (Editorial) Source: Liver Update Function and Disease. 6(4): 1-2. Fall 1992. Summary: This article presents a brief overview of hepatic encephalopathy. Topics include brain edema in acute liver failure; post-shunt encephalopathy; subclinical encephalopathy; research studies that compare treatments for patients with chronic hepatic encephalopathy; how ammonia affects brain function; and the use of flumazenil, a benzodiazepine receptor antagonist, for treatment of hepatic encephalopathy. The author concludes that newer drugs should provide insight into the pathogenesis of hepatic failure and improve the management of encephalopathy.

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Role of Parenteral Nutrition in Inflammatory Bowel Disease, Acute Renal Failure, and Hepatic Encephalopathy Source: International Journal of Technology Assessment in Health Care. 6(4): 655-662. 1990.

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Summary: This article reviews the evidence concerning efficacy and safety of the use of parenteral nutritional support (also called total parenteral nutrition or TPN) in three clinical situations: as a primary therapy for patients with inflammatory bowel disease, for patients with acute renal failure, and for patients with hepatic cirrhosis resulting in encephalopathy. For each of the three situations, the rationale, efficacy, safety, and recommendations for using TPN are given. The authors conclude that the true value of parenteral nutritional support in these three clinical indications remains unknown. It is possible that future clinical trials will demonstrate the value of parenteral nutrition for these patients or for subgroups of these patients. 32 references. •

Hepatic Encephalopathy and Ascites Source: Lancet. 350(9087): 1309-1315. November 1, 1997. Summary: This professional education article discusses hepatic encephalopathy and ascites. Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that occurs only with significant liver dysfunction and has a potential for full reversibility. Two distinct forms (overt and subclinical) can be identified in patients with cirrhosis. Various methods have been described for estimating the severity of HE, but the authors encourage the use of the West-Haven criteria for grading mental state in hepatitic encephalopathy. The authors report on recent developments in the pathogenesis of HE, including alterations in the blood-brain barrier, changes in energy metabolism, the role of gut-derived factors, and changes in cerebral neurotransmission. The authors then review the principles of management of HE, including reduction of ammonia toxicity, cerebral neurotransmission, and other approaches. The second half of the article addresses the problem of ascites in patients with cirrhosis, a major cause of morbidity and a serious prognostic development in these patients. The authors consider the pathogenesis of ascites, including the retention of sodium, retention of water, and the hepatorenal syndrome. The article concludes with a discussion of the management of ascites. 3 figures. 1 table. 62 references.

Federally Funded Research on Hepatic Encephalopathy The U.S. Government supports a variety of research studies relating to hepatic encephalopathy. 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. 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 hepatic encephalopathy. 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 hepatic encephalopathy. The following is typical of

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Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).

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the type of information found when searching the CRISP database for hepatic encephalopathy: •

Project Title: CORTICAL GLUTAMATE, GLUTAMINE & GABA LEVELS IN HEPATIC ENCEPHALOPATHY Principal Investigator & Institution: Shulman, Gerald I.; Professor; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2003 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DISTAL SPLENORENAL INTRAHEPATIC PORTAL SYSTEMIC SHUNT

VERSUS

TRANSJUGULAR

Principal Investigator & Institution: Boyer, Thomas D.; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002 Summary: This is a multicenter, prospective, randomized clinical trial to compare DSRS and TIPS for the management of variceal bleeding in patients with Child's Class A & B cirrhosis. The primary goal of both therapies is to achieve control of variceal bleeding by reducing pressure in the varice, and limit the risk of accelerating the development of liver failure, ascites, and hepatic encephalopathy. The study will randomize patients who have failed or are not candidates for endoscopic therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EFFECT OF CIRRHOSIS AND SHUNTS ON DRUG DISPOSITION Principal Investigator & Institution: Gorski, J. Christopher.; Associate Professor of Medicine; Medicine; Indiana Univ-Purdue Univ at Indianapolis 620 Union Drive, Room 618 Indianapolis, in 462025167 Timing: Fiscal Year 2002; Project Start 15-AUG-2002; Project End 31-JUL-2007 Summary: (provided by applicant): It is well established that hepatic cirrhosis results in reduced clearance of drugs that are highly metabolized and an enhanced sensitivity to the pharmacological and adverse actions of drugs. Chronic alcohol consumption and hepatitis C are the two most common causes of cirrhosis in the United States with an incidence of 3.1 per 1000 people. The development of portal hypertension is the primary mechanism behind several major complications of cirrhosis such as bleeding from gastroesophageal varices, hepatic encephalopathy, and ascites. Transjugular intrahepatic portosystemic shunts (TIPS) and other surgical shunts are performed to manage these complications of portal hypertension. We have demonstrated that in addition to a reduction in hepatic clearance, cirrhotic patients with TIPS experience an increase in intestinal availability of midazolam, a selective cytochrome P450 3A (CYP3A) substrate. This increased bioavailability primarily reflects a functional lack of intestinal wall first-pass metabolism relative to cirrhotics without TIPS and healthy volunteers. The mechanism for this lack of intestinal wall metabolism is unknown. We propose to characterize the mechanism and consequences of this loss of intestinal wall CYP3A activity in cirrhotics with TIPS by directly examining the CYP3A protein and mRNA levels, intestinal permeability, and in vivo hepatic and intestinal CYP3A activity before, immediately after, and I month after TIPS placement. Cirrhotic patients with TIPS, and potentially other types of portosystemic shunts, are expected to be at risk for excessive

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pharmacological effects or suffer from an increased incidence of adverse reactions following CYP3A substrate administration. We will examine the susceptibility of these individuals to adverse drug reactions and drug-drug interaction by examining the ability of erythromycin to prolong the QT interval and clarithromycin to inhibit metabolism of buspirone, a CYP3A substrate. Finally, the expression of other enzymes such as UDP-glucuronosyltransferases (UGTs), sulfotransferases (SULTs) and pglycoprotein may also be altered in cirrhosis. We will characterize the changes in these enzymes using the partial clearance of acetaminophen to glucuronide (UGT) and sulfate (SULT) conjugates and the disposition of fexofenadine in cirrhotics with and without TIPS and healthy volunteers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EXPRESSION OF AMMONIA-SENSITIVE PROTEINS IN THE CNS Principal Investigator & Institution: Weiner, I. David.; Associate Professor; Medicine; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2004; Project Start 01-DEC-2003; Project End 30-NOV-2005 Summary: (provided by applicant): Encephalopathy due to elevated ammonia levels is a common and costly clinical condition associated either with congenital deficiency of hepatic urea cycle enzymes, with acquired liver disease and with a variety of other conditions. Despite a long recognition that elevated ammonia levels can lead to impaired neurologic functioning, the exact mechanism through which this occurs remains incompletely understood. Moreover, treatment of hyperammonemic encephalopathy has been limited by a lack of knowledge of the specific CNS protein(s) with which ammonia directly interacts. The broad, long-term objective of this project is to examine the hypothesis that Rh C Glycoprotein (RhCG) is a central nervous system (CNS) ammonia 'sensor.' We hypothesize that RhCG protein is expressed in specific CNS neuron populations, that ammonia-stimulation of RhCG is coupled to specific intracellular signaling pathways, most likely including MAP kinase, and that RhCG expression is regulated by specific physiology/pathophysiologic stimuli. We will examine this hypothesis with two specific aims. In the first, we will determine whether ammonia's stimulation of RhCG, or, possibly the related proteins, Rh A Glycoprotein (RhAG) or Rh B Glycoprotein (RhBG), activates specific intracellular signaling pathways in cultured neurons. We will use primary neuronal cultures, and will use RNA interference techniques to inhibit RhCG expression to show specificity of response. In parallel, we will determine whether RhCG can function as an ammonia sensor by determining whether it can complement the pseudohyphal transformation-defect of Amep2-Amep2 S. cerevisiae. To examine the second aim, we will determine whether cecal ligation and puncture-induced sepsis increases CNS expression of either RhCG, or of RhAG or RhBG. These studies will combine immunohistochemical analyses of cellular protein expression patterns with quantitative analyses of protein and mRNA expression with immunoblot and real-time RT-PCR, respectively. These studies fit the purpose of the R21 mechanism in two different manners. These studies will provide pilot data to assess the feasibility of a novel avenue of investigation into the role of RhCG, or related proteins, as CNS ammonia 'sensors.' Second, while these studies are admittedly high risk, their results could lead to a breakthrough in the field of hyperammonemic and hepatic encephalopathy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EXTREME AMMONIA TOLERANCE MECHANISMS: A MODEL VERTEBRATE Principal Investigator & Institution: Walsh, Patrick J.; Marine Biology and Fisheries; University of Miami Coral Gables Box 248293 Coral Gables, Fl 33134 Timing: Fiscal Year 2002; Project Start 08-FEB-2002; Project End 30-NOV-2004 Summary: (provided by applicant): Hepatic Encephalopathy (HE), and resultant elevated blood and tissue ammonia concentrations (i.e., hyperammonemia, HA), has profound central nervous system (CNS) effects, and can have environmental causes. In particular, liver damage due to exposure to toxicants such as carbon tetrachloride, toluene, DDT, heptachlor, etc., as well as chronic alcoholism and direct exposure to environmental ammonia, can elicit symptoms of HE/HA. However, there are such a wide variety of CNS effects produced in the disease in humans, and in rodent experimental models, that it is difficult to determine which disease biomarkers are the most critical indicators of disease progression. Furthermore, characteristics of the rodent model present several weaknesses in the study of HE/HA. Because of this gap in our knowledge, no practical and effective clinical intervention strategies are available to prevent or reverse biomarkers or symptoms of the disease. Recently, we have identified a vertebrate model, the gulf toadfish (Opsanus beta), which is both extremely tolerant of ammonia insult, and which, by virtue of its aquatic lifestyle, enables a line of experimentation not practical in mammalian models, namely rapid "ammonia washout" protocols. Therefore, we propose to test several hypotheses aimed at exploiting these and other characteristics of this new model to address the lack of biomarkers and intervention strategies for HE/HA. In particular, we will: (1) test the hypothesis that there are reversible vs. irreversible biomarkers of HE/HA, and that these can be readily identified and distinguished in an aquatic model like the toadfish; (2) test the hypotheses that extreme ammonia tolerance in the toadfish, relative to mammals, is due to an unusual aspect of its physiology, in particular, either to a more robust ammonia detoxification system in the brain, or to an inherent insensitivity of brain mitochondrial metabolism to ammonia insult. As a further test of this second hypothesis, we will also explore the possibility that the toadfish has higher levels of naturally occurring ammonia protectant compounds (e.g., carnitine, trimethylamine oxide, etc.) in its brain tissues than do mammals. In sum, these experiments will lead to information which is not readily obtainable from humans and existing mammalian models concerning the mechanisms of action of ammonia and cellular capacity for tolerance and recovery, and thus to a better understanding of the causes and mechanisms underlying HE/HA that could lead to therapeutic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MRS STUDIES OF NEUROTRANSMITTER CYCLING IN HUMAN BRAIN Principal Investigator & Institution: Rothman, Douglas L.; Professor; Internal Medicine; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2002; Project Start 01-APR-1998; Project End 14-JUN-2003 Summary: Glutamate neurotransmitter release depends on a stable precursor cytosolic glutamate concentration. Loss of glutamate by synaptic release will deplete the nerve terminal cytosolic precursor pool unless compensated for by glutamate reuptake and synthesis. Glial uptake efficiently removes released glutamate from the synaptic cleft in order to maintain a low ECF concentration of glutamate. In vivo and in vitro studies indicate that glutamate taken up by glia is converted to glutamine by glutamine

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synthetase. Glutamine is released from the glia to the ECF where it is taken up by neurons and converted back to glutamate through the action of glutaminase. Despite the critical role of this glutamate/glutamine cycle for normal brain function, little is known about the rate or regulation of this pathway. Recently we have developed and tested in the rat brain a model of this pathway which allows the rate of the glutamate/glutamine cycle to be measured from C MRS measurements of glutamine isotopic labeling. The primary objective of this grant is to determine the rate of the glutamate/glutamine cycle in normal human cortex. C MRS will be used to measured glutamine and glutamate isotopic labeling from infused [1-13C] and [2-13C] glucose. Key aspects of the proposed model of the glutamate/glutamine cycle will be tested through measuring of the effect of altering plasma ammonia concentration on total and anapleurotic glutamine synthesis in subjects with mild hepatic encephalopathy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MUSCARINIC RECEPTOR COUPLING TO INOSITIDES IN CNS Principal Investigator & Institution: Fisher, Stephen K.; Professor; Pharmacology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2003; Project Start 01-SEP-1986; Project End 30-JUN-2007 Summary: (provided by applicant): The regulation of cell volume is of critical importance to the CNS due to the restrictions of the skull. Brain swelling, which may occur in response to a lowering of plasma osmolarity or during cytotoxic edema, is associated with a number of clinical conditions, including congestive heart failure, hepatic encephalopathy, ischemic stroke, or head trauma. To counteract the increased volume, cells release Kv, CI-, and "non-perturbing" organic osmolytes, a major component of which is myo-inositol. Efflux of the osmolytes occurs via a volumesensitive organic anion channel (VSOAC), which primarily gates CI'. Although most attention has been focused on the role played by glia in the process of volume regulation, cultured neuronal cells have also been recently shown to exhibit similar properties. Moreover, recent results from this laboratory indicate that high concentrations of myo-inositol are present in some neuronal populations and that the polyol can be released in a volume-dependent manner. Although the electrophysiological and pharmacological characteristics of VSOAC have been well documented, relatively little is known of the cell signaling pathways that regulate osmolyte efflux through this channel. A central tenet of this proposal is that, in the face of hypoosmotic challenge, the capacity of neural cells to restore their volume via the efflux of inositol and other osmolytes can be regulated by extracellular agonists operating via phosphoinositide-linked receptors, such as the muscarinic cholinergic receptor. Thus we plan to examine the characteristics of myo-inositol efflux from human SH-SY5Y neuroblastoma cells under hypoosmotic conditions and evaluate the relationship between effiux of the polyol and changes in cell volume. In addition, we will test the hypothesis that activation of muscarinic cholinergic and other phosphoinositide-linked receptors leads to an increase in the effiux of inositol, and other osmolytes, from these cells. Furthermore, the possibility that individual osmolytes exit the cell via multiple VSOACs will be explored via a comparison of the effiux characteristics of inositol, taurine, and D-aspartate, all of which can be released from these cells. The ability to manipulate osmolyte effiux could be of potential benefit for a number of clinically relevant conditions. Accordingly, knowledge of the signal transduction pathways that regulate VSOAC is an essential prerequisite for the rational design of therapeutic agents.

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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF 15N UREA ISOTOPOMERS PRODUCTION Principal Investigator & Institution: Nissim, Itzhak; Research Professor Pediatrics; Children's Hospital of Philadelphia 34Th St and Civic Ctr Blvd Philadelphia, Pa 191044399 Timing: Fiscal Year 2002; Project Start 01-APR-1999; Project End 29-FEB-2004 Summary: The biochemistry and physiology of hepatic ureagenesis has posed one of the more complex problems in metabolic regulation. The current proposal entails a comprehensive investigation of the mechanism(s) regulating hepatic ureagenesis in vivo or in liver perfusion, and delineates the determinants of mass isotopomers of [15N]urea production from 15N labeled precursor. We will address two primary hypotheses: (i) The preferential utilization of 5-15N of glutamine (Gln) for carbamoyl- phosphate (CP) synthesis may determine the rate of 15N incorporation into urea nitrogens depending upon acid base homeostasis and/or hormonal states; and (ii) Metabolites of arginine, i.e., nitric oxide (NO) and/or agmatine may have a key role in the synthesis of Nacetylglutamate (NAG), and therefore, the utilization of [5-15N]Gln for CP synthesis and [15N]urea production. An alternative hypothesis is that the partitioning of mitochondrial pyruvate metabolism between the pyruvate dehydrogenase (PDH) pathway (production of acetyl-CoA) and alanine formation via the mitochondrial alanine aminotransferase (MAAT) pathway, may determine the rate of NAG synthesis, and thereby, hepatic ureagenesis at various hormonal or acid-base states. We will use rats and/or liver perfusion as a model system and a perfusate which approximates the complex extracellular fluid taken up by the liver in vivo, with only one substrate labeled with 15N or 13C. We will determine the isotopic enrichment of the immediate nitrogenous precursor pools in urea synthesis, and identify primary site(s) of hormonal or acid-base regulation of [15N]urea mass isotopomers production from 15N labeled precursors by using Gas Chromatography-Mass Spectrometry (GC-MS) and/or Nuclear Magnetic Resonance (NMR). The data to be obtained will have considerable impact on our understanding of liver nitrogen metabolism in normal and disease states. We will provide a rigorous experimental framework for understanding the determinants of urea isotopomers production and delineate the mechanism(s) by which [H+] or hormones regulate hepatic nitrogen metabolism. A long term goal is to apply our experimental approach to human subjects in cases such as sepsis, hepatic encephalopathy and/or perturbed hormonal status, such as in diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: THE CNS AND CIRRHOSIS:PSYCHOBIOLOGICAL APPROACHES Principal Investigator & Institution: Stewart, Charmaine; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-DEC-2002 Summary: (provided by applicant): Hepatic encephalopathy (HE) is one of the most common manifestations of decompensated cirrhosis. Approximately 70% of patients with cirrhosis also have subacute hepatic encephalopathy (SHE), as demonstrated on neuropsychological testing. The use of transjugular intrahepatic portosystemic shunts (TIPS), which acts as a side-to-side shunt, has become common to manage complications of cirrhosis. However, TIPS are associated with adverse effects, including worsening of existing HE or the precipitation of overt HE and liver failure. Liver transplantation has become the ideal management for patients who have decompensated liver disease. The

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principal hypothesis of this proposal is that changes of HE and SHE can be determined by neuropsychological testing and changes in cerebral blood flow (CBF). The Specific Aims are the following: (1) Determine the changes in cognitive function in patients with cirrhosis; (2) Identify changes in CBF and neurotransmitter activity, as assessed by central benzodiazepine receptor binding and serotonin transporter binding after TIPS insertion; (3) Identify changes in CBF and neurotransmitter activity, as assessed by central benzodiazepine receptor binding and serotonin transporter binding after liver transplantation; and (4) Correlate the neuropsychological changes with cognitive function and central benzodiazepine receptor binding and serotonin transporter binding. These Specific Aims will be pursued in 60 subjects: group I will be 20 cirrhotics who will undergo TIPS; group II will be 20 cirrhotic patients who are scheduled to undergo liver transplantation; and group III will be 20 age and sex matched cirrhotic controls. All groups will be studied with a battery of neuropsychological tests and stimulated CBF, using 1502 labeled water, while half of groups I and II will be tested with 11C flumazenil PET or (11C)(+)McN5652 positron emission tomography (PET), in order to determine central benzodiazepine receptor binding and serotonin transporter binding, respectively, before and one month after undergoing TIPS or liver transplantation. The control group will be studied with 11C flumazenil PET or (11C)(+)McN5652 PET at baseline and 1 month, thereafter. In aggregate, these studies will provide a platform to elucidate cognitive and biological mechanisms underlying hepatic encephalopathy with the ultimate goal of enhancing diagnosis and management. Additionally, the proposed studies will be guided by a team of mentors and sponsors and supplemented by a didactic curriculum, all to lay the foundation for eventual independent clinical investigator status. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: THE ENCEPHALOPATHY

PERMEABILITY

TRANSITION

IN

HEPATIC

Principal Investigator & Institution: Norenberg, Michael D.; Professor; Pathology; University of Miami-Medical Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with severe liver failure. Acute HE associated with fulminant hepatic failure has an extremely poor prognosis and specific therapy is not available, short of an emergency liver transplantation. Although its pathogenesis remains poorly understood, ammonia is strongly implicated as a neurotoxin, and astrocytes appear to be the primary target of ammonia neurotoxicity. Additionally, altered bioenergetics and oxidative stress are thought to play a major role in this disorder. These facts led to a consideration of the involvement of mitochondrial permeability transition (MPT) as a factor in the pathogenesis of HE and ammonia neurotoxicity. The MPT is a Ca2+-dependent, cyclosporin A (CsA)-sensitive process due to the opening of a pore in the inner mitochondrial membrane leading to a collapse of ionic gradients and ultimately to mitochondrial dysfunction. We have recently shown that ammonia induced the MPT in cultured astrocytes. We intend to examine the role of the MPT in HE and hyperammonemia using ammonia-treated neural cell cultures and in vivo models of HE/hyperammonemia (HA). Our working hypothesis is that ammonia induces the MPT in astrocytes, culminating in mitochondrial failure and astroglial dysfunction. A corollary of this concept is that inhibition or interference in the development of the MPT in astrocytes may ameliorate CNS dysfunction in HE. The Specific Aims of this proposal are: 1) To identify the factors responsible for the

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ammonia-induced MPT in cultured neural cells. Our focus will be on agents implicated in the pathogenesis of HE/H that have also been shown to induce the MPT in other cells. Specifically, we will examine the role of Ca 2+, reactive oxygen species, nitric oxide, pH and glutamine. We will determine whether these factors are elevated in ammonia-treated cultures, and whether diminishing their production or blocking their actions reduces or abolishes the MPT. Additionally, we will examine possible sequential interrelationships among these factors. 2) To determine whether ammonia-induced abnormalities in astrocytes (morphological alterations, defects in neurotransmitter uptake, and cell swelling) are mediated by the MPT, we will investigate whether inhibitors of the MPT (CsA, bongkrekik acid) are capable of diminishing or blocking the deleterious effects of ammonia. 3) To investigate the involvement of mitochondrial dysfunction as a potential factor in MPT-mediated cell injury. We will determine the state of mitochondrial function after ammonia treatment, and then investigate whether improving energy metabolism will inhibit ammonia-induced cellular injury. 4) To clarify whether the MPT occurs in in vivo models of HE (thioacetarnide treatment) and hyperammonemia. We will also determine whether factors that inhibit the MPT in vitro (e.g., CsA, trifluoperazine) are also capable of doing so in vivo. Additionally, we will assess the ability of MPT blockers to improve the clinical, histopathologic, neurochemical abnormalities, and the extent of brain swelling observed in HE/HA. We believe that these studies will yield critical data bearing on the pathogenesis of HE, and may potentially aid in the development of novel therapeutic strategies for the treatment of this condition. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: TWO-DIMENSIONAL MR SPECTROSCOPIC CHARACTERIZATION OF HE Principal Investigator & Institution: Thomas, Michael A.; Associate Professor; Radiology; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2003; Project Start 04-DEC-2002; Project End 30-NOV-2006 Summary: (provided by applicant): The major goals of this application are to evaluate a localized two-dimensional (2D) MR spectroscopic technique (MRS) and to detect cerebral metabolites unequivocally in hepatic encephalopathy (HE). Detection of early changes is very critical in the diagnosis of HE. Localized MR Spectroscopy is a major biochemical tool in characterizing noninvasively several metabolites in human tissues. Excellent one-dimensional (1D) MR spectra of HE and other pathologies have been reported with promising results. However, spectral overlap of various metabolites has been a major concern with the conventional 1D MRS. Spectral analysis of certain metabolites, namely glutamate, glutamine, GABA, myo-inositol, aspartate, glutathione, and the aspartyl groups of NAA and NAAG, has been complicated by severe overlap at 1.5T. 2D MRS seems well suited to address this problem of overlap. It has revolutionized the applications of NMR in biological macromolecules. Previous attempts by other researchers to implement the localized versions of the twodimensional MR techniques mainly used phantom solutions, although some results were reported from animal brains using a non-localized 2D technique. In addition to the major metabolites successfully assigned and analyzed so far with 1D MRS, more metabolites are yet to be detected and their respective roles in different pathologiesare yet to be explored using 2D MRS. A major hypothesis to be tested in this work is whether the changes of glutamine/glutamate, myo-inositol, aspartate, GABA and other cerebral metabolites can be detected using the localized 2D COSY more unambiguously

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in HE than the conventional 1D MRS. Three specific goals of this project will be: 1) to acquire the single-voxel based 2D COSY spectra in the anterior cingulate and the basal ganglia regions of HE patients; 2) to record the global pallidal Mill changes in HE patients; 3) to perform the neuropsychiatric and neurocognitive assessment in HE patients, and to correlate the MR findings with the neuropsycho-logical, blood ammonia and liver function test results using multivariate regression analysis. AGE 1.5T MRI scanner with a bilateral surface "receive" coil (MRI Devices Corp.) in combination with a body rf "transmit" coil will be used to achieve improved signal detection. Minimal spectral overlap leading to less ambiguous assignment and better quantitation of glutamate/glutamine, GABA, myo-inositol, threonine, glucose, taurine and glutathione, will be a major outcome of this work. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “hepatic encephalopathy” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for hepatic encephalopathy in the PubMed Central database: •

Dietary management of hepatic encephalopathy in cirrhotic patients: survey of current practice in United Kingdom. by Soulsby CT, Morgan MY.; 1999 May 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27883

The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals.

3 4

Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.

With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print. 6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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To generate your own bibliography of studies dealing with hepatic encephalopathy, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “hepatic encephalopathy” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for hepatic encephalopathy (hyperlinks lead to article summaries): •

A controlled study of sorbent suspension dialysis in chronic liver disease and hepatic encephalopathy. Author(s): Kramer L, Gendo A, Madl C, Mullen KD, Kaminski-Russ K, SunderPlassmann G, Schaffer A, Bauer E, Roth E, Ferenci P. Source: Int J Artif Organs. 2001 July; 24(7): 434-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11510914

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A new clinical application of MR spectroscopy in hepatic encephalopathy. Author(s): Bryan RN, Barker P. Source: Ajnr. American Journal of Neuroradiology. 1998 October; 19(9): 1593-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9802476

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A non-absorbable rifamycin for treatment of hepatic encephalopathy. Author(s): Testa R, Eftimiadi C, Sukkar GS, De Leo C, Rovida S, Schito GC, Celle G. Source: Drugs Exp Clin Res. 1985; 11(6): 387-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3836135

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A proposed therapy for the encephalopathies of Reye's syndrome and hepatic encephalopathy. Author(s): Anderson B. Source: Medical Hypotheses. 1984 December; 15(4): 415-20. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6098803

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Accumulation of manganese and copper in pallidum of cirrhotic patients: role in the pathogenesis of hepatic encephalopathy? Author(s): Layrargues GP, Shapcott D, Spahr L, Butterworth RF. Source: Metabolic Brain Disease. 1995 December; 10(4): 353-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8847998

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Acute hepatic encephalopathy with diffuse cortical lesions. Author(s): Arnold SM, Els T, Spreer J, Schumacher M. Source: Neuroradiology. 2001 July; 43(7): 551-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11512584

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Altered striatal dopamine D2 receptor density and dopamine transport in a patient with hepatic encephalopathy. Author(s): Weissenborn K, Berding G, Kostler H. Source: Metabolic Brain Disease. 2000 September; 15(3): 173-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11206586

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Amino acid challenge in patients with cirrhosis: a model for the assessment of treatments for hepatic encephalopathy. Author(s): Douglass A, Al Mardini H, Record C. Source: Journal of Hepatology. 2001 May; 34(5): 658-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11434611

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Amino acid, ammonia and neurotransmitter concentrations in hepatic encephalopathy: serial analysis in plasma and cerebrospinal fluid during treatment with an adapted amino acid solution. Author(s): Rossle M, Luft M, Herz R, Klein B, Lehmann M, Gerok W. Source: Klin Wochenschr. 1984 September 17; 62(18): 867-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6149332

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Ammonia and endogenous benzodiazepine-like compounds in the pathogenesis of hepatic encephalopathy. Author(s): Venturini I, Corsi L, Avallone R, Farina F, Bedogni G, Baraldi C, Baraldi M, Zeneroli ML. Source: Scandinavian Journal of Gastroenterology. 2001 April; 36(4): 423-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11336169

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Ammonia and GABA-ergic neurotransmission: interrelated factors in the pathogenesis of hepatic encephalopathy. Author(s): Basile AS, Jones EA. Source: Hepatology (Baltimore, Md.). 1997 June; 25(6): 1303-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9185743

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Analysis of risk factors for chronic hepatic encephalopathy: the role of Helicobacter pylori infection. Author(s): Dasani BM, Sigal SH, Lieber CS. Source: The American Journal of Gastroenterology. 1998 May; 93(5): 726-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9625117

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Arterial ammonia with Blood Ammonia Checker II and with indophenol reaction to assess presence of hepatic encephalopathy. Author(s): Huizenga JR, van Dam GM, Gips CH. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1996 August 15; 252(1): 73-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8814363

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Assessing the severity of hepatic encephalopathy. Author(s): Venkataraman S, Peter S, Chandy GM. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S7-10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025245

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Assessment of hepatic encephalopathy with visual evoked potentials compared with conventional methods. Author(s): Sandford NL, Saul RE. Source: Hepatology (Baltimore, Md.). 1988 September-October; 8(5): 1094-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3417229

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Astrocytic-ammonia interactions in hepatic encephalopathy. Author(s): Norenberg MD. Source: Seminars in Liver Disease. 1996 August; 16(3): 245-53. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8989810

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Astroglial dysfunction in hepatic encephalopathy. Author(s): Norenberg MD. Source: Metabolic Brain Disease. 1998 December; 13(4): 319-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10206824

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Attention deficits in minimal hepatic encephalopathy. Author(s): Weissenborn K, Heidenreich S, Ennen J, Ruckert N, Hecker H. Source: Metabolic Brain Disease. 2001 June; 16(1-2): 13-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726083

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Auditory event-related cerebral potentials (P300) in hepatic encephalopathy-topographic distribution and correlation with clinical and psychometric assessment. Author(s): Hollerbach S, Kullmann F, Frund R, Lock G, Geissler A, Scholmerich J, Holstege A. Source: Hepatogastroenterology. 1997 July-August; 44(16): 1002-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9261590

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Auditory P300 event-related potentials and number connection test for evaluation of subclinical hepatic encephalopathy in patients with cirrhosis of the liver: a follow-up study. Author(s): Saxena N, Bhatia M, Joshi YK, Garg PK, Tandon RK. Source: Journal of Gastroenterology and Hepatology. 2001 March; 16(3): 322-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11339425

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Bacterial infections associated with hepatic encephalopathy: prevalence and outcome. Author(s): Strauss E, Gomes de Sa Ribeiro Mde F. Source: Ann Hepatol. 2003 January-March; 2(1): 41-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15094705

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Benzodiazepine receptor antagonism improves reaction time in latent hepatic encephalopathy. Author(s): Gooday R, Hayes PC, Bzeizi K, O'Carroll RE. Source: Psychopharmacology. 1995 June; 119(3): 295-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7675964

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Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy. Author(s): Als-Nielsen B, Kjaergard LL, Gluud C. Source: Cochrane Database Syst Rev. 2001; (4): Cd002798. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11687160

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Benzodiazepine-receptor antagonists and hepatic encephalopathy: where do we stand? Author(s): Mullen KD, Basile AS. Source: Gastroenterology. 1993 September; 105(3): 937-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8395446

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Benzodiazepine-receptor ligands and hepatic encephalopathy: a causal relationship? Author(s): Rothstein JD. Source: Hepatology (Baltimore, Md.). 1994 January; 19(1): 248-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8276362

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Benzodiazepines in hepatic encephalopathy: sleeping with the enemy. Author(s): Dasarathy S, Mullen KD. Source: Gut. 1998 June; 42(6): 764-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9691910

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Biochemical mechanisms of hepatic encephalopathy. Author(s): Crossley IR, Wardle EN, Williams R. Source: Clinical Science (London, England : 1979). 1983 March; 64(3): 247-52. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6129935

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Biocompatibility of a cuprophane charcoal-based detoxification device in cirrhotic patients with hepatic encephalopathy. Author(s): Kramer L, Gendo A, Madl C, Ferrara I, Funk G, Schenk P, Sunder-Plassmann G, Horl WH. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2000 December; 36(6): 1193-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11096044

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Biocompatibility of sorbent suspension dialysis in cirrhotic patients with hepatic encephalopathy. Author(s): Ash SR. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2001 July; 38(1): 219-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11431210

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Brain edema and hepatic encephalopathy. Author(s): Cordoba J, Blei AT. Source: Seminars in Liver Disease. 1996 August; 16(3): 271-80. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8989813

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Brain edema in acute liver failure. A window to the pathogenesis of hepatic encephalopathy. Author(s): Vaquero J, Chung C, Blei AT. Source: Ann Hepatol. 2003 January-March; 2(1): 12-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15094701

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Brain electrical activity mapping of EEG for the diagnosis of (sub)clinical hepatic encephalopathy in chronic liver disease. Author(s): Kullmann F, Hollerbach S, Lock G, Holstege A, Dierks T, Scholmerich J. Source: European Journal of Gastroenterology & Hepatology. 2001 May; 13(5): 513-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11396530

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Brain energy metabolism and function during hepatic encephalopathy. Author(s): Hawkins RA. Source: European Journal of Clinical Investigation. 1984 October; 14(5): 313-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6437827

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Brain indoles in human hepatic encephalopathy. Author(s): al Mardini H, Harrison EJ, Ince PG, Bartlett K, Record CO. Source: Hepatology (Baltimore, Md.). 1993 June; 17(6): 1033-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7685732

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Brain metabolism in hepatic encephalopathy and hyperammonemia. Author(s): Hawkins RA, Mans AM. Source: Advances in Experimental Medicine and Biology. 1993; 341: 13-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8116483

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Brain SPECT imaging with Tc-99m HMPAO in hepatic encephalopathy. Author(s): Mouratidis B, Lomas F. Source: Clinical Nuclear Medicine. 1995 September; 20(9): 842. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8521669

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Brain tryptophan perturbation in hepatic encephalopathy: implications for effects by neuropsychoactive drugs in clinical practice. Author(s): Bengtsson F, Bergqvist PB, Apelqvist G. Source: Advances in Experimental Medicine and Biology. 1997; 420: 1-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9286423

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Branched-chain amino acids for hepatic encephalopathy. Author(s): Als-Nielsen B, Koretz RL, Kjaergard LL, Gluud C. Source: Cochrane Database Syst Rev. 2003; (2): Cd001939. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12804416

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Branched-chain amino acids in the treatment of chronic hepatic encephalopathy. Author(s): Eriksson LS, Persson A, Wahren J. Source: Gut. 1982 October; 23(10): 801-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6749604

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Bright basal ganglia in T1-weighted magnetic resonance images are frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy. Author(s): Nolte W, Wiltfang J, Schindler CG, Unterberg K, Finkenstaedt M, Niedmann PD, Hartmann H, Ramadori G. Source: Journal of Hepatology. 1998 September; 29(3): 443-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9764992

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Cerebral 1H MR spectroscopy and neuropsychologic status of patients with hepatic encephalopathy. Author(s): Thomas MA, Huda A, Guze B, Curran J, Bugbee M, Fairbanks L, Ke Y, Oshiro T, Martin P, Fawzy F. Source: Ajr. American Journal of Roentgenology. 1998 October; 171(4): 1123-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9763008

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Cerebral benzodiazepine receptor binding in vivo in patients with recurrent hepatic encephalopathy. Author(s): Macdonald GA, Frey KA, Agranoff BW, Minoshima S, Koeppe RA, Kuhl DE, Shulkin BL, Lucey MR. Source: Hepatology (Baltimore, Md.). 1997 August; 26(2): 277-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9252134

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Cerebral blood flow in basal ganglia is correlated with clinical signs of hepatic encephalopathy in patients with liver cirrhosis. Author(s): Iwasa M, Kaito M, Adachi Y, Watanabe Y, Matsumura K, Takeda K. Source: The American Journal of Gastroenterology. 2002 March; 97(3): 763-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11922581

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Cerebral changes in hepatic encephalopathy. Author(s): Watanabe A. Source: Journal of Gastroenterology and Hepatology. 1998 July; 13(7): 752-60. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9715431

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Cerebral energy metabolism in hepatic encephalopathy and hyperammonemia. Author(s): Rao KV, Norenberg MD. Source: Metabolic Brain Disease. 2001 June; 16(1-2): 67-78. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726090

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Cerebral proton and phosphorus-31 magnetic resonance spectroscopy in patients with subclinical hepatic encephalopathy. Author(s): Taylor-Robinson SD, Buckley C, Changani KK, Hodgson HJ, Bell JD. Source: Liver. 1999 October; 19(5): 389-98. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10533796

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Changes in cerebral receptors for gamma aminobutyric acid in patients with hepatic encephalopathy. Author(s): Ferenci P, Riederer P, Jellinger K, Schafer DF, Jones EA. Source: Liver. 1988 August; 8(4): 225-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2843723

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Charcoal-based hemodiabsorption liver support for episodic type C hepatic encephalopathy. Author(s): Hill K, Hu KQ, Cottrell A, Teichman S, Hillebrand DJ. Source: The American Journal of Gastroenterology. 2003 December; 98(12): 2763-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14687830

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Cirrhosis, hepatic encephalopathy, and propranolol. Author(s): Watson P, Hayes JR. Source: British Medical Journal (Clinical Research Ed.). 1983 October 8; 287(6398): 1067. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6412951

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Clinical correlation of neuropsychological tests with 1H magnetic resonance spectroscopy in hepatic encephalopathy. Author(s): Huda A, Guze BH, Thomas A, Bugbee M, Fairbanks L, Strouse T, Fawzy FI. Source: Psychosomatic Medicine. 1998 September-October; 60(5): 550-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9773757

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Clinical efficacy of lactulose in cirrhotic patients with and without subclinical hepatic encephalopathy. Author(s): Watanabe A, Sakai T, Sato S, Imai F, Ohto M, Arakawa Y, Toda G, Kobayashi K, Muto Y, Tsujii T, Kawasaki H, Okita K, Tanikawa K, Fujiyama S, Shimada S. Source: Hepatology (Baltimore, Md.). 1997 December; 26(6): 1410-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9397979

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Cognitive function and Epworth Sleepiness Scale in 'minimal' hepatic encephalopathy. Author(s): Vignatelli L, Mattarozzi K, Zanatta C, Stracciari A. Source: European Journal of Neurology : the Official Journal of the European Federation of Neurological Societies. 2001 July; 8(4): 369. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11422439

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Complications of cirrhosis III. Hepatic encephalopathy. Author(s): Butterworth RF. Source: Journal of Hepatology. 2000; 32(1 Suppl): 171-80. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10728803

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Conjunctival edema: a marker of increased mortality in patients with advanced hepatic encephalopathy and hepatocellular failure. Author(s): Akhtar AJ. Source: Digestive Diseases and Sciences. 2002 February; 47(2): 373-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11855552

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Constrictive pericarditis and hepatic encephalopathy. Author(s): Kerzner R, Barzilai B, Satyanarayana R. Source: Lancet. 2002 June 1; 359(9321): 1895. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12057551

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Correlation between a psychometric test and biochemical indices of hepatic encephalopathy in alcoholics. Author(s): Manganaro M, Zardi EM, Ceccanti M, Spada S, Attilia ML, Pancheri P, Biondi M, Paga G. Source: Hepatogastroenterology. 2000 March-April; 47(32): 455-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10791212

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Cortical origin of mini-asterixis in hepatic encephalopathy. Author(s): Timmermann L, Gross J, Kircheis G, Haussinger D, Schnitzler A. Source: Neurology. 2002 January 22; 58(2): 295-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11805261

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Cortico-spinal pathways and inhibitory mechanisms in hepatic encephalopathy. Author(s): Nolano M, Guardascione MA, Amitrano L, Perretti A, Fiorillo F, Ascione A, Santoro L, Caruso G. Source: Electroencephalography and Clinical Neurophysiology. 1997 February; 105(1): 72-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9118841

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Could an endogenous benzodiazepine ligand contribute to hepatic encephalopathy? Author(s): Mullen KD, Martin JV, Mendelson WB, Bassett ML, Jones EA. Source: Lancet. 1988 February 27; 1(8583): 457-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2893876

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Critical flicker frequency for quantification of low-grade hepatic encephalopathy. Author(s): Kircheis G, Wettstein M, Timmermann L, Schnitzler A, Haussinger D. Source: Hepatology (Baltimore, Md.). 2002 February; 35(2): 357-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11826409

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Decompressive shunts and hepatic encephalopathy. Author(s): Sachdev A, Duseja A. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S21-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025248

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Detection of benzodiazepine in hepatic encephalopathy. Author(s): Mullen KD. Source: Hepatology (Baltimore, Md.). 1995 February; 21(2): 604-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7843738

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Determination of 3-hydroxykynurenine in human brain and plasma by highperformance liquid chromatography with electrochemical detection. Increased concentrations in hepatic encephalopathy. Author(s): Pearson SJ, Reynolds GP. Source: Journal of Chromatography. 1991 April 19; 565(1-2): 436-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1874889

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Diagnosis and therapy of hepatic encephalopathy. Author(s): Mas A, Salmeron JM, Rodes J. Source: Advances in Experimental Medicine and Biology. 1994; 368: 119-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7741003

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Diagnosis and treatment of chronic hepatic encephalopathy. Author(s): Seery JP, Aspinall RJ, Taylor-Robinson SD. Source: Hosp Med. 1998 March; 59(3): 200-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9722346

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Diagnosis and treatment of hepatic encephalopathy. Author(s): Blei AT. Source: Bailliere's Best Practice & Research. Clinical Gastroenterology. 2000 December; 14(6): 959-74. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11139349

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Diagnosis of hepatic encephalopathy: will in vivo proton MRS play a role? Author(s): Jalan R, Olde Damink SW, Hayes PC, Wardlaw JM. Source: Hepatology (Baltimore, Md.). 1999 May; 29(5): 1605-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10216150

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Diagnostic tools for the detection of subclinical hepatic encephalopathy: comparison of standard and computerized psychometric tests with spectral-EEG. Author(s): Amodio P, Quero JC, Del Piccolo F, Gatta A, Schalm SW. Source: Metabolic Brain Disease. 1996 December; 11(4): 315-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8979251

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Dietary management of hepatic encephalopathy in cirrhotic patients: survey of current practice in United Kingdom. Author(s): Soulsby CT, Morgan MY. Source: Bmj (Clinical Research Ed.). 1999 May 22; 318(7195): 1391. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10334749

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Dietary management of hepatic encephalopathy. Author(s): Seymour CA, Whelan K. Source: Bmj (Clinical Research Ed.). 1999 May 22; 318(7195): 1364-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10334724

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Dietary management of patients with hepatic encephalopathy in hospitals in the United Kingdom. Author(s): Soulsby CT. Source: Nutrition (Burbank, Los Angeles County, Calif.). 1998 September; 14(9): 714-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9760596

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Disappearance of hepatic encephalopathy and improvement of liver function after surgical treatment of portal-systemic shunt in a patient with liver cirrhosis. Author(s): Moriya K, Kojima H, Matsumura M, Sakurai S, Imazu H, Uemura M, Honda H, Fukui H. Source: Hepatogastroenterology. 2003 July-August; 50(52): 1128-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12845996

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Disposition of venlafaxine enantiomers in rats with hepatic encephalopathy after chronic drug treatment. Author(s): Wikell C, Eap CB, Josefsson M, Apelqvist G, Ahlner J, Baumann P, Bengtsson F. Source: Chirality. 2002 May 5; 14(4): 347-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11968077

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Distinctive pattern of Bergmann glial pathology in human hepatic encephalopathy. Author(s): Kril JJ, Flowers D, Butterworth RF. Source: Mol Chem Neuropathol. 1997 August; 31(3): 279-87. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9336769

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Do benzodiazepine ligands contribute to hepatic encephalopathy? Author(s): Jones EA, Basile AS, Yurdaydin C, Skolnich P. Source: Advances in Experimental Medicine and Biology. 1993; 341: 57-69. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8116487

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Does brain damage (hepatic encephalopathy) improve without any complication and sequellae after liver transplantation? Author(s): Ichida T. Source: Intern Med. 2000 November; 39(11): 871-2. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11065233

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Double-blind randomized clinical trial comparing neomycin and placebo in the treatment of exogenous hepatic encephalopathy. Author(s): Strauss E, Tramote R, Silva EP, Caly WR, Honain NZ, Maffei RA, de Sa MF. Source: Hepatogastroenterology. 1992 December; 39(6): 542-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1483668

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Double-blind, double-dummy comparison between treatment with rifaximin and lactulose in patients with medium to severe degree hepatic encephalopathy. Author(s): Bucci L, Palmieri GC. Source: Current Medical Research and Opinion. 1993; 13(2): 109-18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8325041

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Driving under the influence of minimal hepatic encephalopathy. Author(s): Cordoba J, Lucke R. Source: Hepatology (Baltimore, Md.). 2004 March; 39(3): 599-601. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14999676

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Drug therapy in patients with hepatic encephalopathy--suggested guidelines for sedation and treatment of delirium tremens. Author(s): Pillans PI, Robins AH, Straughan JL. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1984 November 10; 66(19): 711. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6495116

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Early detection and treatment of hepatic encephalopathy. Author(s): Lockwood AH. Source: Current Opinion in Neurology. 1998 December; 11(6): 663-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9870134

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Early detection of hepatic encephalopathy by recording visual evoked potential (VEP). Author(s): Zamir D, Storch S, Kovach I, Storch R, Zamir C. Source: Rocz Akad Med Bialymst. 2002; 47: 186-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12533959

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Effect of bromocriptin therapy on the electroencephalogram in chronic hepatic encephalopathy. Author(s): Ahmed I, Sisk C. Source: Clin Electroencephalogr. 1983 April; 14(2): 86-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6851191

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Effects of an infusion of branched-chain amino acids on neurophysiological and psychometric testings in cirrhotic patients with mild hepatic encephalopathy. Author(s): Higuchi K, Shimizu Y, Nambu S, Miyabayashi C, Takahara T, Saito S, Hioki O, Kuwabara Y, Watanabe A. Source: Journal of Gastroenterology and Hepatology. 1994 July-August; 9(4): 366-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7948819

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Effects of high-normal and low-normal serum potassium levels on hepatic encephalopathy: facts, half-facts or artifacts? Author(s): Conn HO. Source: Hepatology (Baltimore, Md.). 1994 December; 20(6): 1637-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7982665

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Effects of sorbent suspension dialysis on plasma amino acid levels in cirrhotic patients with refractory hepatic encephalopathy. Author(s): Bauer E, Gendo A, Madl C, Garo F, Roth E, Kramer L. Source: Int J Artif Organs. 2002 October; 25(10): 923-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12456032

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Efficacy of lactulose in cirrhotic patients with subclinical hepatic encephalopathy. Author(s): Dhiman RK, Sawhney MS, Chawla YK, Das G, Ram S, Dilawari JB. Source: Digestive Diseases and Sciences. 2000 August; 45(8): 1549-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11007104

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Electrophysiological alterations in hepatic encephalopathy detected by brain mapping. Author(s): Malaguarnera M, Pistone G, Trovato BA, Scuderi M, Vinci M, Romano M, Marletta F. Source: Panminerva Medica. 1996 June; 38(2): 84-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8979739

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Embolization of portal-systemic shunts in cirrhotic patients with chronic recurrent hepatic encephalopathy. Author(s): Sakurabayashi S, Sezai S, Yamamoto Y, Hirano M, Oka H. Source: Cardiovascular and Interventional Radiology. 1997 March-April; 20(2): 120-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9030502

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Embolization of the left portal vein to inferior vena cava shunts for chronic recurrent hepatic encephalopathy via the mesenteric vein. Author(s): Takayama Y, Moriura S, Nagata J, Akutagawa A, Hirano A, Ishiguro S, Matsumoto T, Sato T. Source: Journal of Gastroenterology and Hepatology. 2001 December; 16(12): 1425-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11851846

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Embolization to reverse severe recurrent hepatic encephalopathy. Author(s): Uflacker R, d'Albuquerque LA, de Oliveira e Silva A, de Freitas JM, GamaRodrigues JJ. Source: Arquivos De Gastroenterologia. 1988; 25 Spec No: 21-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3202707

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Endoscopically placed nasogastrojejunal feeding tubes: a safe route for enteral nutrition in patients with hepatic encephalopathy. Author(s): Lee SS, Mathiasen RA, Lipkin CA, Colquhoun SD, Margulies DR. Source: The American Surgeon. 2002 February; 68(2): 196-200. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11842970

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Endotoxin and tumor necrosis factor-alpha in the pathogenesis of hepatic encephalopathy. Author(s): Odeh M. Source: Journal of Clinical Gastroenterology. 1994 September; 19(2): 146-53. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7963364

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Epileptiform abnormalities in hepatic encephalopathy. Author(s): Ficker DM, Westmoreland BF, Sharbrough FW. Source: Journal of Clinical Neurophysiology : Official Publication of the American Electroencephalographic Society. 1997 May; 14(3): 230-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9244163

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Evaluation of the efficacy and safety of rifaximin in the treatment of hepatic encephalopathy: a double-blind, randomized, dose-finding multi-centre study. Author(s): Williams R, James OF, Warnes TW, Morgan MY. Source: European Journal of Gastroenterology & Hepatology. 2000 February; 12(2): 2038. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10741936

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Evidence for an astrocytic glutamate transporter deficit in hepatic encephalopathy. Author(s): Chan H, Butterworth RF. Source: Neurochemical Research. 1999 November; 24(11): 1397-401. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10555780

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Evidence for the involvement of the benzodiazepine receptor complex in hepatic encephalopathy. Implications for treatment with benzodiazepine receptor antagonists. Author(s): Basile AS, Gammal SH. Source: Clinical Neuropharmacology. 1988 October; 11(5): 401-22. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2905934

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Evoked potentials for the evaluation of latent hepatic encephalopathy in pediatric liver transplant candidates. Author(s): Nora DB, Amaral OB, Busnello JV, Quevedo J, Vieira S, da Silveira TR, Kapczinski F. Source: Journal of Pediatric Gastroenterology and Nutrition. 2000 October; 31(4): 371-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11045832

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Experimental hepatic encephalopathy: changes in the binding of gammaaminobutyric acid. Author(s): Baraldi M, Zeneroli ZL. Source: Science. 1982 April 23; 216(4544): 427-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6280279

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Extracorporeal blood detoxification by sorbents in treatment of hepatic encephalopathy. Author(s): Ash SR. Source: Adv Ren Replace Ther. 2002 January; 9(1): 3-18. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11927902

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Factors in the aetiology of hepatic encephalopathy in the tropics. Author(s): Olubuyide IO, Atoba MA, Ayoola EA. Source: West Afr J Med. 1990 January-March; 9(1): 50-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2271422

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Factors predicting chronic hepatic encephalopathy after distal splenorenal shunt: a multivariate analysis of clinical and hemodynamic variables. Author(s): Spina GP, Santambrogio R, Opocher E, Pisani-Ceretti A, Ongari B, Rashidi B, Garancini P, Gallus G. Source: Surgery. 1993 September; 114(3): 519-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8367806

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Fatal acute tumor lysis syndrome, hepatic encephalopathy and flare phenomenon following combined androgen blockade. Author(s): Tanvetyanon T, Choudhury AM. Source: The Journal of Urology. 2004 April; 171(4): 1627. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15017238

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Figures or numbers: what determines hepatic encephalopathy? Author(s): Dhar A, Dilawari JB. Source: Trop Gastroenterol. 1996 April-June; 17(2): 84-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8783982

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First and second generation non absorbable disaccharides in the treatment of hepatic encephalopathy. Author(s): Capocaccia L, Riggio O, Merli M. Source: Ital J Gastroenterol. 1990 December; 22(6): 365-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2131958

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Flumazenil and hepatic encephalopathy. Author(s): Amaral OB, Quevedo J, Walz R, Kapczinski F. Source: Hepatology (Baltimore, Md.). 1999 April; 29(4): 1338-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10336339

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Flumazenil as a diagnostic test for latent hepatic encephalopathy. Author(s): Bruha R, Marecek Z, Brodanova M, Votruba M. Source: Journal of Hepatology. 1994 June; 20(6): 844. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7930489

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Flumazenil for hepatic encephalopathy grade III and IVa in patients with cirrhosis: an Italian multicenter double-blind, placebo-controlled, cross-over study. Author(s): Barbaro G, Di Lorenzo G, Soldini M, Giancaspro G, Bellomo G, Belloni G, Grisorio B, Annese M, Bacca D, Francavilla R, Barbarini G. Source: Hepatology (Baltimore, Md.). 1998 August; 28(2): 374-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9695999

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Flumazenil in the treatment of acute hepatic encephalopathy in cirrhotic patients: a double blind randomized placebo controlled study. Author(s): Laccetti M, Manes G, Uomo G, Lioniello M, Rabitti PG, Balzano A. Source: Dig Liver Dis. 2000 May; 32(4): 335-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11515632

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Flumazenil in the treatment of hepatic encephalopathy in children with fulminant liver failure. Author(s): Devictor D, Tahiri C, Lanchier C, Navelet Y, Durand P, Rousset A. Source: Intensive Care Medicine. 1995 March; 21(3): 253-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7790615

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Flumazenil in the treatment of hepatic encephalopathy. Author(s): Howard CD, Seifert CF. Source: The Annals of Pharmacotherapy. 1993 January; 27(1): 46-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8431621

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Flumazenil therapy for hepatic encephalopathy in cirrhotic patients: a double-blind pragmatic randomized, placebo study. Author(s): Cadranel JF, el Younsi M, Pidoux B, Zylberberg P, Benhamou Y, Valla D, Opolon P. Source: European Journal of Gastroenterology & Hepatology. 1995 April; 7(4): 325-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7600138

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Flumazenil therapy for hepatic encephalopathy. A double-blind cross over study. Author(s): Van der Rijt CC, Schalm SW, Meulstee J, Stijnen T. Source: Gastroenterologie Clinique Et Biologique. 1995 June-July; 19(6-7): 572-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7590022

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Flumazenil vs. placebo in hepatic encephalopathy in patients with cirrhosis: a metaanalysis. Author(s): Goulenok C, Bernard B, Cadranel JF, Thabut D, Di Martino V, Opolon P, Poynard T. Source: Alimentary Pharmacology & Therapeutics. 2002 March; 16(3): 361-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11876688

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Flumazenil: potential implications for hepatic encephalopathy. Author(s): Jones EA, Basile AS, Mullen KD, Gammal SH. Source: Pharmacology & Therapeutics. 1990; 45(3): 331-43. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2105510

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Flumazenil-induced psychotic disorder in hepatic encephalopathy. Author(s): Seebach J, Jost R. Source: Lancet. 1992 February 22; 339(8791): 488-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1346834

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Focal hepatic encephalopathy with status epilepticus: incomplete recovery after hepatic transplantation. Author(s): Annoni JM, Giostra E, Goumaz M, Slosman D, Hadengue A, Mentha G. Source: Digestive Diseases and Sciences. 1997 April; 42(4): 792-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9125651

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Focal neurological signs in cirrhotic patients with episodes of hepatic encephalopathy. Author(s): Kyprianou A, Hanna J, Mullen KD. Source: The American Journal of Gastroenterology. 2001 February; 96(2): 273-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11232663

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Focal neurological signs in hepatic encephalopathy in cirrhotic patients: an underestimated entity? Author(s): Cadranel JF, Lebiez E, Di Martino V, Bernard B, El Koury S, Tourbah A, Pidoux B, Valla D, Opolon P. Source: The American Journal of Gastroenterology. 2001 February; 96(2): 515-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11232699

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Further comments on the importance of serum potassium concentrations on early hepatic encephalopathy. Author(s): Conn HO. Source: Hepatology (Baltimore, Md.). 1996 January; 23(1): 190. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8550041

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GABA, benzodiazepines and hepatic encephalopathy. Author(s): Wilkinson SP. Source: European Journal of Gastroenterology & Hepatology. 1995 April; 7(4): 323-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7600137

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gamma-Aminobutyric acid (GABA) and hepatic encephalopathy: testing the validity of electroencephalographic evidence of the GABA hypothesis. Author(s): Myslobodsky MS. Source: Hepatogastroenterology. 1987 April; 34(2): 58-64. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3036678

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Gastrointestinal transit in cirrhotic patients: effect of hepatic encephalopathy and its treatment. Author(s): Van Thiel DH, Fagiuoli S, Wright HI, Chien MC, Gavaler JS. Source: Hepatology (Baltimore, Md.). 1994 January; 19(1): 67-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8276369

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Glial fibrillary acidic protein and S-100 protein in human hepatic encephalopathy: immunocytochemical demonstration of dissociation of two glia-associated proteins. Author(s): Kimura T, Budka H. Source: Acta Neuropathologica. 1986; 70(1): 17-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3727931

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Glial fibrillary acidic protein in hepatic encephalopathy. An immunohistochemical study. Author(s): Sobel RA, DeArmond SJ, Forno LS, Eng LF. Source: Journal of Neuropathology and Experimental Neurology. 1981 November; 40(6): 625-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7028923

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Glucuronidation of oxazepam is not spared in patients with hepatic encephalopathy. Author(s): Sonne J, Andreasen PB, Loft S, Dossing M, Andreasen F. Source: Hepatology (Baltimore, Md.). 1990 June; 11(6): 951-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2365292

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Glutamatergic neurotransmission in hepatic encephalopathy. Author(s): Maddison JE, Watson WE, Johnston GA. Source: Alcohol Alcohol Suppl. 1993; 2: 169-73. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7538300

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Glutamic acid and glutamine levels in serum and cerebrospinal fluid in hepatic encephalopathy. Author(s): Watanabe A, Takei N, Higashi T, Shiota T, Nakatsukasa H, Fujiwara M, Sakata T, Nagashima H. Source: Biochem Med. 1984 October; 32(2): 225-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6150706

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Glutamine as a pathogenic factor in hepatic encephalopathy. Author(s): Albrecht J, Dolinska M. Source: Journal of Neuroscience Research. 2001 July 1; 65(1): 1-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11433423

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Glycogen in leukocytes from patients with hepatic encephalopathy. Author(s): Yokoi S, Amano N. Source: Acta Neuropathologica. 1984; 62(4): 284-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6375238

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Growth hormone (GH) secretion in hepatic encephalopathy. Author(s): Langer M, Masala A, Alagna S, Rassu S, Madeddu G, Solinas A, Chiandussi L. Source: Clinical Endocrinology. 1981 February; 14(2): 189-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6790202

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Helicobacter pylori and hepatic encephalopathy. Author(s): Duseja A, Sachdev A, Dhiman RK, Chawla YK. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S31-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025251

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Helicobacter pylori infection and hepatic encephalopathy. Author(s): Zullo A, Hassan C, Chakrabarti P, Morini S. Source: Dig Liver Dis. 2002 January; 34(1): 86. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11926579

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Helicobacter pylori infection does not correlate with plasma ammonia concentration and hepatic encephalopathy in patients with cirrhosis. Author(s): Huber M, Rossle M, Siegerstetter V, Ochs A, Haag K, Kist M, Blum HE. Source: Hepatogastroenterology. 2001 March-April; 48(38): 541-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11379349

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Helicobacter pylori infection is not associated with subclinical hepatic encephalopathy in stable cirrhotic patients. Author(s): Scotiniotis IA, Lucey MR, Metz DC. Source: Digestive Diseases and Sciences. 2001 December; 46(12): 2744-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11768268

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Helicobacter pylori is not a risk factor for hepatic encephalopathy. Author(s): Calvet X, Nogueras C, Roque M, Sanfeliu I. Source: Dig Liver Dis. 2001 June-July; 33(5): 414-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11529653

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Hepatic encephalopathy and nitric oxide. Author(s): Schliess F, Haussinger D. Source: Journal of Hepatology. 2001 April; 34(4): 610-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11394664

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Hepatic encephalopathy as a complication of liver disease. Author(s): vom Dahl S, Kircheis G, Haussinger D. Source: World Journal of Gastroenterology : Wjg. 2001 April; 7(2): 152-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11819754

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Hepatic encephalopathy caused by congenital extrahepatic portosystemic venous shunt. Author(s): Ishii Y, Inagaki Y, Hirai K, Aoki T. Source: Journal of Hepato-Biliary-Pancreatic Surgery. 2000; 7(5): 524-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11180882

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Hepatic encephalopathy in liver cirrhosis: pathogenesis, diagnosis and management. Author(s): Gerber T, Schomerus H. Source: Drugs. 2000 December; 60(6): 1353-70. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11152016

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Hepatic encephalopathy in pregnancy. Author(s): Aggarwal R. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S78-80. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025263

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Hepatic encephalopathy secondary to intrahepatic portosystemic venous shunt: balloon-occluded retrograde transvenous embolization with n-butyl cyanoacrylate and microcoils. Author(s): Yamagami T, Nakamura T, Iida S, Kato T, Tanaka O, Matsushima S, Ito H, Okuyama C, Ushijima Y, Shiga K, Nishimura T. Source: Cardiovascular and Interventional Radiology. 2002 May-June; 25(3): 219-21. Epub 2002 March 27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12058220

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Hepatic encephalopathy syndromes. Author(s): Tandon BN. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S4-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025244

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Hepatic encephalopathy. Author(s): Lockwood AH. Source: Neurologic Clinics. 2002 February; 20(1): 241-6, Vii. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11754309

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Hepatic Encephalopathy. Author(s): Blei AT, Cordoba J; Practice Parameters Committee of the American College of Gastroenterology. Source: The American Journal of Gastroenterology. 2001 July; 96(7): 1968-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11467622

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Hepatic encephalopathy. Author(s): Ong JP, Mullen KD. Source: European Journal of Gastroenterology & Hepatology. 2001 April; 13(4): 325-34. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11338058

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Hepatic encephalopathy. Metabolic consequence of cirrhosis often is reversible. Author(s): Abou-Assi S, Vlahcevic ZR. Source: Postgraduate Medicine. 2001 February; 109(2): 52-4, 57-60, 63-5 Passim. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11272694

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Hepatic encephalopathy: a neuropsychiatric disorder involving multiple neurotransmitter systems. Author(s): Butterworth RF. Source: Current Opinion in Neurology. 2000 December; 13(6): 721-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11148676

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Hepatic encephalopathy: a review. Author(s): Lizardi-Cervera J, Almeda P, Guevara L, Uribe M. Source: Ann Hepatol. 2003 July-September; 2(3): 122-30. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15115963

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Hepatic encephalopathy--definition, nomenclature, diagnosis, and quantification: final report of the working party at the 11th World Congresses of Gastroenterology, Vienna, 1998. Author(s): Ferenci P, Lockwood A, Mullen K, Tarter R, Weissenborn K, Blei AT. Source: Hepatology (Baltimore, Md.). 2002 March; 35(3): 716-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11870389

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Home lactulose enema: prevention of hepatic encephalopathy at home. Author(s): Saito T, Shinzawa H, Watanabe H, Togashi H, Kawata S. Source: Journal of Gastroenterology. 2002 January; 37(1): 68-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11824804

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Improvement in cerebral perfusion after MARS therapy: further clues about the pathogenesis of hepatic encephalopathy? Author(s): Jalan R, Williams R. Source: Liver Transplantation : Official Publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society. 2001 August; 7(8): 713-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11510017

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Improvement of hepatic encephalopathy treated with flumazenil. Author(s): Grimm G, Ferenci P, Katzenschlager R, Madl C, Schneeweiss B, Laggner AN, Lenz K, Gangl A. Source: Lancet. 1988 December 17; 2(8625): 1392-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2904525

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Improvement of magnetic resonance spectroscopic abnormalities but not pallidal hyperintensity followed amelioration of hepatic encephalopathy after occlusion of a large spleno-renal shunt. Author(s): Cordoba J, Olive G, Alonso J, Rovira A, Segarra A, Perez M, Jacas C, Vargas V. Source: Journal of Hepatology. 2001 January; 34(1): 176-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11211900

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In vivo brain magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) in hepatic encephalopathy. Author(s): Chamuleau RA, Vogels BA, Bosman DK, Bovee WM. Source: Advances in Experimental Medicine and Biology. 1994; 368: 23-31. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7741013

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Increased activities of MAOA and MAOB in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy. Author(s): Rao VL, Giguere JF, Layrargues GP, Butterworth RF. Source: Brain Research. 1993 September 10; 621(2): 349-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8242348

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Increased availability of central benzodiazepine receptors in patients with chronic hepatic encephalopathy and alcohol related cirrhosis. Author(s): Jalan R, Turjanski N, Taylor-Robinson SD, Koepp MJ, Richardson MP, Wilson JA, Bell JD, Brooks DJ. Source: Gut. 2000 April; 46(4): 546-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10716686

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Increased density of brain histamine H(1) receptors in rats with portacaval anastomosis and in cirrhotic patients with chronic hepatic encephalopathy. Author(s): Lozeva V, Tuomisto L, Sola D, Plumed C, Hippelainen M, Butterworth R. Source: Hepatology (Baltimore, Md.). 2001 June; 33(6): 1370-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11391525

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Increased density of catalytic sites and expression of brain monoamine oxidase A in humans with hepatic encephalopathy. Author(s): Mousseau DD, Baker GB, Butterworth RF. Source: Journal of Neurochemistry. 1997 March; 68(3): 1200-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9048767

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Increased intracranial pressure and hepatic encephalopathy in chronic liver disease. Author(s): Crippin JS, Gross JB Jr, Lindor KD. Source: The American Journal of Gastroenterology. 1992 July; 87(7): 879-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1615943

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Increased signals seen in globus pallidus in T1-weighted magnetic resonance imaging in cirrhotics are not suggestive of chronic hepatic encephalopathy. Author(s): Thuluvath PJ, Edwin D, Yue NC, deVilliers C, Hochman S, Klein A. Source: Hepatology (Baltimore, Md.). 1995 February; 21(2): 440-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7843718

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Increased turnover of Gc-globulin in patients with hepatic encephalopathy. Author(s): Schiodt FV, Clemmesen JO, Bondesen S, Dahl B, Ott P. Source: Scandinavian Journal of Gastroenterology. 2001 September; 36(9): 998-1003. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11521994

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Infection and the progression of hepatic encephalopathy in acute liver failure. Author(s): Vaquero J, Polson J, Chung C, Helenowski I, Schiodt FV, Reisch J, Lee WM, Blei AT. Source: Gastroenterology. 2003 September; 125(3): 755-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12949721

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Influence of hepatic encephalopathy on health-related quality of life in patients with cirrhosis. Author(s): Arguedas MR, DeLawrence TG, McGuire BM. Source: Digestive Diseases and Sciences. 2003 August; 48(8): 1622-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12924658

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Infusion of branched-chain enriched amino acid solution in patients with hepatic encephalopathy. Author(s): Freund H, Dienstag J, Lehrich J, Yoshimura N, Bradford RR, Rosen H, Atamian S, Slemmer E, Holroyde J, Fischer JE. Source: Annals of Surgery. 1982 August; 196(2): 209-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6284073

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Intensive enteral feeding in advanced cirrhosis: reversal of malnutrition without precipitation of hepatic encephalopathy. Author(s): Charlton CP, Buchanan E, Holden CE, Preece MA, Green A, Booth IW, Tarlow MJ. Source: Archives of Disease in Childhood. 1992 May; 67(5): 603-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1599297

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Interplay of portal pressure, portal perfusion and hepatic arterial inflow in modulating expression of hepatic encephalopathy in patients with spontaneous or artificially created portosystemic shunts. Author(s): Mullen KD. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S25-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025249

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Intractable hepatic encephalopathy after tips with polytetrafluoroethylene-covered stent-graft. Author(s): Riggio O, Nicolao F, Angeloni S, Masini A, Salvatori F, Fanelli F, Efrati C, Merli M. Source: Scandinavian Journal of Gastroenterology. 2003 May; 38(5): 570-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12795474

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Is intravenous administration of branched chain amino acids effective in the treatment of hepatic encephalopathy? A multicenter study. Author(s): Wahren J, Denis J, Desurmont P, Eriksson LS, Escoffier JM, Gauthier AP, Hagenfeldt L, Michel H, Opolon P, Paris JC, Veyrac M. Source: Hepatology (Baltimore, Md.). 1983 July-August; 3(4): 475-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6345330

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Is it a medical error if we do not screen cirrhotic patients for minimal hepatic encephalopathy? Author(s): Quero Guillen JC, Groeneweg M, Jimenez Saenz M, Schalm SW, Herrerias Gutierrez JM. Source: Rev Esp Enferm Dig. 2002 September; 94(9): 544-57. Review. English, Spanish. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12587235

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Is serum prolactin of prognostic value in hepatic encephalopathy? Author(s): Nanivadekar SA, Sainani GS. Source: J Assoc Physicians India. 1988 March; 36(3): 193-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3182662

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Lack of preventive effect of branched-chain amino acid solution on postoperative hepatic encephalopathy in patients with cirrhosis: a randomized, prospective trial. Author(s): Kanematsu T, Koyanagi N, Matsumata T, Kitano S, Takenaka K, Sugimachi K. Source: Surgery. 1988 September; 104(3): 482-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2842882

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Lactitol and lactulose for the treatment of subclinical hepatic encephalopathy in cirrhotic patients. A randomised, cross-over study. Author(s): Morgan MY, Alonso M, Stanger LC. Source: Journal of Hepatology. 1989 March; 8(2): 208-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2654285

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Lactitol in prevention of recurrent episodes of hepatic encephalopathy in cirrhotic patients with portal-systemic shunt. Author(s): Riggio O, Balducci G, Ariosto F, Merli M, Pieche U, Pinto G, Tremiterra S, Ziparo V, Capocaccia L. Source: Digestive Diseases and Sciences. 1989 June; 34(6): 823-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2656134

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Lactitol in the treatment of chronic hepatic encephalopathy: an open comparison with lactulose. Author(s): Lanthier PL, Morgan MY. Source: Gut. 1985 April; 26(4): 415-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3979914

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Lactitol in the treatment of chronic hepatic encephalopathy--a randomized cross-over comparison with lactulose. Author(s): Riggio O, Balducci G, Ariosto F, Merli M, Tremiterra S, Ziparo V, Capocaccia L. Source: Hepatogastroenterology. 1990 October; 37(5): 524-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2253931

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Lactitol in treatment of chronic hepatic encephalopathy. A meta-analysis. Author(s): Camma C, Fiorello F, Tine F, Marchesini G, Fabbri A, Pagliaro L. Source: Digestive Diseases and Sciences. 1993 May; 38(5): 916-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8482191

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Lactitol or lactulose in the treatment of chronic hepatic encephalopathy: results of a meta-analysis. Author(s): Blanc P, Daures JP, Rouillon JM, Peray P, Pierrugues R, Larrey D, Gremy F, Michel H. Source: Hepatology (Baltimore, Md.). 1992 February; 15(2): 222-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1531204

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Lactitol versus lactulose in the treatment of chronic hepatic encephalopathy. A double-blind, randomised, cross-over study. Author(s): Morgan MY, Hawley KE, Stambuk D. Source: Journal of Hepatology. 1987 April; 4(2): 236-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3295020

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Lactitol vs. lactulose in the treatment of acute hepatic encephalopathy in cirrhotic patients: a double-blind, randomized trial. Author(s): Morgan MY, Hawley KE. Source: Hepatology (Baltimore, Md.). 1987 November-December; 7(6): 1278-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3315932

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Lactulose and combination therapy of hepatic encephalopathy: the role of the intestinal microflora. Author(s): Weber FL Jr. Source: Digestive Diseases (Basel, Switzerland). 1996; 14 Suppl 1: 53-63. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8872452

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Lactulose or lactose in hepatic encephalopathy? Author(s): Desai HG. Source: Indian J Gastroenterol. 1983 April; 2(1): 7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6565636

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Lactulose: a crucial element in treating hepatic encephalopathy. Author(s): Gever LN. Source: Nursing. 1982 August; 12(8): 76-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6920588

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L-Carnitine in the treatment of mild or moderate hepatic encephalopathy. Author(s): Malaguarnera M, Pistone G, Astuto M, Dell'Arte S, Finocchiaro G, Lo Giudice E, Pennisi G. Source: Digestive Diseases (Basel, Switzerland). 2003; 21(3): 271-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14571103

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Liver assist devices (LADs) will not be used to treat fulminant hepatic failure (FHF), but its consequences, namely hepatic encephalopathy (HE) Author(s): Sussman NL, Kelly JH. Source: Artificial Organs. 1993 January; 17(1): 43-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8422234

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Liver function, cerebral blood flow autoregulation, and hepatic encephalopathy in fulminant hepatic failure. Author(s): Strauss G, Hansen BA, Kirkegaard P, Rasmussen A, Hjortrup A, Larsen FS. Source: Hepatology (Baltimore, Md.). 1997 April; 25(4): 837-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9096585

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Localized 1H NMR spectroscopy in patients with chronic hepatic encephalopathy. Analysis of changes in cerebral glutamine, choline and inositols. Author(s): Kreis R, Farrow N, Ross BD. Source: Nmr in Biomedicine. 1991 April; 4(2): 109-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1650239

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Long-term effects of Enterococcus faecium SF68 versus lactulose in the treatment of patients with cirrhosis and grade 1-2 hepatic encephalopathy. Author(s): Loguercio C, Abbiati R, Rinaldi M, Romano A, Del Vecchio Blanco C, Coltorti M. Source: Journal of Hepatology. 1995 July; 23(1): 39-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8530808

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Long-term oral branched-chain amino acid treatment in chronic hepatic encephalopathy. A randomized double-blind casein-controlled trial. The Italian Multicenter Study Group. Author(s): Marchesini G, Dioguardi FS, Bianchi GP, Zoli M, Bellati G, Roffi L, Martines D, Abbiati R. Source: Journal of Hepatology. 1990 July; 11(1): 92-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2204661

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Long-term results of balloon-occluded retrograde transvenous obliteration for the treatment of gastric varices and hepatic encephalopathy. Author(s): Fukuda T, Hirota S, Sugimura K. Source: Journal of Vascular and Interventional Radiology : Jvir. 2001 March; 12(3): 32736. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11287510

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Low serum total thyroxine and free triiodothyronine in patients with hepatic encephalopathy due to non-alcoholic cirrhosis. Author(s): Kayacetin E, Kisakol G, Kaya A. Source: Swiss Medical Weekly : Official Journal of the Swiss Society of Infectious Diseases, the Swiss Society of Internal Medicine, the Swiss Society of Pneumology. 2003 April 5; 133(13-14): 210-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12811678

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Magnetic resonance imaging and spectroscopy in hepatic encephalopathy. Author(s): Gupta RK, Dhiman RK. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S45-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025255

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Magnetic resonance spectroscopy in the study of hyperammonemia and hepatic encephalopathy. Author(s): Kanamori K, Bluml S, Ross B. Source: Advances in Experimental Medicine and Biology. 1997; 420: 185-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9286434

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Management of agitation and convulsions in hepatic encephalopathy. Author(s): Prabhakar S, Bhatia R. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S54-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025257

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Management of hepatic encephalopathy. Author(s): Plauth M, Merli M, Kondrup J. Source: The New England Journal of Medicine. 1997 December 25; 337(26): 1921-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9417530

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Manganese and chronic hepatic encephalopathy. Author(s): Krieger D, Krieger S, Jansen O, Gass P, Theilmann L, Lichtnecker H. Source: Lancet. 1995 July 29; 346(8970): 270-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7630246

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Manganese toxicity, dopaminergic dysfunction and hepatic encephalopathy. Author(s): Butterworth RF, Spahr L, Fontaine S, Layrargues GP. Source: Metabolic Brain Disease. 1995 December; 10(4): 259-67. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8847990

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Markers of reversible hepatic encephalopathy. Author(s): Krieger D, Krieger S. Source: Neurology. 1997 October; 49(4): 1187-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9339732

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Methods for assessing hepatic encephalopathy. Author(s): Pappas SC, Jones EA. Source: Seminars in Liver Disease. 1983 November; 3(4): 298-307. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6359425

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Mini-asterixis in hepatic encephalopathy induced by pathologic thalamo-motorcortical coupling. Author(s): Timmermann L, Gross J, Butz M, Kircheis G, Haussinger D, Schnitzler A. Source: Neurology. 2003 September 9; 61(5): 689-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12963765

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Minimal hepatic encephalopathy impairs fitness to drive. Author(s): Wein C, Koch H, Popp B, Oehler G, Schauder P. Source: Hepatology (Baltimore, Md.). 2004 March; 39(3): 739-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14999692

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Minimal hepatic encephalopathy: a permanent source of discussion. Author(s): Weissenborn K. Source: Hepatology (Baltimore, Md.). 2002 February; 35(2): 494-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11826427

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Minimal hepatic encephalopathy: diagnosis by neuropsychological and neurophysiologic methods. Author(s): Kharbanda PS, Saraswat VA, Dhiman RK. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S37-41. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025253

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Minimal hepatic encephalopathy: longitudinal effects of liver transplantation. Author(s): Mattarozzi K, Stracciari A, Vignatelli L, D'Alessandro R, Morelli MC, Guarino M. Source: Archives of Neurology. 2004 February; 61(2): 242-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14967773

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Minimal hepatic encephalopathy: natural history, impact on daily functioning, and role of treatment. Author(s): Duseja A, Dhiman RK, Saraswat VA, Chawla Y. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S42-4. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025254

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Movement dysfunction and hepatic encephalopathy. Author(s): Layrargues GP. Source: Metabolic Brain Disease. 2001 June; 16(1-2): 27-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726085

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MR and 1H MR spectroscopy of the brain in patients with liver cirrhosis and early stages of hepatic encephalopathy. Author(s): Tarasow E, Panasiuk A, Siergiejczyk L, Orzechowska-Bobkiewicz A, Lewszuk A, Walecki J, Prokopowicz D. Source: Hepatogastroenterology. 2003 November-December; 50(54): 2149-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14696484

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MR imaging and (1)H spectroscopy of brain metabolites in hepatic encephalopathy: time-course of renormalization after liver transplantation. Author(s): Naegele T, Grodd W, Viebahn R, Seeger U, Klose U, Seitz D, Kaiser S, Mader I, Mayer J, Lauchart W, Gregor M, Voigt K. Source: Radiology. 2000 September; 216(3): 683-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10966695

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MRI findings in chronic hepatic encephalopathy depend on portosystemic shunt: results of a controlled prospective clinical investigation. Author(s): Krieger S, Jauss M, Jansen O, Stiehl A, Sauer P, Geissler M, Theilmann L, Krieger D. Source: Journal of Hepatology. 1997 July; 27(1): 121-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9252084

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Myocarditis associated with hepatic encephalopathy. Author(s): Gopinathan VP, Choudhary NR, Hazra NK. Source: J Indian Med Assoc. 1983 November; 81(9-10): 167-8. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6674355

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Natural benzodiazepines and hepatic encephalopathy. Author(s): Mullen KD, Jones EA. Source: Seminars in Liver Disease. 1996 August; 16(3): 255-64. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8989811

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Neomycin should not be used to treat hepatic encephalopathy. Author(s): Curioso WH, Monkemuller KE. Source: Bmj (Clinical Research Ed.). 2001 July 28; 323(7306): 233. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11496883

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Neuroactive amino acids in hepatic encephalopathy. Author(s): Butterworth RF. Source: Metabolic Brain Disease. 1996 June; 11(2): 165-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8776718

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Neurological deficits in "awake" cirrhotic patients on hepatic encephalopathy treatment: missed metabolic or metal disorder? Author(s): Mullen KD, Cole M, Foley JM. Source: Gastroenterology. 1996 July; 111(1): 256-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8698210

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Neuronal nitric oxide synthase and Hepatic Encephalopathy. Author(s): Rao VL, Butterworth RF. Source: Metabolic Brain Disease. 1998 September; 13(3): 175-89. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9804363

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Neurophysiological evidence of cognitive impairment in patients without hepatic encephalopathy after transjugular intrahepatic portosystemic shunts. Author(s): Kramer L, Bauer E, Gendo A, Funk G, Madl C, Pidlich J, Gangl A. Source: The American Journal of Gastroenterology. 2002 January; 97(1): 162-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11808942

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Neuropsychiatric condition must be thoroughly assessed before treatment of hepatic encephalopathy. Author(s): Lewis MB. Source: Bmj (Clinical Research Ed.). 1999 August 14; 319(7207): 455. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10445943

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Neuropsychiatric implications of brain tryptophan perturbations appearing in hepatic encephalopathy. Author(s): Bengtsson F, Bergqvist P. Source: Advances in Experimental Medicine and Biology. 1996; 398: 387-95. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8906294

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Neuropsychological characterization and detection of subclinical hepatic encephalopathy. Author(s): McCrea M, Cordoba J, Vessey G, Blei AT, Randolph C. Source: Archives of Neurology. 1996 August; 53(8): 758-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8759982

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Neuropsychological characterization of hepatic encephalopathy. Author(s): Weissenborn K, Ennen JC, Schomerus H, Ruckert N, Hecker H. Source: Journal of Hepatology. 2001 May; 34(5): 768-73. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11434627

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Neurospectroscopic alterations and globus pallidus hyperintensity as related magnetic resonance markers of reversible hepatic encephalopathy. Author(s): Pujol J, Kulisevsky J, Moreno A, Deus J, Alonso J, Balanzo J, Marti-Vilalta JL, Capdevila A. Source: Neurology. 1996 December; 47(6): 1526-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8960739

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Neurotransmitter dysfunction in hepatic encephalopathy: new approaches and new findings. Author(s): Butterworth RF. Source: Metabolic Brain Disease. 2001 June; 16(1-2): 55-65. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726089

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Newer approaches to therapy of hepatic encephalopathy. Author(s): Ferenci P, Herneth A, Steindl P. Source: Seminars in Liver Disease. 1996 August; 16(3): 329-38. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8989818

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Newer aspects of hepatic encephalopathy. Author(s): Mullen KD. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S17-20. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025247

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Nitric oxide in hepatic encephalopathy and hyperammonemia. Author(s): Rao VL. Source: Neurochemistry International. 2002 August-September; 41(2-3): 161-70. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12020616

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Non-absorbable disaccharides for hepatic encephalopathy: systematic review of randomised trials. Author(s): Als-Nielsen B, Gluud LL, Gluud C. Source: Bmj (Clinical Research Ed.). 2004 May 1; 328(7447): 1046. Epub 2004 March 30. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15054035

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Nonalcoholic cirrhosis associated with neuropsychological dysfunction in the absence of overt evidence of hepatic encephalopathy. Author(s): Tarter RE, Hegedus AM, Van Thiel DH, Schade RR, Gavaler JS, Starzl TE. Source: Gastroenterology. 1984 June; 86(6): 1421-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6714571

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Nutrition in the management of hepatic encephalopathy. Author(s): Srivastava N, Singh N, Joshi YK. Source: Trop Gastroenterol. 2003 April-June; 24(2): 59-62. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14603821

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Nutritional management of hepatic encephalopathy. Author(s): Bower RH, Fischer JE. Source: Adv Nutr Res. 1983; 5: 1-11. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6133418

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Nutritional support in hepatic encephalopathy. Author(s): Mizock BA. Source: Nutrition (Burbank, Los Angeles County, Calif.). 1999 March; 15(3): 220-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10198918

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Objective measurement of hepatic encephalopathy by means of automated EEG analysis. Author(s): Van der Rijt CC, Schalm SW, De Groot GH, De Vlieger M. Source: Electroencephalography and Clinical Neurophysiology. 1984 May; 57(5): 423-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6201336

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Obliteration of portal systemic shunts as therapy for hepatic encephalopathy in patients with non-cirrhotic portal hypertension. Author(s): Ito T, Ikeda N, Watanabe A, Sue K, Kakio T, Mimura H, Tsuji T. Source: Gastroenterol Jpn. 1992 December; 27(6): 759-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1468606

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Opioid receptor ligands in human hepatic encephalopathy. Author(s): Yurdaydin C, Karavelioglu D, Onaran O, Celik T, Yasa MH, Uzunalimoglu O. Source: Journal of Hepatology. 1998 November; 29(5): 796-801. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9833918

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Oral BCAA in the treatment of chronic hepatic encephalopathy. Author(s): Marchesini G, Bianchi G, Zoli M. Source: Journal of Hepatology. 1991 March; 12(2): 267. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1888373

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Oral L-ornithine-L-aspartate therapy of chronic hepatic encephalopathy: results of a placebo-controlled double-blind study. Author(s): Stauch S, Kircheis G, Adler G, Beckh K, Ditschuneit H, Gortelmeyer R, Hendricks R, Heuser A, Karoff C, Malfertheiner P, Mayer D, Rosch W, Steffens J. Source: Journal of Hepatology. 1998 May; 28(5): 856-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9625322

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Orthograde whole gut irrigation with mannite versus paromomycine + lactulose as prophylaxis of hepatic encephalopathy in patients with cirrhosis and upper gastrointestinal bleeding: results of a controlled randomized trial. Author(s): Tromm A, Griga T, Greving I, Hilden H, Huppe D, Schwegler U, Micklefield GH, May B. Source: Hepatogastroenterology. 2000 March-April; 47(32): 473-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10791216

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Overt hepatic encephalopathy precipitated by zinc deficiency. Author(s): Van der Rijt CC, Schalm SW, Schat H, Foeken K, De Jong G. Source: Gastroenterology. 1991 April; 100(4): 1114-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2001810

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Overview of randomized clinical trials of oral branched-chain amino acid treatment in chronic hepatic encephalopathy. Author(s): Fabbri A, Magrini N, Bianchi G, Zoli M, Marchesini G. Source: Jpen. Journal of Parenteral and Enteral Nutrition. 1996 March-April; 20(2): 15964. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8676537

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Oxidative injury and other metabolic disorders in hepatic encephalopathy. Author(s): Negru T, Ghiea V, Pasarica D. Source: Rom J Physiol. 1999 January-June; 36(1-2): 29-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11068602

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Oxindole in pathogenesis of hepatic encephalopathy. Author(s): Moroni F, Carpenedo R, Venturini I, Baraldi M, Zeneroli ML. Source: Lancet. 1998 June 20; 351(9119): 1861. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9652676

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Partial pressure of ammonia versus ammonia in hepatic encephalopathy. Author(s): Kramer L, Tribl B, Gendo A, Zauner C, Schneider B, Ferenci P, Madl C. Source: Hepatology (Baltimore, Md.). 2000 January; 31(1): 30-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10613724

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Pathogenesis of hepatic encephalopathy in acute liver failure. Author(s): Vaquero J, Chung C, Cahill ME, Blei AT. Source: Seminars in Liver Disease. 2003 August; 23(3): 259-69. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14523679

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Pathogenesis of hepatic encephalopathy. Author(s): Jones EA. Source: Clinics in Liver Disease. 2000 May; 4(2): 467-85. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11232201

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Pathogenesis of hepatic encephalopathy: update on molecular mechanisms. Author(s): Butterworth RF. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S11-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025246

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Persistence of mild parkinsonism 4 months after liver transplantation in patients with preoperative minimal hepatic encephalopathy: a study on neuroradiological and blood manganese changes. Author(s): Lazeyras F, Spahr L, DuPasquier R, Delavelle J, Burkhard P, Hadengue A, Hochstrasser D, Mentha G, Giostra E, Terrier F, Vingerhoets F. Source: Transplant International : Official Journal of the European Society for Organ Transplantation. 2002 April; 15(4): 188-95. Epub 2002 April 04. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11976741

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Plasma levels of pipecolic acid, both L- and D-enantiomers, in patients with chronic liver diseases, especially hepatic encephalopathy. Author(s): Fujita T, Amuro Y, Hada T, Higashino K. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 1999 September; 287(1-2): 99-109. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10509899

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Prevalence and natural history of subclinical hepatic encephalopathy in cirrhosis. Author(s): Das A, Dhiman RK, Saraswat VA, Verma M, Naik SR. Source: Journal of Gastroenterology and Hepatology. 2001 May; 16(5): 531-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11350549

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Primary hypothyroidism masquerading as hepatic encephalopathy: case report and review of the literature. Author(s): Thobe N, Pilger P, Jones MP. Source: Postgraduate Medical Journal. 2000 July; 76(897): 424-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10878207

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Prognostic value of altered oral glutamine challenge in patients with minimal hepatic encephalopathy. Author(s): Romero-Gomez M, Grande L, Camacho I. Source: Hepatology (Baltimore, Md.). 2004 April; 39(4): 939-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15057897

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Proton MR spectroscopy of neurometabolites in hepatic encephalopathy during Lornithine-L-aspartate treatment--results of a pilot study. Author(s): Delcker A, Turowski B, Mihm U, Raab P, Rusch O, Pilatus U, Zeuzem S, Zanella FE. Source: Metabolic Brain Disease. 2002 June; 17(2): 103-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12083335

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Quality of life in cirrhotics with minimal hepatic encephalopathy. Author(s): Schomerus H, Hamster W. Source: Metabolic Brain Disease. 2001 June; 16(1-2): 37-41. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726087

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Quantitative EEG analysis and evoked potentials to measure (latent) hepatic encephalopathy. Author(s): van der Rijt CC, Schalm SW. Source: Journal of Hepatology. 1992 March; 14(2-3): 141-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1500675

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Quantitative psychometric testing and subclinical hepatic encephalopathy-comparative study between encephalopathic and non-encephalopathic patients with liver cirrhosis. Author(s): Shiota T. Source: Acta Medica Okayama. 1984 April; 38(2): 193-205. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6731029

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Quantitative T1 mapping of hepatic encephalopathy using magnetic resonance imaging. Author(s): Shah NJ, Neeb H, Zaitsev M, Steinhoff S, Kircheis G, Amunts K, Haussinger D, Zilles K. Source: Hepatology (Baltimore, Md.). 2003 November; 38(5): 1219-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14578860

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Raised intracranial pressure in hepatic encephalopathy. Author(s): Mukherjee KK, Chhabra R, Khosla VK. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S62-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025259

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Re: management of TIPS-related refractory hepatic encephalopathy with reduced Wallgraft endoprostheses. Author(s): York JA. Source: Journal of Vascular and Interventional Radiology : Jvir. 2003 November; 14(11): 1469; Author Reply 1469. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14605116

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Reversal of diuretic-induced hepatic encephalopathy with infusion of albumin but not colloid. Author(s): Jalan R, Kapoor D. Source: Clinical Science (London, England : 1979). 2004 May; 106(5): 467-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14678008

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Reversal of transjugular intrahepatic portosystemic shunt (TIPS)-induced hepatic encephalopathy using a strictured self-expanding covered stent. Author(s): Cox MW, Soltes GD, Lin PH, Bush RL, Lumsden AB. Source: Cardiovascular and Interventional Radiology. 2003 November-December; 26(6): 539-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15061178

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Role of circulating neurotoxins in the pathogenesis of hepatic encephalopathy: potential for improvement following their removal by liver assist devices. Author(s): Butterworth RF. Source: Liver International : Official Journal of the International Association for the Study of the Liver. 2003; 23 Suppl 3: 5-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12950954

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Role of gut bacteria in the therapy of hepatic encephalopathy with lactulose and antibiotics. Author(s): Dasarathy S. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S50-3. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025256

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Role of Helicobacter pylori infection and its eradication in patients with subclinical hepatic encephalopathy. Author(s): Miquel J, Barcena R, Boixeda D, Fernandez J, SanRoman AL, Martin-deArgila C, Ramosa F. Source: European Journal of Gastroenterology & Hepatology. 2001 September; 13(9): 1067-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11564957

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Role of Helicobacter pylori infection in hyperammonemia and subclinical hepatic encephalopathy in cirrhosis of liver. Author(s): Kini D, Aggarwal R, Saraswat VA, Naik SR. Source: Indian J Gastroenterol. 2001 November-December; 20(6): 237-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11817778

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Role of trace elements in hepatic encephalopathy: zinc and manganese. Author(s): Chetri K, Choudhuri G. Source: Indian J Gastroenterol. 2003 December; 22 Suppl 2: S28-30. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15025250

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Role of zinc in subclinical hepatic encephalopathy: comparison with somatosensoryevoked potentials. Author(s): Yang SS, Lai YC, Chiang TR, Chen DF, Chen DS. Source: Journal of Gastroenterology and Hepatology. 2004 April; 19(4): 375-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15012773

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Screening of subclinical hepatic encephalopathy. Author(s): Groeneweg M, Moerland W, Quero JC, Hop WC, Krabbe PF, Schalm SW. Source: Journal of Hepatology. 2000 May; 32(5): 748-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10845661

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Serum levels of tumor necrosis factor-alpha correlate with severity of hepatic encephalopathy due to chronic liver failure. Author(s): Odeh M, Sabo E, Srugo I, Oliven A. Source: Liver International : Official Journal of the International Association for the Study of the Liver. 2004 April; 24(2): 110-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15078474

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Spectral versus visual EEG analysis in mild hepatic encephalopathy. Author(s): Amodio P, Marchetti P, Del Piccolo F, de Tourtchaninoff M, Varghese P, Zuliani C, Campo G, Gatta A, Guerit JM. Source: Clinical Neurophysiology : Official Journal of the International Federation of Clinical Neurophysiology. 1999 August; 110(8): 1334-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10454268

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Stage IV hepatic encephalopathy associated with acute blindness after liver transplantation. Author(s): Arikan C, Tekgul H, Egilmez S, Kilic M, Yagci RV, Tokat Y, Aydogdu S. Source: Pediatric Transplantation. 2003 December; 7(6): 497-500. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14870902

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Subclinical hepatic encephalopathy predicts the development of overt hepatic encephalopathy. Author(s): Romero-Gomez M, Boza F, Garcia-Valdecasas MS, Garcia E, Aguilar-Reina J. Source: The American Journal of Gastroenterology. 2001 September; 96(9): 2718-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11569701

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Subclinical hepatic encephalopathy: elusive 'gold standard'. Author(s): Kharbanda PS, Prabhakar S. Source: Journal of Gastroenterology and Hepatology. 2004 January; 19(1): 1-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14675235

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Subclinical hepatic encephalopathy: role of tryptophan binding to albumin and the competition with indole-3-acetic acid. Author(s): Greco AV, Mingrone G, Favuzzi A, Bertuzzi A, Gandolfi A, DeSmet R, Vanholder R, Gasbarrini G. Source: Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research. 2000 July; 48(4): 274-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10916286

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Successful surgical treatment for hepatic encephalopathy caused by a pancreatic siphon: report of a case. Author(s): Nozaki H, Shimada T, Fukushima Y, Inou T, Takeda Y. Source: Surgery Today. 1998; 28(10): 1069-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9786582

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Surgical treatment of a patient with idiopathic portal hypertension and hepatic encephalopathy. Author(s): Ohta M, Shimada T, Matsufuji H, Yukizane T, Yamada H, Sugimachi K. Source: Hepatogastroenterology. 2001 September-October; 48(41): 1461-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11677987

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The importance of bacterial infections as precipating factors of chronic hepatic encephalopathy in cirrhosis. Author(s): Strauss E, da Costa MF. Source: Hepatogastroenterology. 1998 May-June; 45(21): 900-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9684155

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The number connection tests A and B: interindividual variability and use for the assessment of early hepatic encephalopathy. Author(s): Weissenborn K, Ruckert N, Hecker H, Manns MP. Source: Journal of Hepatology. 1998 April; 28(4): 646-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9566834

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The pathophysiology, diagnosis, and management of acute hepatic encephalopathy. Author(s): Colquhoun SD, Lipkin C, Connelly CA. Source: Adv Intern Med. 2001; 46: 155-76. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11147252

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The prognostic significance of subclinical hepatic encephalopathy. Author(s): Hartmann IJ, Groeneweg M, Quero JC, Beijeman SJ, de Man RA, Hop WC, Schalm SW. Source: The American Journal of Gastroenterology. 2000 August; 95(8): 2029-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10950053

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TIPS-related hepatic encephalopathy: management options with novel endovascular techniques. Author(s): Madoff DC, Wallace MJ, Ahrar K, Saxon RR. Source: Radiographics : a Review Publication of the Radiological Society of North America, Inc. 2004 January-February; 24(1): 21-36; Discussion 36-7. Review. Erratum In: Radiographics. 2004 March-April; 24(2): 418. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14730033

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Treatment of hepatic encephalopathy. Author(s): Ferenci P. Source: Indian J Gastroenterol. 2001 March; 20 Suppl 1: C90-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11293190

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Treatment of hepatic encephalopathy. Author(s): Cordoba J, Blei AT. Source: The American Journal of Gastroenterology. 1997 September; 92(9): 1429-39. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9317058

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Treatment of hepatic encephalopathy. Author(s): Riordan SM, Williams R. Source: The New England Journal of Medicine. 1997 August 14; 337(7): 473-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9250851

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Treatment of hepatic encephalopathy: it's not lactulose. Author(s): Shawcross DL, Jalan R. Source: Bmj (Clinical Research Ed.). 2004 July 10; 329(7457): 112; Author Reply 112. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15242927

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Tryptophan metabolism and hepatic encephalopathy. Studies on the sedative properties of oxindole. Author(s): Mannaioni G, Carpenedo R, Corradetti R, Carla V, Venturini I, Baraldi M, Zeneroli ML, Moroni F. Source: Advances in Experimental Medicine and Biology. 1999; 467: 155-67. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10721052

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Urinary p-hydroxyphenyllactic acid as indicator of hepatic encephalopathy in patients with hepatic cirrhosis. Author(s): Muting D, Wuzel H, Bucsis L, Flasshoff HJ. Source: Lancet. 1985 December 14; 2(8468): 1365-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2866417

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Use of balloon-occluded retrograde transvenous obliteration with ethanolamine oleate for the treatment of hepatic encephalopathy in a cirrhotic patient with a large spontaneous splenorenal shunt. Author(s): Numata K, Tanaka K, Kiba T, Saito S, Shirato K, Kitamura T, Sekihara H. Source: Journal of Gastroenterology. 1998 June; 33(3): 424-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9658325

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Use of branched chain amino acids for treating hepatic encephalopathy: clinical experiences. Author(s): Rossi Fanelli F, Cangiano C, Capocaccia L, Cascino A, Ceci F, Muscaritoli M, Giunchi G. Source: Gut. 1986 November; 27 Suppl 1: 111-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3539709

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Usefulness of magnetic resonance spectroscopy for diagnosis of hepatic encephalopathy in a patient with relapsing confusional syndrome. Author(s): Cordoba J, Hinojosa C, Sampedro F, Alonso J, Rovira A, Quiroga S, Esteban R, Guardia J. Source: Digestive Diseases and Sciences. 2001 November; 46(11): 2451-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11713951

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Value of plasmapheresis in hepatic encephalopathy. Author(s): Riviello JJ Jr, Halligan GE, Dunn SP, Widzer SJ, Foley CM, Breningstall GN, Grover WD. Source: Pediatric Neurology. 1990 November-December; 6(6): 388-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2073301

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Value of regional cerebral blood flow in the evaluation of chronic liver disease and subclinical hepatic encephalopathy. Author(s): Yazgan Y, Narin Y, Demirturk L, Saracoglu M, Ercan M, Akyatan N, Dalkanat N, Ozel AM, Cetin M. Source: Journal of Gastroenterology and Hepatology. 2003 October; 18(10): 1162-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12974903

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Vancomycin in resistant hepatic encephalopathy. Author(s): Forbes A, Murray-Lyon I. Source: Gut. 1990 December; 31(12): 1424. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2265794

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Vegetable protein diet and hepatic encephalopathy. Author(s): Gumaste VV. Source: Gastroenterology. 1993 November; 105(5): 1578-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8224668

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Venous, arterial, and arterialized-venous blood ammonia levels and their relationship to hepatic encephalopathy after propranolol. Author(s): Snady H, Lieber CS. Source: The American Journal of Gastroenterology. 1988 March; 83(3): 249-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3344727

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Visual attention orienting in liver cirrhosis without overt hepatic encephalopathy. Author(s): Amodio P, Marchetti P, Del Piccolo F, Sartori G, Prior M, Merkel C, Gatta A. Source: Metabolic Brain Disease. 1995 December; 10(4): 335-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8847996

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Visual evoked potential: a diagnostic tool for the assessment of hepatic encephalopathy. Author(s): Zeneroli ML, Pinelli G, Gollini G, Penne A, Messori E, Zani G, Ventura E. Source: Gut. 1984 March; 25(3): 291-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6421664

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Visual evoked potential--a tool in the diagnosis of hepatic encephalopathy? Author(s): Johansson U, Andersson T, Persson A, Eriksson LS. Source: Journal of Hepatology. 1989 September; 9(2): 227-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2809163

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Visual evoked potentials in hepatic encephalopathy. Author(s): Casellas F, Sagales T, Calzada MD, Accarino A, Vargas V, Guarner L. Source: Lancet. 1985 February 16; 1(8425): 394-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2857443

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Zinc levels in the cerebrospinal fluid, serum & urine in acute hepatic encephalopathy. Author(s): Singh V, Bhattacharya SK, Sundar S, Kachhawaha JS. Source: The Indian Journal of Medical Research. 1988 June; 87: 594-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3240938

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CHAPTER 2. NUTRITION AND HEPATIC ENCEPHALOPATHY Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and hepatic encephalopathy.

Finding Nutrition Studies on Hepatic Encephalopathy The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail: [email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “hepatic encephalopathy” (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 information is typical of that found when using the “Full IBIDS Database” to search for “hepatic encephalopathy” (or a synonym): •

Chronic hepatic encephalopathy following portacaval shunt: management by loop ileostomy. Author(s): Department of Gastroenterology, Royal Melbourne Hospital, Victoria, Australia. Source: Hebbard, G S Jenney, A W Gibson, P R Jacobs, R Penfold, J C Aust-N-Z-J-Surg. 1993 March; 63(3): 231-4 0004-8682

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Metabolic disorders of the brain in chronic hepatic encephalopathy detected with H-1 MR spectroscopy. Author(s): Magnetic Resonance Spectroscopy Laboratory, Huntington Medical Research Institute, Pasadena, CA 91105. Source: Kreis, R Ross, B D Farrow, N A Ackerman, Z Radiology. 1992 January; 182(1): 19-27 0033-8419

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Prostaglandin E1 improves hepatic encephalopathy produced by ischaemiareperfusion liver injury in rats. Author(s): Department of Anaesthesiology and Resuscitology, Ehime University School of Medicine, Osen-gun, Japan. Source: Adachi, N Ochi, T Tabo, E Nagaro, T Arai, T Intensive-Care-Med. 2000 November; 26(11): 1681-4 0342-4642

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Proton MR spectroscopic measurement of neurometabolites in hepatic encephalopathy during oral lactulose therapy. Author(s): Center for Noninvasive Diagnosis, University of New Mexico School of Medicine, Albuquerque, USA. Source: Haseler, L J Sibbitt, W L Mojtahedzadeh, H N Reddy, S Agarwal, V P McCarthy, D M AJNR-Am-J-Neuroradiol. 1998 October; 19(9): 1681-6 0195-6108

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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WebMDHealth: 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 hepatic encephalopathy; 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: •

Minerals Manganese Source: Healthnotes, Inc.; www.healthnotes.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND HEPATIC ENCEPHALOPATHY Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to hepatic encephalopathy. At the conclusion of this chapter, we will provide additional sources.

National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to hepatic encephalopathy 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 “hepatic encephalopathy” (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 hepatic encephalopathy: •

Acute encephalopathy: a new toxicity associated with high-dose paclitaxel. Author(s): Nieto Y, Cagnoni PJ, Bearman SI, Shpall EJ, Matthes S, DeBoom T, Baron A, Jones RB. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 1999 March; 5(3): 501-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10100699

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An analysis for death causes in 45 cases of liver cancer treated with traditional Chinese drugs. Author(s): Yang Z, Sui X. Source: J Tradit Chin Med. 1999 June; 19(2): 97-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10681863

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Behavioral model of early hepatic encephalopathy in rats. Author(s): Warbritton JD, Geyer MA, Jeppsson BW, Fischer JE. Source: Surg Forum. 1979; 30: 394-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=538643

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Beneficial effect of vegetable protein diet supplemented with psyllium plantago in patients with hepatic encephalopathy and diabetes mellitus. Author(s): Uribe M, Dibildox M, Malpica S, Guillermo E, Villallobos A, Nieto L, Vargas F, Garcia Ramos G. Source: Gastroenterology. 1985 April; 88(4): 901-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2982694

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Chaparral-associated hepatotoxicity. Author(s): Sheikh NM, Philen RM, Love LA. Source: Archives of Internal Medicine. 1997 April 28; 157(8): 913-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9129552

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Chronic camphor ingestion mimicking Reye's syndrome. Author(s): Jimenez JF, Brown AL, Arnold WC, Byrne WJ. Source: Gastroenterology. 1983 February; 84(2): 394-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6848413

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Comparison of dietary protein with an oral, branched chain-enriched amino acid supplement in chronic portal-systemic encephalopathy: a randomized controlled trial. Author(s): Horst D, Grace ND, Conn HO, Schiff E, Schenker S, Viteri A, Law D, Atterbury CE. Source: Hepatology (Baltimore, Md.). 1984 March-April; 4(2): 279-87. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6706302

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Fatal hepatic coma attributed to paclitaxel. Author(s): Feenstra J, Vermeer RJ, Stricker BH. Source: Journal of the National Cancer Institute. 1997 April 16; 89(8): 582-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9106649

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Management of hepatic encephalopathy with oral zinc supplementation: a long-term treatment. Author(s): Bresci G, Parisi G, Banti S. Source: Eur J Med. 1993 August-September; 2(7): 414-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8258031

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Oral zinc supplementation improves hepatic encephalopathy. Results of a randomised controlled trial. Author(s): Reding P, Duchateau J, Bataille C.

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Source: Lancet. 1984 September 1; 2(8401): 493-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6147551 •

Plasma neutral amino acid ratios in normal man and in patients with hepatic encephalopathy: correlations with self-selected protein and energy consumption. Author(s): Anderson GH, Blendis LM. Source: The American Journal of Clinical Nutrition. 1981 March; 34(3): 377-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6111214

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Plasma polyunsaturated fatty acids in liver cirrhosis with or without chronic hepatic encephalopathy: a preliminary study. Author(s): Cabre E, Periago JL, Gonzalez J, Gonzalez-Huix F, Abad-Lacruz A, Gil A, Sanchez-Medina F, Esteve-Comas M, Fernandez-Banares F, Planas R, et al. Source: Jpen. Journal of Parenteral and Enteral Nutrition. 1992 July-August; 16(4): 35963. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1386392

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Probiotics can treat hepatic encephalopathy. Author(s): Solga SF. Source: Medical Hypotheses. 2003 August; 61(2): 307-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12888324

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Reversible hepatic coma possibly induced by docetaxel treatment. Author(s): Chen YM, Tsai CM, Perng RP. Source: Lung Cancer (Amsterdam, Netherlands). 2001 February-March; 31(2-3): 347-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11305259

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Short-term oral zinc supplementation does not improve chronic hepatic encephalopathy. Results of a double-blind crossover trial. Author(s): Riggio O, Ariosto F, Merli M, Caschera M, Zullo A, Balducci G, Ziparo V, Pedretti G, Fiaccadori F, Bottari E, et al. Source: Digestive Diseases and Sciences. 1991 September; 36(9): 1204-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1893805

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Synbiotic modulation of gut flora: effect on minimal hepatic encephalopathy in patients with cirrhosis. Author(s): Liu Q, Duan ZP, Ha da K, Bengmark S, Kurtovic J, Riordan SM. Source: Hepatology (Baltimore, Md.). 2004 May; 39(5): 1441-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15122774

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The protective effect of HD-03 in CCl4-induced hepatic encephalopathy in rats. Author(s): Mitra SK, Venkataranganna MV, Gopumadhavan S, Anturlikar SD, Seshadri SJ, Venkatesha Udupa U.

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Source: Phytotherapy Research : Ptr. 2001 September; 15(6): 493-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11536377 •

Vegetarian diets in hepatic encephalopathy: facts or fantasies? Author(s): Amodio P, Caregaro L, Patteno E, Marcon M, Del Piccolo F, Gatta A. Source: Dig Liver Dis. 2001 August-September; 33(6): 492-500. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11572577

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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Chinese Medicine: http://www.newcenturynutrition.com/

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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html

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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm

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Google: http://directory.google.com/Top/Health/Alternative/

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Healthnotes: http://www.healthnotes.com/

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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine

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Open Directory Project: http://dmoz.org/Health/Alternative/

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HealthGate: http://www.tnp.com/

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WebMDHealth: 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 hepatic encephalopathy; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •

General Overview Liver Cirrhosis Source: Healthnotes, Inc.; www.healthnotes.com

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•

Herbs and Supplements Branched-Chain Amino Acids Source: Healthnotes, Inc.; www.healthnotes.com Neomycin Source: Healthnotes, Inc.; www.healthnotes.com Ornithine Source: Healthnotes, Inc.; www.healthnotes.com

General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.

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CHAPTER 4. PATENTS ON HEPATIC ENCEPHALOPATHY 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.8 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 “hepatic encephalopathy” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on hepatic encephalopathy, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Hepatic Encephalopathy By performing a patent search focusing on hepatic encephalopathy, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. 8Adapted

from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

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The following is an example of the type of information that you can expect to obtain from a patent search on hepatic encephalopathy: •

Infusion solutions for the treatment of hepatic encephalopathy and method of using them Inventor(s): Kleinberger; Gunter (Vienna, AT) Assignee(s): Leopold & Co., Chem. Pharm. Fabrik Gesellschaft m. b. H. (Graz, AT) Patent Number: 4,259,353 Date filed: November 3, 1978 Abstract: Infusion solution for the treatment of human patients with heptic encephalopathy which consists essentially of a sterile aqueous solution of L-valine and has a pH-value of 7,4 to 7,5. This infusion solution when intravenously administered to patients in an amount of 20-85 mg/kg of body weight per hour influences hepatic encephalopathy in a very advantageous manner. Excerpt(s): It is known that in patients with hepatic encephalopathy, especially those in praecoma or coma hepaticum, the content of the branched amino acids valine, leucine and isoleucine is lower than normal and the content of the aromatic amino acids phenylalanine, tyrosine and tryptophane is higher than normal, see Fisher et al., Am. J. Surg, volume 127, page 40 (1974). Since such patients also require parenteral feeding, it has been proposed according to U.S. Pat. No. 3,950,529 to use nutrient solutions which contain at least the essential amino acids and in which very specific relationships between the branched-chain amino acids and the aromatic amino acids must be maintained, the content of tryptophane and of phenylalanine being limited in particular. By this means, excessive tryptophane transport to the brain is said to be prevented and it is said to be ensured that too high a phenylalanine content does not arise in the plasma. In the paper by E. Fisher et al., Surgery Vol. 80, No. 1, 77-91, 1976, it was finally pointed out that the degree of hepatic encephalopathy is decisively dependent on the factor of the concentration of the branched amino acids valine, leucine and isoleucine to that of the aromatic amino acids phenylalanine, tyrosine and tryptophane. It is suggested that the branched chain amino acids are competing with the aromatic amino acids for entry across the blood brain barrier and a higher dosage level of branched chain amino acids leads to a lower concentration of aromatic amino acids in the brain. It is presumed, that by this action the brain neurotransmitter profile, which is deranged in hepatic encephalopathy, can be improved. It is therefore pointed out that with nutrient solutions which are of a composition calculated so that it aims to normalize the amino acid level in the plasma, an amelioration of the encephalopathy is also achieved although the solutions also contain some amount of aromatic amino acids. Web site: http://www.delphion.com/details?pn=US04259353__

Patent Applications on Hepatic Encephalopathy As of December 2000, U.S. patent applications are open to public viewing.9 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take

9

This has been a common practice outside the United States prior to December 2000.

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several years.) The following patent applications have been filed since December 2000 relating to hepatic encephalopathy: •

Dihydrofuran cyclic tanshinones used in treating hyperammonemia and hepatic encephalopathy Inventor(s): Bu, Xianzhang; (Guangzhan, CN), Gu, Lianquan; (Guangzhou, CN), Ma, Lin; (Guangzhan, CN) Correspondence: Banner & Witcoff; 1001 G Street N W; Suite 1100; Washington; DC; 20001; US Patent Application Number: 20040024056 Date filed: September 4, 2003 Abstract: The present invention relates to use of dihydrofuran cyclic tanshinones represented by the formula (I): 1wherein R.sub.1 is selected from a group consisting of -CH.sub.2CH.sub.2CH.sub.2C(CH.sub.3).sub.2--, --CHCHCHC(CH.sub.3)--, -CH.sub.2CH.sub.2CHC(CH.sub.3)--, or --CH.sub.2CH.sub.2CH.sub.2C(CH.sub.- 2)--, R.sub.2 is H or C.sub.1-C.sub.3 alkyl etc. or a pharmaceutical composition containing the same manufacturing medicine in preventing or treatment of hypermmonemia caused by chronic hepatitis and hepatocirrhosis, including hepatic encephalopathy and subclinical hepatic encephalopathy caused by hypermmonemia etc. Excerpt(s): The present invention relates to use of dihydrofuran cyclic tanshinones, especially Cryptotanshinone and Dihydortanshinone I for manufacturing medicine in preventing or treating hypermmonemia (over concentration of ammonia and phenethylamine in the blood) caused by chronic hepatitis and hepatocirrhosis etc., especially hepatic encephalopathy (HE) and subclinical hepatic encephalopathy (SHE) caused by hypermmonemia, and so on. Hypermmonemia is one of the major symptoms of chronic hepatitis and hepatocirrhosis. There are mainly two sources of ammonia production in the body: intestine and kidney. Most of the ammonia produced by them can be detoxicated through the ornithine cycle for synthesizing urea in the liver when its function is normal. However, the liver function of the chronic hepatitis and hepatocirrhosis patients is abnormal, and the ability of the liver to eliminate ammonia toxin is weakened, so there is increased amount of ammonia infiltrated into the blood, especially to the hepatocirrhosis patients for their greatly increased ammonia production caused by intestine congestion with portal vein diffluence formation and refluence blockage. Meanwhile, the kidney function of the chronic hepatitis and hepatocirrhosis patients is also impaired which also leads to apparently increased production of ammonia. Therefore, hypermmonemia is a symptom commonly shown by chronic hepatitis and hepatocirrhosis patients. Ammonia is a kind of basic toxic substance with poisoning effect to many major organs especially the brain. Long-term hypermmonemia is a major cause of aggravation and deterioration of chronic hepatitis and hepatocirrhosis, and initiation of hepatic encephalopathy (HE) and subclinical hepatic encephalopathy (SHE). Hepatic encephalopathy (HE) is a syndrome of central nervous system dysfunction based on metabolizing disturbance. Its main clinical manifestation is consciousness disorder, behavior disorder and coma (Pathology, edited by Li Yu-Lin, People's Health Press, 2000, p340-350). There are primarily two mechanisms for hepatic encephalopathy (HE). The first mechanism is the high concentrated blood ammonia caused by liver dysfunction permeating through bloodbrain barrier and entering into the brain tissue. The toxic effect of ammonia to brain tissue chiefly exists in its influence to the energy metabolism of brain cells, resulting in a decrease of the concentration of energy-rich phosphate compounds, some coenzymes and.alpha.-ketoglutarate. In normal situation, the liver can transform most of the

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ammonia produced in metabolism in the body into urea which is then removed form the kidney. In the situation of liver dysfunction, the ammonia eliminating ability will be weakened, thus the blood ammonia concentration increased. Moreover, at the time of alkalosis, the ionic type ammonium in the body will be transformed into molecular type ammonia, which also leads to a raise of blood ammonia concentration. The second mechanism is the action of the pseudo-neurotransmitter. The phenethylamine formed through decarboxylase effect by some amino acid such as phenylalanine can be decomposed and eliminated in the liver in normal situation, however, the blood phenethylamine concentration will rise and enter into the brain tissue through the blood-brain barrier, and converse into phenylethanol amine through the action of the enzyme in the neurocyte when the liver function is abnormal. Phenylethanol amine is a kind of pseudo-neurotransmitter with a similar structure to normal neurotransmitters such as dopamine, norepinephrine etc., but far weaker physiological functions. Phenylethanol amine can compete with normal neurotransmitter and so cause the dysfunction of cranial nerves. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Remedy for hepatopathy Inventor(s): Chin, Masahiro; (Miyagi, JP), Doi, Hideyuki; (Miyagi, JP), Koga, Hiroshi; (Tokyo, JP), Komatsu, Hiromichi; (Shizuoka, JP), Satomi, Susumu; (Miyagi, JP) Correspondence: Browdy And Neimark, P.L.L.C.; 624 Ninth Street, NW; Suite 300; Washington; DC; 20001-5303; US Patent Application Number: 20040022827 Date filed: July 30, 2003 Abstract: Compositions that contain valine as an active ingredient but which are entirely free of other amino acids or substantially free of amino other acids as an active ingredient are used as drugs or foods for treating or ameliorating hepatic diseases, whereupon less side effects are caused than in the conventional regimens of pharmacotherapy and yet the compositions ameliorate, palliate or gain recovery from symptoms and abnormalities that are caused by such hepatic diseases, for example, fever, lassitude, loss of appetite, vomiting stomachache, ascites and pleural effusion, or complications of hepatic disease (not including hepatic encephalopathy). Excerpt(s): The present application is a continuation of U.S. Ser. No. 09/509,680, filed Mar. 30, 2000, which is the national stage under 35 U.S.C.371 of PCT/JP98/04495, filed Sep. 30, 1998. This invention relates to compositions for treating hepatic diseases or improving the hepatic function that are characterized by containing valine as an active ingredient and being substantially free of other amino acids as an active ingredient. More specifically, the invention relates to pharmaceutical or food compositions that contain valine as an active ingredient capable of treating or ameliorating hepatic diseases such as acute hepatitis, hepatic insufficiency, chronic hepatitis and cirrhosis but which are substantially free of other amino acids as an active ingredient. Various amino acid preparations are conventionally used against hepatic diseases such as hepatic insufficiency and cirrhosis. For example, amino acid preparations such as Aminoleban (registered trademark), Morihepamin (registered trademark), Aminoleban (registered trademark) EN, Hepan (registered trademark) ED and Livact (registered trademark) granule are used for such purposes as ameliorating hepatic encephalopathy and hypoalbuminemia that accompany hepatic diseases such as cirrhosis and hepatic insufficiency. In fact, however, these amino acid preparations are used not for direct

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treatment or amelioration of the mentioned hepatic diseases but rather in anticipation of an improvement in impaired nutrition due to hepatic diseases, namely, for such purposes as improving nitrogen metabolism by correcting the imbalance in plasma amino acids and lowering the blood ammonia level. In addition, these preparations are mixtures of amino acids and single amino acids are little known to be capable of ameliorating the mentioned hepatic diseases. Referring to the official gazette of Examined Japanese Patent Publication No. 29446/1982, it is taught that an injection of Lvaline, when administered alone, is useful in the treatment of hepatic encephalopathy; however, hepatic encephalopathy is one of the complications of worsened hepatic disease and toxic substances such as ammonia that accumulate in blood impair the central nervous system to cause various neurotic symptoms; hence, hepatic encephalopathy is different from "hepatic disease" in the sense of term used in the present invention. What is more, the official gazette, supra, makes no suggestion that Lvaline is capable of direct treatment or amelioration of hepatic diseases per se. As a matter of fact, hepatic encephalopathy is currently treated with blood ammonia lowering agents such as lactulose and there have been reported no cases of using therapeutics for hepatic diseases in the treatment of hepatic encephalopathy, of which fact shows that the present invention is by no means easy to derive from the official gazette, supra. 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 hepatic encephalopathy, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “hepatic encephalopathy” (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 hepatic encephalopathy. You can also use this procedure to view pending patent applications concerning hepatic encephalopathy. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 5. BOOKS ON HEPATIC ENCEPHALOPATHY Overview This chapter provides bibliographic book references relating to hepatic encephalopathy. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on hepatic encephalopathy 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 “hepatic encephalopathy” (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 hepatic encephalopathy: •

Diseases of the Liver and Biliary System, Eleventh Edition Source: Malden, MA: Blackwell Science, Inc. 2002. 706 p. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail: [email protected]. Website: www.blackwell-science.com. PRICE: $178.95. ISBN: 0632055820. Summary: Designed to serve practicing physicians, surgeons and pathologists, as well as clinical students, this textbook presents a comprehensive and up-to-date account of diseases of the liver and biliary system. The text offers 38 chapters: anatomy and function; the assessment of liver function; biopsy of the liver; the hematology of liver disease; ultrasound, computed tomography (CT scan) and magnetic resonance imaging (MRI); hepatocellular failure; hepatic encephalopathy; acute liver failure; ascites (fluid

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accumulation); the portal venous system and portal hypertension; the hepatic artery and hepatic vein, and the liver in circulatory failure; jaundice; cholestasis; primary biliary cirrhosis (PBC); sclerosing cholangitis; viral hepatitis, including general features, hepatitis A, hepatitis E, and other viruses; hepatitis B virus and hepatitis Delta virus; hepatitis C virus; chronic hepatitis, its general features and autoimmune chronic disease; drugs and the liver; hepatic cirrhosis (scarring); alcohol and the liver; iron overload states; Wilson's disease; nutritional and metabolic liver diseases; the liver in infancy and childhood; the liver in pregnancy; the liver is systemic disease, granulomas, and hepatic trauma; the liver in infections; nodules and benign liver lesions; malignant liver tumors; the role of interventional radiology and endoscopy in imaging of the biliary tract; cysts and congenital biliary abnormalities; gallstones and inflammatory gallbladder diseases; benign stricture of the bile ducts; diseases of the ampulla of Vater and the pancreas; tumors of the gallbladder and bile ducts; and hepatic transplantation. The text includes full-color and black-and-white illustrations and photographs. A detailed subject index concludes the volume. •

Gastroenterology and Hepatology: The Comprehensive Visual Reference. Volume 1: The Liver Source: Philadelphia, PA: Current Medicine. 1996. [200 p.]. Contact: Available from Current Medicine. 400 Market Street, Suite 700, Philadelphia, PA 19106. (800) 427-1796 or (215) 574-2266. Fax (215) 574-2270. E-mail: [email protected]. Website: current-medicine.com. PRICE: $125.00 plus shipping and handling. ISBN: 1878132784. Summary: This atlas is one in an 8-volume collection of images that pictorially displays the gastrointestinal tract, liver, biliary tree, and pancreas in health and disease, both in children and adults. This volume includes 14 chapters on the liver. Several chapters deal with the major manifestations of liver disease, providing reviews of jaundice, portal hypertension, hepatic encephalopathy, ascites, hepatorenal syndrome, and spontaneous bacterial peritonitis. The spectrum of manifestations of hepatitis (viral, autoimmune, and drug induced) is interwoven throughout the book. In addition, there is a comprehensive discussion of the problems attendant to the development of acute liver failure. The various causes of acute and chronic hepatitis are covered in depth and Hepatitis B and hepatitis C receive individual attention in separate chapters. The spectrum of drug-induced liver disease and the mechanisms by which drug-related liver injuries develop (and can be detected or prevented) is discussed. Liver disease caused by copper and iron receive special attention as do those disorders predominantly affecting the hepatic vasculature or the parnechyma in the form of abscesses or cysts. The volume describes tumors of the liver, once considered therapeutically hopeless, with emphasis on recently acquired information regarding the pathogenic roles of hepatitis B, hepatitis C, iron, and environmental toxins. The book includes a status report evaluating the roles of hepatic resection and transplantation as treatments for tumors. The last chapter of the book covers liver transplantation. The format of the atlas is visual images supported by relatively brief text. Tables, charts, diagrams, and photomicrographs are used extensively.

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Evidence Based Gastroenterology and Hepatology Source: London, UK: BMJ Publishing Group. 1999. 557 p.

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Contact: Available from BMJ Publishing Group. BMA Books, BMA House, Tavistock Square, London WCIH 9JR. Fax 44 (0)20 7383 6402. E-mail: [email protected]. Website: www.bmjbooks.com. PRICE: Contact publisher for price. ISBN: 0727911821. Summary: This book emphasizes the approaches of evidence based medicine in gastroenterology (the study of the gastrointestinal tract and gastrointestinal diseases) and hepatology (the study of the liver and liver diseases). The authors use clinical epidemiology to present the strongest and most current evidence for interventions for the major diseases of the gastrointestinal tract and liver. Thirty chapters are included: an introduction to evidence based gastroenterology and hepatology; gastroesophageal reflux disease (GERD); ulcer disease and Helicobacter pylori; ulcer disease and nonsteroidal antiinflammatory drugs; treatment options for non-variceal gastrointestinal hemorrhage; the diagnosis and treatment of functional dyspepsia (indigestion); the diagnosis, treatment, and prognosis of celiac disease (gluten intolerance); the treatment of Crohn's disease; the diagnosis, prognosis, and treatment of ulcerative colitis (UC); pouchitis after restorative proctocolectomy; metabolic bone disease in gastrointestinal disorders; colorectal cancer in UC and the role of surveillance; population based screening and surveillance for colorectal cancer; irritable bowel syndrome (IBS); the surgical treatment of gallstone disease; the prognosis and treatment of acute pancreatitis; hepatitis C; hepatitis B; the screening and treatment of alcoholic liver disease; hemochromatosis and Wilson disease; primary biliary cirrhosis (PBC); autoimmune hepatitis; primary sclerosing cholangitis (PSC); the prevention and treatment of portal hypertensive bleeding; ascites, hepatorenal syndrome, and spontaneous bacterial peritonitis; hepatic encephalopathy; hepatocellular carcinoma; fulminant hepatic failure; the prevention and treatment of rejection after liver transplantation; and the prevention and treatment of infection after liver transplantation. Each chapter features the grading of recommendations and levels of evidence used by the authors to note the research basis on which their clinical guidelines are formed. Chapters conclude with extensive reference lists; the text concludes with a subject index. A glossary of acronyms is also provided. •

Handbook of Liver Disease Source: Philadelphia, PA: Churchill-Livingstone. 1998. 534 p. Contact: Available from W.B. Saunders Company. Book Order Fulfillment Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. Email: [email protected]. PRICE: $73.00 plus shipping and handling. ISBN: 0443055203. Summary: This comprehensive handbook in outline format offers easy access to information on the full range of liver disorders, and covers symptoms, signs, differential diagnoses, and treatments. A total of 34 chapters cover the following topics: assessment of liver function and diagnostic studies, acute liver failure, chronic viral hepatitis, acute viral hepatitis, autoimmune hepatitis, alcoholic liver disease, fatty liver and nonalcoholic steatohepatitis, drug induced and toxic liver disease, cirrhosis and portal hypertension, portal hypertension and gastrointestinal bleeding, ascites and spontaneous bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy, primary biliary cirrhosis, primary sclerosing cholangitis, hemochromatosis, Wilson's disease and related disorders, alpha 1 antitrypsin deficiency and other metabolic liver diseases, Budd Chiari syndrome and other vascular disorders, the liver in heart failure, the liver in pregnancy, the liver in systemic disease, pediatric liver disease, liver disease in the elderly, HIV and the liver, granulomatous liver disease, hepatic tumors, hepatic abscesses and cysts, other infections involving the liver, surgery in the patient with liver disease and postoperative

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jaundice, liver transplantation, cholelithiasis and cholecystitis, diseases of the bile ducts, and tumors of the biliary tract. The book features lists that summarize key information and numerous figures and tables on topics such as acetaminophen toxicity, classifications of chronic hepatitis, and indications for liver transplantation. Each chapter was written by an acknowledged expert in the field and includes references for additional study. A subject index concludes the volume. •

Clinical Practice of Gastroenterology. Volume Two Source: Philadelphia, PA: Current Medicine. 1999. 861 p. Contact: Available from W.B. Saunders Company. Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887. (800) 545-2522. Fax (800) 874-6418 or (407) 352-3445. Website: www.wbsaunders.com. PRICE: $235.00 plus shipping and handling. ISBN: 0443065209 (two volume set); 0443065217 (volume 1); 0443065225 (volume 2). Summary: This lengthy textbook brings practitioners up to date on the complexities of gastroenterology practice, focusing on the essentials of patient care. This second volume includes 113 chapters in five sections: liver, gallbladder and biliary tract, pancreas, pediatric gastroenterology, and special topics. Specific topics include hepatic (liver) structure and function, jaundice, viral hepatitis, alcoholic liver injury, liver tumors, parasitic diseases of the liver, Wilson's disease, hemochromatosis, the pregnancy patient with liver disease, portal hypertension, hepatic encephalopathy, fulminant hepatic failure, liver transplantation, the anatomy of the gallbladder and biliary tract, gallstones, laparoscopic cholecystectomy (gallbladder removal), cholecystitis (gallbladder infection), primary sclerosing cholangitis, biliary obstruction, pancreatic anatomy and physiology, acute pancreatitis, pancreatic fistulas and ascites (fluid accumulation), chronic pancreatitis, cancer of the pancreas, endoscopic retrograde cholangiopancreatography, esophageal atresia, gastroesophageal reflux in infants and children, achalasia and esophageal motility disorders, caustic and foreign body ingestion, vomiting, chronic abdominal pain, gastritis and peptic ulcer disease in children, malabsorption syndromes in children, inflammatory bowel disease in children and adolescents, acute appendicitis, cystic fibrosis, constipation and fecal soiling (incontinence), hepatitis in children, liver transplantation in children, failure to thrive, pediatric AIDS, the gastrointestinal manifestations of AIDS, the evaluation and management of acute upper gastrointestinal bleeding, principles of endoscopy, eating disorders, nutritional assessment, enteral and parenteral nutrition, gastrointestinal diseases in the elderly and in pregnancy, nosocomial infections, and the psychosocial aspects of gastroenterology (doctor patient interactions). The chapters include figures, algorithms, charts, graphs, radiographs, endoscopic pictures, intraoperative photographs, photomicrographs, tables, and extensive references. The volume concludes with a detailed subject index and a section of color plates.

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Diseases of the Liver and Biliary System. 10th ed Source: Oxford, England: Blackwell Science. 1997. 714 p. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail: [email protected]. PRICE: $150.00. ISBN: 0865429065. Summary: This medical textbook presents a comprehensive account of diseases of the liver and biliary system, designed to be of use to physicians, surgeons and pathologists, and also as a reference text for the clinical student. Chapters cover anatomy and function; assessment of liver function; needle biopsy of the liver; the hematology of liver

Books

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disease; ultrasound, computed tomography, and magnetic resonance imaging; hepatocellular failure; hepatic encephalopathy; fulminant hepatic failure; ascites; the portal venous system and portal hypertension; the hepatic artery and hepatic veins, i.e., the liver in circulatory failure; jaundice; cholestasis; primary biliary cirrhosis; sclerosing cholangitis; virus hepatitis; chronic hepatitis; drugs and the liver; hepatic cirrhosis; alcohol and the liver; iron overload states; Wilson's disease; nutritional and metabolic liver disease; the liver in infancy and childhood; the liver in pregnancy; the liver in systemic disease and hepatic trauma; the liver in infections; hepatic tumors, including hepato-cellular carcinoma; imaging of the biliary tract, including interventional radiology and endoscopy; cysts and congenital biliary abnormalities; gallstones and inflammatory gallbladder diseases; benign stricture of the bile ducts; diseases of the ampulla of Vater and pancreas; tumors of the gallbladder and bile ducts; and hepatic transplantation. The volume includes full color photographs, extensive reference lists with each chapter, and a detailed subject index. •

Oxford Textbook of Clinical Hepatology: Volume I Source: New York, NY: Oxford University Press. 1991. 837 p. Contact: Available from Oxford University Press. 200 Madison Avenue, New York, NY 10016. PRICE: $275 for 2-volume set. ISBN: 0192621556 (Volume 1); 0192619683 (2volume set). Summary: This textbook provides a comprehensive account of clinical hepatology. In Volume I, 69 chapters are presented in 13 sections: structure of the liver; functions of the liver; hepatic metabolism of drugs and toxins; general pathology; symptoms and signs of liver disease; investigation of hepatobiliary disease; cirrhosis and chronic active hepatitis; portal hypertension and gastrointestinal bleeding; ascites, renal failure and electrolyte disorders in cirrhosis; hepatic encephalopathy; the spleen, hypersplenism, and other relationships between the liver and spleen; embryology and non-parasitic cystic diseases; and infections of the liver. The subject index for both volumes in appended.

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Wilson's Disease Source: Saint Louis, MO: W.B. Saunders Company. 1996. 210 p. Contact: Available from W.B. Saunders Company. Book Order Fulfillment Department, 11830 Westline Industrial Drive, Saint Louis, MO 63146-9988. (800) 545-2522 or (314) 4537010. Fax (800) 568-5236 or (314) 453-7095. E-mail: [email protected]. Website: www.wbsaunders.com. PRICE: $66.00 plus shipping and handling. ISBN: 0702018422. Summary: Wilson's disease, an inherited copper toxicosis, is a condition that affects the central nervous system and liver, and appears in childhood or early adulthood. Though the condition is rare, it is vital that the physician be aware of its clinical manifestations, since treatment can be very successful if instituted before irreversible organ damage has occurred. This book offers a comprehensive guide to the early diagnosis and treatment of Wilson's disease, using case studies to bring out the nuances of effective patient management. In addition, the author provides a review of the etiology and pathogenesis of the disease, plus practical guidance on new diagnostic tests and therapies. There is a genetic basis for the difference in the age of presentation. Patients with late (usually neurological) presentation have the H714X mutation; patients with early (usually hepatic) presentation have other, thus far unknown, mutations. Increase of free plasma copper, and not copper accumulation, is the central feature of Wilson's disease. High concentrations of copper in the liver and brain are a sign of copper detoxification by

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metallothionein. The neuropathological abnormalities in Wilson's disease and hepatic encephalopathy are similar at a microscopic level. Three clinical forms of neurological Wilson's disease can be distinguished: the dyskinetic, the pseudosclerotic, and the pseudoparkinsonian forms. The neuropsychiatric symptoms of Wilson's disease are those of subacute metabolic encephalopathy. The essential diagnostic indices of Wilson's disease are Kayser-Fleischer ring (in the eyes), low caeruloplasmin, high urinary copper excretion and high hepatic copper content. Pencillamine and zinc sulphate are both effective in the treatment of Wilson's disease. Because chelating (removal) agents may cause paradoxical deterioration, penicillamine should not be used as initial treatment. The author advocates starting treatment with zinc sulphate and to add penicillamine only if decoppering with zinc therapy alone is insufficient. The book includes a section of color plates, an extensive references list, and a subject index. 404 references.

Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “hepatic encephalopathy” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “hepatic encephalopathy” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “hepatic encephalopathy” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

Advances in ammonia metabolism and hepatic encephalopathy; ISBN: 0444809570; http://www.amazon.com/exec/obidos/ASIN/0444809570/icongroupinterna

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Advances in Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy (Advances in Experimental Medicine and Biology, 420) by Vicente Felipo, et al; ISBN: 0306455986; http://www.amazon.com/exec/obidos/ASIN/0306455986/icongroupinterna

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Advances in Hepatic Encephalopathy and Metabolic Nitrogen Exchange by Livio Capocaccia, et al; ISBN: 084938964X; http://www.amazon.com/exec/obidos/ASIN/084938964X/icongroupinterna

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Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy (Advances in Experimental Medicine and Biology, 341) by Santiago Grisolia, Vicente Felipo; ISBN: 0306445956; http://www.amazon.com/exec/obidos/ASIN/0306445956/icongroupinterna

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Glial and neuronal changes in experimental hepatic encephalopathy by Nils Henrik Diemer; ISBN: 8716082052; http://www.amazon.com/exec/obidos/ASIN/8716082052/icongroupinterna

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Progress in Hepatic Encephalopathy and Metabolic Nitrogen Exchange by Fin Bengtsson, et al; ISBN: 0849301807; http://www.amazon.com/exec/obidos/ASIN/0849301807/icongroupinterna

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Chapters on Hepatic Encephalopathy In order to find chapters that specifically relate to hepatic encephalopathy, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and hepatic encephalopathy 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 “hepatic encephalopathy” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on hepatic encephalopathy: •

Approach to the Patient with Fulminant (Acute) Liver Failure Source: in Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 983-991. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-6423. Fax: (301) 223-2400. Website: www.lww.com. PRICE: $289.00. ISBN: 781728614. Summary: Fulminant (acute) liver failure (FLF) is a relatively uncommon condition characterized by hepatocyte necrosis (liver tissue death) and disruption of liver function in proportion to the degree of liver cell death. With extensive liver cell death comes the development of clinically obvious hepatic encephalopathy, which defines the clinical condition of FLF. This chapter on the approach to patients with FLF is from a lengthy, two-volume textbook that integrates the various demands of science, technology, expanding information, good judgment, and common sense into the diagnosis and management of gastrointestinal patients. The chapter first discusses the definition, pathogenesis, and etiology of FLF. Thereafter, the authors discuss the clinical management of these patients, divided into pre-intensive care unit (ICU) and ICU management of patients with FLF. Subsequently, liver transplantation and developments in transplantation are discussed, as well as the available bioreactors for use in patients with FLF. Supportive therapy allows both functional and structural regeneration of the liver after FLF, without the development of chronic liver disease. However, in certain cases, the prognosis is grave and is greatly improved by emergency liver transplantation. 2 tables. 58 references.

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Hepatic Failure Source: in Farthing, M.J.G.; Ballinger, A.B., eds. Drug Therapy for Gastrointestinal and Liver Diseases. Florence, KY: Martin Dunitz. 2001. p. 313-330. Contact: Available from Martin Dunitz. Fulfillment Center, Taylor and Francis, 7625 Empire Drive, Florence, KY 41042. (800) 634-7064. E-mail: cserve@routledge_ny.com. Website: www.dunitz.co.uk. PRICE: $75.00 plus shipping and handling. ISBN: 1853177334. Summary: Patients with liver (hepatic) failure frequently require drug therapy both for the primary hepatic disease and for other complicating conditions. The liver has a central role in drug metabolism and disposition and, consequently, impairment of hepatic function may have profound effects on drug handling. Since inappropriate drug administration may worsen hepatic failure or even precipitate serious complications, the administration of many drugs often needs to be modified radically in patients with liver failure. This chapter on hepatic failure is from a textbook that reviews the drug therapy

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for gastrointestinal and liver diseases. The authors discuss general principles of prescribing for patients with liver failure, outline areas of importance in their supportive care, and examine practical therapeutic approaches to the treatment of hepatic encephalopathy, a frequent and important complication of hepatic failure. The chapter concludes with a drug list that summarizes mode of action, and other aspects of clinical pharmacology where appropriate, drug doses, common adverse affects, and drug interactions. 2 figures. 1 table. 79 references. •

Portal Hypertension-2: Ascites, Encephalopathy, and Other Conditions Source: in Beckingham, I.J., ed. ABC of Liver, Pancreas and Gallbladder. London, UK: BMJ Publishing Group. 2001. p.22-24. Contact: Available from BMJ Publishing Group. BMA Books, BMA House, Tavistock Square, London WCIH 9JR. Fax 44 (0)20 7383 6402. E-mail: [email protected]. Website: www.bmjbooks.com. PRICE: Contact publisher for price. ISBN: 0727915312. Summary: Portal hypertension is abnormally increased blood pressure in the portal venous system; it is a frequent complication of cirrhosis (scarring) of the liver. Ascites is the accumulation of serous fluid in the abdominal cavity. Hepatic encephalopathy is a reversible state of impaired cognitive function or altered consciousness that occurs in patients with liver disease or portosystemic shunts. This chapter on portal hypertension, ascites, and hepatic encephalopathy is from an atlas of the liver, pancreas and gallbladder. The authors describe each condition, its diagnosis, and treatment strategies. The authors also briefly cover hepatorenal syndrome, an acute state of kidney failure resulting from intense constriction of the blood flow in the kidneys in otherwise normal kidneys; and spontaneous bacterial peritonitis. The chapter concludes with summary points of the concepts discussed. 2 figures. 8 tables. 2 references.

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Acute Liver Failure Source: in Friedman, L.S. and Keeffe, E.B., eds. Handbook of Liver Disease. Philadelphia, PA: Churchill-Livingstone. 1998. p. 15-26. Contact: Available from W.B. Saunders Company. Book Order Fulfillment Department, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. Email: [email protected]. PRICE: $73.00 plus shipping and handling. ISBN: 0443055203. Summary: This chapter on acute liver failure is from a comprehensive handbook in outline format that offers easy access to information on the full range of liver disorders and covers symptoms, signs, differential diagnoses, and treatments. The authors define acute liver failure as a syndrome of rapidly evolving hepatic synthetic dysfunction that is complicated by coagulopathy and, in advanced stages, hepatic encephalopathy. Acute liver failure can be divided into two subgroups: fulminant hepatic failure, with hepatic encephalopathy developing within 8 weeks of the onset of illness (or at least 2 weeks after the onset of jaundice); and subfulminant hepatic failure, with hepatic encephalopathy developing 8 weeks to 6 months after the onset of illness (or 2 weeks to 3 months after the onset of jaundice). Fuliminant hepatic failure is most often caused by acute hepatitis A, acute hepatitis B, or acetaminophen overdose, while subfulminant hepatic failure is more often caused by drug induced hepatotoxicity or unknown factors. The major complications of acute liver failure that require preventive measures or specific therapy include cerebral edema, coagulopathy, renal failure, hypoglycemia, and infection. Management of acute liver failure is directed toward aggressive supportive care in an intensive care unit and determination of whether liver transplantation is

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indicated. The authors conclude that applying prognostic criteria associated with death from acute liver failure is critical in determining which patients are likely to recover and which are likely to die and should be considered for liver transplantation. 4 tables. 9 references. (AA-M). •

Hepatobiliary Disorders Source: in Norris, J., et al., eds. Professional Guide to Diseases. 5th edition. Springhouse, PA: Springhouse Corporation. 1995. p. 721-745. Contact: Available from Springhouse Corporation. 1111 Bethlehem Pike, P.O. Box 908, Springhouse, PA 19477-0908. (800) 346-7844 or (215) 646-8700. Fax (215) 646-4508. PRICE: $34.95 (as of 1995). ISBN: 0874347696. Summary: This chapter on hepatobiliary disorders is from an extensive reference guide to diseases. After an introduction, the chapter covers viral hepatitis, nonviral hepatitis, cirrhosis and fibrosis, liver abscess, fatty liver, Wilson's disease, hepatic encephalopathy, cholelithiasis, choledocholithiasis, cholangitis, cholecystitis, cholesterolosis, biliary cirrhosis, and gallstone ileus. For each disease, the authors include a definition and discussion of the causes, signs and symptoms, diagnosis, treatment options, and special considerations. 8 references.

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Central Nervous System and Pulmonary Complications of End-Stage Liver Diseases Source: in Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 2445-2468. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-6423. Fax: (301) 223-2400. Website: www.lww.com. PRICE: $289.00. ISBN: 781728614. Summary: This chapter on the central nervous system and pulmonary (lung) complications of end stage liver diseases is from a comprehensive gastroenterology textbook that provides an encyclopedic discussion of virtually all the disease states encountered in a gastroenterology practice. In this chapter, the authors discuss hepatic encephalopathy, hepatopulmonary syndrome, and portopulmonary hypertension. Specific topics include definitions and pathophysiology of each syndrome, the role of gut-derived neurotoxins, the role of altered neurotransmitters, modifications in energy metabolism, mechanisms involved in fulminant hepatic failure, the signs and symptoms of overt hepatic encephalopathy, imaging modalities, biochemical markers, hepatic encephalopathy without liver disease, prognosis, differential diagnosis, pulmonary vasodilation, and treatment strategies. 5 figures. 6 tables. 216 references.

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Diagnosis and Therapy of Cirrhosis and Its Complications Source: in Danzi, J.T.; Scopelliti, J.A., eds. Office Management of Digestive Diseases. Malvern, PA: Lea and Febiger. 1992. p. 152-167. Contact: Available from Lea and Febiger. Box 3024, Malvern, PA 19355-9725. (215) 2512230. PRICE: $39.50. ISBN: 0812114361. Summary: This chapter, from a medical textbook about the office management of common gastrointestinal diseases, discusses the diagnosis and therapy of cirrhosis and its complications. Topics include ascites, including mechanism of formation, a rational approach to treatment, and the use of diuretics; spontaneous bacterial peritonitis, including the source of bacteria, immunologic disturbances in cirrhotics, its clinical

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features, and recommended treatment; and hepatic encephalopathy, its manifestations and treatment. One appendix lists a sample 1000-mg sodium diet plan. 2 figures. 3 tables. 57 references. •

Aging Gut Source: in Chernoff, R. Geriatric Nutrition: The Health Professional's Handbook. Frederick, MD: Aspen Publishers, Inc. 1991. p. 183-227. Contact: Available from Aspen Publishers, Inc. 7201 McKinney Circle, Frederick, MD 21701-9782. (800) 638-8437 or (301) 417-7500. PRICE: $59; plus shipping and handling. ISBN: 083420228X. Summary: This lengthy chapter, from a book about the interplay of nutrition and aging, discusses the aging gastrointestinal system. Topics covered include the morphologic and functional changes of the gastrointestinal system with aging; the incidence and character of feeding and swallowing disorders; oropharyngeal physiology, function, and dysphagia; esophageal dysphagia; changes in the stomach and pancreas with aging; diseases of the pancreas in the elderly population; the morphology, function, and motility of the small intestine; intestinal disorders, including disaccharidase deficiency, celiac disease, bacterial overgrowth, inflammatory bowel disease, and radiation enteritis; liver function and aging; liver disease in the elderly population, including the role of nutrition in liver diseases such as fatty liver, acute hepatitis, cholestasis, cirrhosis, hepatic encephalopathy, and ascites; and functional problems of the colon, including constipation and diverticulosis. 5 figures. 195 references.

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Nutrition Support in Hepatic Failure Source: in American Dietetic Association. Manual of Clinical Dietetics. Chicago, IL: American Dietetic Association. 1996. p. 343-346. Contact: Available from American Dietetic Association. 216 West Jackson Boulevard, Chicago, IL 60606. (800) 877-1600 or (312) 899-0040. Fax (312) 899-4899. PRICE: $59.95 for members, $70.00 for nonmembers. ISBN: 0880911530. Summary: This section on the nutrition management of the patient with hepatic (liver) failure is from a manual that serves as a nutrition care guide for dietetics professionals, physicians, nurses, and other health professionals. The manual integrates current knowledge of nutrition, medical science, and food to set forth recommendations for healthy individuals and those for whom medical nutrition therapy (MNT) is indicated. The challenge of nutrition support during hepatic failure is to provide absorbable nutrients in sufficient quantity to promote hepatic regeneration (liver healing) while preventing or minimizing nutrient intolerance and hepatic encephalopathy. Nutrition support is indicated for the patient with advanced hepatic disease who cannot meet his or her nutritional needs through oral intake. The text outlines the purpose, use, modifications, and adequacy of the diet. The section also outlines the related physiology, noting problems with malabsorption and the changes in mental status that may accompany hepatic failure. The section provides guidelines for enteral support and parenteral support. 12 references. (AA-M).

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CHAPTER 6. MULTIMEDIA ON HEPATIC ENCEPHALOPATHY Overview In this chapter, we show you how to keep current on multimedia sources of information on hepatic encephalopathy. 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 hepatic encephalopathy is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “hepatic encephalopathy” 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 “hepatic encephalopathy” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on hepatic encephalopathy: •

Postgraduate Gastroenterology Program Source: Mt. Laurel, NJ: CME Conference Video, Inc. 1992. (videocassettes and syllabus). Contact: Available from P.O. Box 5077, Cherry Hill, NJ 08034-5077. (800) 284-8433. Fax (800) 284-5964. PRICE: $675. Group practice packages available. Summary: This continuing education video series is designed to enhance understanding of pathophysiology and patient management of gastrointestinal (GI) organ systems and GI disorders and to improve viewers' diagnostic and treatment abilities. Six sections cover gastroduodenal disorders; clinical applications of research; liver diseases; pancreatic and biliary tract diseases; inflammatory bowel syndrome (IBS); and esophageal disorders. Specific topics include helicobacter pylori and peptic ulcer disease; gastric emptying; gastroparesis; hormones and neuropeptides; interferon therapy of chronic liver disease; liver transplantation; hepatic encephalopathy; sclerosing cholangitis; chronic pancreatitis; endoscopic retrograde

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cholangiopancreatography (ECRP); colorectal polyps; surgical therapy for IBS; IBS and constipation; swallowing physiology; and Barrett's esophagus. The video includes interactive sessions between experts in the field of gastroenterology. (AA-M). •

Cirrhosis of the Liver Source: Los Angeles, CA: National Health Video, Inc. 1998. (videocassette). Contact: Available from National Health Video, Inc. 12021 Wilshire Blvd., Suite 550, Los Angeles, CA 90025. (800) 543-6803. Fax (310) 477-8198. E-mail: [email protected]. PRICE: $89.00 plus shipping and handling. Summary: This health education videotape is designed to convince viewers of the liver damage caused by alcohol intake. Narrated by a registered dietitian, the program first briefly reviews the anatomy of the liver and then describes the liver's functions: making clotting factors, supporting the immune system, filtering out chemical and alcohol toxins (regardless of how they enter the body), maintaining glycogen (stored food energy), aiding digestion of fats, protein and carbohydrates, and making bile for digesting fats and accessing vitamins. The main factor in keeping the liver healthy is the avoidance of alcohol, but the program also discusses the importance of a healthy diet and regular exercise. The program then focuses on cirrhosis, a condition in which normal liver cells are replaced by scar tissue. The program offers mortality statistics and reviews the causes of cirrhosis, including hepatitis, genetic disease, drug effects, and alcohol (which causes 75 percent of cirrhosis cases). There are no adequate warning signs that become apparent before the liver has been damaged. The program discusses the consequences of cirrhosis, including malnutrition, hepatic encephalopathy (ammonia induced mental impairment), swollen abdomen (ascites), fatty liver (in which fat cells replace normal liver cells), and reduced ability to manage medications and toxins. A final section discusses liver failure and liver transplantation, emphasizing that there are never enough donor livers available and that people who have alcohol induced liver disease are often not acceptable transplant candidates. The program features interviews and scenes with patients and physicians.

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CHAPTER 7. PERIODICALS AND NEWS ON HEPATIC ENCEPHALOPATHY Overview In this chapter, we suggest a number of news sources and present various periodicals that cover hepatic encephalopathy.

News Services and Press Releases One of the simplest ways of tracking press releases on hepatic encephalopathy 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 “hepatic encephalopathy” (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 hepatic encephalopathy. 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 “hepatic encephalopathy” (or synonyms). The following was recently listed in this archive for hepatic encephalopathy: •

Minimal hepatic encephalopathy may impair driving ability Source: Reuters Medical News Date: April 21, 2004

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Plasma ammonia levels reflect hepatic encephalopathy severity Source: Reuters Medical News Date: March 24, 2003 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 “hepatic encephalopathy” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “hepatic encephalopathy” (or synonyms). If you know the name of a company that is relevant to hepatic encephalopathy, 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 “hepatic encephalopathy” (or synonyms).

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Academic Periodicals covering Hepatic Encephalopathy Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to hepatic encephalopathy. In addition to these sources, you can search for articles covering hepatic encephalopathy that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”

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CHAPTER 8. 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 hepatic encephalopathy. 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 non-profit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with hepatic encephalopathy. 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,

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etc.). The following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to hepatic encephalopathy: Acetaminophen •

Systemic - U.S. Brands: Aceta Elixir; Aceta Tablets; Acetaminophen Uniserts; Actamin; Actamin Extra; Actamin Super; Aminofen; Aminofen Max; Apacet Capsules; Apacet Elixir; Apacet Extra Strength Caplets; Apacet Extra Strength Tablets; Apacet Regular Strength Tablets; Apacet, Infants'; Aspirin Free Anacin Maximum Strength Caplets; Aspirin Free Anacin Maximum Strength Gel Caplets; Aspirin Free Anacin Maximum Strength Tablets; Aspirin-Free Excedrin Caplets; Banesin; Bayer Select Maximum Strength Headache Pain Relief Formula; Dapa; Dapa X-S; Datril Extra-Strength; Feverall Junior Strength; Feverall Sprinkle Caps Junior Strength; Feverall Sprinkle Caps, Children's; Feverall, Children's; Feverall, Infants'; Genapap Children's Elixir; Genapap Children's Tablets; Genapap Extra Strength Caplets; Genapap Extra Strength Tablets; Genapap Regular Strength Tablets; Genapap, Infants'; Genebs Extra Strength Caplets; Genebs Regular Strength Tablets; Genebs X-Tra; Liquiprin Children's Elixir; Liquiprin Infants' Drops; Neopap; Oraphen-PD; Panadol Junior Strength Caplets; Panadol Maximum Strength Caplets; Panadol Maximum Strength Tablets; Panadol, Children's; Panadol, Infants'; Phenaphen Caplets; Redutemp; SnapletsFR; St. Joseph Aspirin-Free Fever Reducer for Children; Suppap-120; Suppap325; Suppap-650; Tapanol Extra Strength Caplets; Tapanol Extra Strength Tablets; Tempra; Tempra D.S; Tempra Syrup; Tempra, Infants'; Tylenol Arthritis Extended Relief; Tylenol Children's Chewable Tablets; Tylenol Children's Elixir; Tylenol Children's Suspension Liquid; Tylenol Extra Strength Caplets; Tylenol Extra Strength Gelcaps; Tylenol Extra Strength Tablets; Tylenol Extra-Strength Adult Liquid Pain Reliever; Tylenol Infants' Drops; Tylenol Infants' Suspension Drops; Tylenol Junior Strength Caplets; Tylenol Junior Strength Chewable Tablets; Tylenol Regular Strength Caplets; Tylenol Regular Strength Tablets; Valorin; Valorin Extra http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202001.html

Antacids •

Oral - U.S. Brands: Advanced Formula Di-Gel; Alamag; Alamag Plus; Alenic Alka; Alenic Alka Extra Strength; Alka-Mints; Alkets; Alkets Extra Strength; Almacone; Almacone II; AlternaGEL; Alu-Cap; Aludrox; Alu-Tab; Amitone; Amphojel; Antacid Gelcaps; Antacid Liquid; Antacid Liquid Double Strength; Basaljel; Calglycine; Chooz; Dicarbosil; Di-Gel; Equilet; Foamicon; Gaviscon; Gaviscon Extra Strength Relief Formula; Gaviscon-2; Gelusil; Genaton; Genaton Extra Strength; Kudrox Double Strength; Losopan; Losopan Plus; Lowsium Plus; Maalox; Maalox Antacid Caplets; Maalox Heartburn Relief Formula; Maalox Plus; Maalox Plus, Extra Strength; Maalox TC; Magnalox; Magnalox Plus; MagOx 400; Mallamint; Maox 420; Marblen; Mi-Acid; Mi-Acid Double Strength; Mintox; Mintox Extra Strength; Mygel; Mygel II; Mylanta; Mylanta Double Strength; Mylanta Gelcaps; Nephrox; Phillips'; Phillips' Chewable; Phillips' Concentrated Double Strength; Riopan; Riopan Plus; Riopan Plus Double Strength; Rolaids; Rulox; Rulox No. 1; Rulox No. 2; Rulox Plus; Simaal 2 Gel; Simaal Gel; Tempo; Titralac; Titralac Extra Strength; Titralac Plus; Tums; Tums Anti-gas/Antacid; Tums E-X; Tums Ultra; Uro-Mag http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202047.html

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Bromocriptine •

Systemic - U.S. Brands: Parlodel; Parlodel SnapTabs http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202094.html

Diclofenac •

Topical - U.S. Brands: Solaraze http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500247.html

Erythromycin •

Ophthalmic - U.S. Brands: Ilotycin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202220.html

Isoniazid •

Systemic - U.S. Brands: Laniazid; Nydrazid http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202307.html

Kanamycin •

Oral - U.S. Brands: Kantrex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202312.html

Methyldopa •

Systemic - U.S. Brands: Aldomet http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202359.html

Metronidazole •

Systemic - U.S. Brands: Flagyl; Flagyl 375; Flagyl ER; Flagyl I.V.; Flagyl I.V. RTU; Metric 21; Metro I.V.; Protostat http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202365.html

•

Vaginal - U.S. Brands: MetroGel-Vaginal http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202704.html

Neomycin •

Oral - U.S. Brands: Mycifradin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202396.html

•

Topical - U.S. Brands: Myciguent http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202397.html

Urea •

Intra-amniotic - U.S. Brands: Ureaphil http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202584.html

Vancomycin •

Oral - U.S. Brands: Vancocin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202589.html

•

Systemic - U.S. Brands: Vancocin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202590.html

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Vitamin K •

Systemic - U.S. Brands: AquaMEPHYTON; Mephyton http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202599.html

Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.

Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.

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 hepatic encephalopathy 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 “hepatic encephalopathy” (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.

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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 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 hepatic encephalopathy: •

Rifaximin (trade name: Normix) http://www.rarediseases.org/nord/search/nodd_full?code=907

If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.

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APPENDICES

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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.

NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •

Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm

•

National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/

•

National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html

•

National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25

•

National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm

•

National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm

•

National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375

•

National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/

10

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

•

National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

•

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

•

National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

•

National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

•

National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

•

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm

•

National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html

•

National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

•

National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

•

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

•

National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html

•

National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

•

Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

•

National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

•

National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp

•

Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html

•

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.11 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:12 •

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

•

HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html

•

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

•

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/

•

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

•

Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html

•

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/

•

Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html

•

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

•

Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html

•

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

11

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). 12 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

•

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 NLM Gateway13 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.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “hepatic encephalopathy” (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. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total

Items Found 7813 69 901 9 76 8868

HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 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.17 Simply search by “hepatic encephalopathy” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

13

Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

14

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). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17

The HSTAT URL is http://hstat.nlm.nih.gov/.

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.

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Coffee Break: Tutorials for Biologists18 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.19 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.20 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/.

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/.

18 Adapted 19

from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.

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. 20 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.

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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 hepatic encephalopathy 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 hepatic encephalopathy. 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 hepatic encephalopathy. 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 “hepatic encephalopathy”:

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Cirrhosis http://www.nlm.nih.gov/medlineplus/cirrhosis.html Hepatitis http://www.nlm.nih.gov/medlineplus/hepatitis.html Hepatitis B http://www.nlm.nih.gov/medlineplus/hepatitisb.html Hepatitis C http://www.nlm.nih.gov/medlineplus/hepatitisc.html Laboratory Tests http://www.nlm.nih.gov/medlineplus/laboratorytests.html Liver Diseases http://www.nlm.nih.gov/medlineplus/liverdiseases.html Metabolic Disorders http://www.nlm.nih.gov/medlineplus/metabolicdisorders.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 hepatic encephalopathy. 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: •

Hepatic Encephalopathy Source: Toronto, Ontario: Canadian Liver Foundation. 200x. 3 p. Contact: Available from Canadian Liver Foundation. Suite 1500, 2235 Sheppard Avenue East, Toronto Ontario, M2J 5B5. (416) 491-3353 or (800) 563-5483. Fax (416) 491-4952. Email: [email protected]. Website: [email protected]. PRICE: Full-text available online at no charge; Contact organization for print copies. Summary: This fact sheet, from the Canadian Liver Foundation, reviews hepatic encephalothy (HE), a disorder of mental activity, neuromuscular function, and consciousness that occurs as a result of either chronic or acute liver failure (ALF). This complex neuropsychiatric syndrome is primarily caused by metabolic abnormalities. Written in question-and-answer format, the fact sheet covers the normal function of the liver, cirrhosis (scarring) of the liver, the different types of HE, symptoms of the different stages of HE, diagnostic approaches to HE, the pathogenesis of HE, and

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treatment options. The author notes that the most important aspect of management of HE is the prompt recognition and correction of precipitating factors, when possible. These factors include kidney failure, use of sedatives or narcotics, gastrointestinal bleeding, hypokalemia or alkalosis, dietary protein increase, infection, constipation, and exacerbation of liver disease. The fact sheet concludes with the contact information for the Canadian Liver Foundation (www.liver.ca or 800-563-5483). 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 hepatic encephalopathy. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •


•

Family Village: http://www.familyvillage.wisc.edu/specific.htm

•

Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/

•

Med Help International: http://www.medhelp.org/HealthTopics/A.html

•

Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/

•

Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/

•

WebMDHealth: http://my.webmd.com/health_topics

Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to hepatic encephalopathy. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with hepatic encephalopathy. 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 hepatic encephalopathy. For more

108


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 “hepatic encephalopathy” (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 “hepatic encephalopathy”. 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 “hepatic encephalopathy” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “hepatic encephalopathy” (or a synonym) into the search box, and click “Submit Query.”

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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.

Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.21

Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.

Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of

21

Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.

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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)22: •

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

•

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/

22

Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.

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•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

•

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

•

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

•

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/

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Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/

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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10

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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/

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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html

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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp

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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp

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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/

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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm

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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330

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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/

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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

Finding Medical Libraries

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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm

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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/

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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •

ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html

•

MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp

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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 hepatic encephalopathy: •

Basic Guidelines for Hepatic Encephalopathy CVA Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000726.htm Delirium Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000740.htm Hepatic encephalopathy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm Meningitis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000680.htm Wernicke-Korsakoff syndrome Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000771.htm

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Signs & Symptoms for Hepatic Encephalopathy Agitation Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003212.htm Behavior changes Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003255.htm Change in mental state Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003205.htm Changes in consciousness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Changes in mood Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003213.htm Coma Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Confusion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003205.htm Decreased alertness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Drowsiness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003208.htm Edema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Erythema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Forgetfulness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003257.htm Gynecomastia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003165.htm Hematemesis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003118.htm Hepatomegaly Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm Hyperactive Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003256.htm Icterus Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003243.htm

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Jaundice Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003243.htm Loss of memory Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003257.htm Melena Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003130.htm Movement, dysfunctional Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003203.htm Movement, uncontrollable Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003201.htm Muscle Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003193.htm Seizures Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003200.htm Sleepiness Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003208.htm Speech impairment Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003204.htm Stupor Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003202.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Yellow skin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003243.htm •

Diagnostics and Tests for Hepatic Encephalopathy Albumin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003480.htm ALT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003473.htm AST Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003472.htm Bilirubin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003479.htm Blood chemistry Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003468.htm

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Blood gases Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003855.htm BUN Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003474.htm CBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm Creatinine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm CT scan of the head Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003786.htm EEG Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003931.htm Electroencephalogram Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003931.htm MRI Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003335.htm Partial thromboplastin time Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003653.htm Platelet count Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003647.htm Prothrombin time Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003652.htm PT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003652.htm PTT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003653.htm Toxicology screen Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003578.htm Urinalysis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003579.htm •

Nutrition for Hepatic Encephalopathy Protein Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002467.htm Protein in diet Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002467.htm

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Vitamin K Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002407.htm •

Surgery and Procedures for Hepatic Encephalopathy Liver transplant Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003006.htm

•

Background Topics for Hepatic Encephalopathy Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm Ammonia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002759.htm Cardiovascular Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002310.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Hepatic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002378.htm Intravenous Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002383.htm Precipitating Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002275.htm Respiratory Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002290.htm Sedative overdose Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002545.htm Shock Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000039.htm Toxins Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002331.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

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•

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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HEPATIC ENCEPHALOPATHY DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 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] Abscess: A localized, circumscribed collection of pus. [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] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] 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] Adenocarcinoma: A malignant 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] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Aetiology: Study of the causes of disease. [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

122


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] Aggravation: An increasing in seriousness or severity; an act or circumstance that intensifies, or makes worse. [EU] Agmatine: Decarboxylated arginine, isolated from several plant and animal sources, e.g., pollen, ergot, herring sperm, octopus muscle. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkalosis: A pathological condition that removes acid or adds base to the body fluids. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] 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] 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] Ameliorating: A changeable condition which prevents the consequence of a failure or

Dictionary 123

accident from becoming as bad as it otherwise would. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino acid: 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] 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] Amnestic: Nominal aphasia; a difficulty in finding the right name for an object. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] 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] 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] Anastomosis: A procedure to connect healthy sections of tubular structures in the body after the diseased portion has been surgically removed. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] 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] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [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] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU]

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Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [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] Antidote: A remedy for counteracting a poison. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]

Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]

Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipruritic: Relieving or preventing itching. [EU] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU]

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Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Anxiolytic: An anxiolytic or antianxiety agent. [EU] Appendicitis: Acute inflammation of the vermiform appendix. [NIH] Aqueous: Having to do with water. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Artifacts: Any visible result of a procedure which is caused by the procedure itself and not by the entity being analyzed. Common examples include histological structures introduced by tissue processing, radiographic images of structures that are not naturally present in living tissue, and products of chemical reactions that occur during analysis. [NIH] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Aspartate: A synthetic amino acid. [NIH] Asterixis: A motor disturbance marked by intermittency of sustained contraction of groups of muscles. [NIH] 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] Auditory: Pertaining to the sense of hearing. [EU] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune Hepatitis: A liver disease caused when the body's immune system destroys liver cells for no known reason. [NIH] Autonomic: Self-controlling; functionally independent. [EU] 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] 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] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH]

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Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] 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]

Benzene: Toxic, volatile, flammable liquid hydrocarbon biproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide. [NIH] Benzodiazepines: A two-ring heterocyclic compound consisting of a benzene ring fused to a diazepine ring. Permitted is any degree of hydrogenation, any substituents and any Hisomer. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile 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] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Bioreactors: Tools or devices for generating products using the synthetic or chemical conversion capacity of a biological system. They can be classical fermentors, cell culture perfusion systems, or enzyme bioreactors. For production of proteins or enzymes, recombinant microorganisms such as bacteria, mammalian cells, or insect or plant cells are usually chosen. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived

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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] Bivalent: Pertaining to a group of 2 homologous or partly homologous chromosomes during the zygotene stage of prophase to the first metaphase in meiosis. [NIH] Bladder: The organ that stores urine. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [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 vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Body Fluids: Liquid components of living organisms. [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] 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] 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] Bronchial: Pertaining to one or more bronchi. [EU] Buspirone: An anxiolytic agent and a serotonin receptor agonist belonging to the azaspirodecanedione class of compounds. Its structure is unrelated to those of the benzodiazepines, but it has an efficacy comparable to diazepam. [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]

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Camphor: A bicyclic monoterpene ketone found widely in plant (primarily the camphor tree, Cinnamomum camphora). Natural camphor is used topically as a skin antipruritic and as an anti-infective agent. [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] Carbohydrates: The largest class of organic compounds, including starches, glycogens, cellulose, gums, and simple sugars. Carbohydrates are composed of carbon, hydrogen, and oxygen in a ratio of Cn(H2O)n. [NIH] 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] Carcinogenic: Producing carcinoma. [EU] 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] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardioselective: Having greater activity on heart tissue than on other tissue. [EU] Cardiovascular: Having to do with the heart and blood vessels. [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] 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] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Caustic: An escharotic or corrosive agent. Called also cauterant. [EU] Celiac Artery: The arterial trunk that arises from the abdominal aorta and after a short course divides into the left gastric, common hepatic and splenic arteries. [NIH] Celiac Disease: A disease characterized by intestinal malabsorption and precipitated by gluten-containing foods. The intestinal mucosa shows loss of villous structure. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Division: The fission of a cell. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH]

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Cerebral: Of or pertaining of the cerebrum or the brain. [EU] 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] 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] 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] 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] 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] Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking dopamine receptors. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholecystectomy: Surgical removal of the gallbladder. [NIH] Cholecystitis: Inflammation of the gallbladder. [NIH] Choledocholithiasis: Gallstones in the bile ducts. [NIH] Cholelithiasis: Presence or formation of gallstones. [NIH] Cholestasis: Impairment of biliary flow at any level from the hepatocyte to Vater's ampulla. [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] Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] 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] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] Clarithromycin: A semisynthetic macrolide antibiotic derived from erythromycin that is

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active against a variety of microorganisms. It can inhibit protein synthesis in bacteria by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [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] 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] Coenzymes: Substances that are necessary for the action or enhancement of action of an enzyme. Many vitamins are coenzymes. [NIH] 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] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] 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] 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] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative

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pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the 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] 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 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] 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

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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] 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] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] 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 study: An experiment or clinical trial that includes a comparison (control) group. [NIH]

Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [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 Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Corpus: The body of the uterus. [NIH] Corpus Striatum: Striped gray and white matter consisting of the neostriatum and paleostriatum (globus pallidus). It is located in front of and lateral to the thalamus in each cerebral hemisphere. The gray substance is made up of the caudate nucleus and the lentiform nucleus (the latter consisting of the globus pallidus and putamen). The white matter is the internal capsule. [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] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Cranial Nerves: Twelve pairs of nerves that carry general afferent, visceral afferent, special afferent, somatic efferent, and autonomic efferent fibers. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] 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]

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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] Cysteinyl: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [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] 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] Cytotoxic: Cell-killing. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] 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] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [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] Diastolic: Of or pertaining to the diastole. [EU]

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Dietetics: The study and regulation of the diet. [NIH] Dietitian: An expert in nutrition who helps people plan what and how much food to eat. [NIH]

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] Dilatation, Pathologic: The condition of an anatomical structure's being dilated beyond normal dimensions. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disaccharides: Sugars composed of two monosaccharides linked by glycoside bonds. [NIH] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] Disposition: A tendency either physical or mental toward certain diseases. [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] Diuretic: A drug that increases the production of urine. [NIH] Diverticula: Plural form of diverticulum. [NIH] Diverticulitis: Inflammation of a diverticulum or diverticula. [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] Docetaxel: An anticancer drug that belongs to the family of drugs called mitotic inhibitors. [NIH]

Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for

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its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Double-blind: Pertaining to a clinical trial or other experiment in which neither the subject nor the person administering treatment knows which treatment any particular subject is receiving. [EU] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenum: The first part of the small intestine. [NIH] Dyspepsia: Impaired digestion, especially after eating. [NIH] Dysphagia: Difficulty in swallowing. [EU] Dyspnea: Difficult or labored breathing. [NIH] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] 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] Efferent: Nerve fibers which conduct impulses from the central nervous system to muscles and glands. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] 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] 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] Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e.,

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radiation. [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] 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] Embryology: The study of the development of an organism during the embryonic and fetal stages of life. [NIH] Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used for the broader group. [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] Endoscopic retrograde cholangiopancreatography: ERCP. A procedure to x-ray the pancreatic duct, hepatic duct, common bile duct, duodenal papilla, and gallbladder. In this procedure, a thin, lighted tube (endoscope) is passed through the mouth and down into the first part of the small intestine (duodenum). A smaller tube (catheter) is then inserted through the endoscope into the bile and pancreatic ducts. A dye is injected through the catheter into the ducts, and an x-ray is taken. [NIH] Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] Enema: The injection of a liquid through the anus into the large bowel. [NIH] Enkephalins: One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla. [NIH] Enteral Nutrition: Nutritional support given via the alimentary canal or any route connected to the gastrointestinal system (i.e., the enteral route). This includes oral feeding, sip feeding, and tube feeding using nasogastric, gastrostomy, and jejunostomy tubes. [NIH] Enteritis: Inflammation of the intestine, applied chiefly to inflammation of the small intestine; see also enterocolitis. [EU]

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Enterocolitis: Inflammation of the intestinal mucosa of the small and large bowel. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]

Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Ergot: Cataract due to ergot poisoning caused by eating of rye cereals contaminated by a fungus. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophageal Atresia: Congenital failure of the full esophageal lumen to develop that commonly occurs with tracheoesophageal fistula. Symptoms include excessive salivation, gagging, cyanosis, and dyspnea. [NIH] Esophageal Motility Disorders: Disorders affecting the motor function of the upper or lower esophageal sphincters, the esophageal body, or a combination of these parts. The failure of the sphincters to maintain a tonic pressure may result in the impeding of the passage of food, regurgitation of food, or reflux of gastric acid into the esophagus. [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. [NIH]

Estrogen: One of the two female sex hormones. [NIH] Ethanolamine: A viscous, hygroscopic amino alcohol with an ammoniacal odor. It is widely distributed in biological tissue and is a component of lecithin. It is used as a surfactant, fluorimetric reagent, and to remove CO2 and H2S from natural gas and other gases. [NIH] Evacuation: An emptying, as of the bowels. [EU] 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]

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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] Excrete: To get rid of waste from the body. [NIH] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Extracellular: Outside a cell or cells. [EU] Extrapyramidal: Outside of the pyramidal tracts. [EU] Failure to Thrive: A condition in which an infant or child's weight gain and growth are far below usual levels for age. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]

Fatty 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] 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] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fine-needle aspiration: The removal of tissue or fluid with a needle for examination under a microscope. Also called needle biopsy. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flatus: Gas passed through the rectum. [NIH] Fluid Therapy: Therapy whose basic objective is to restore the volume and composition of the body fluids to normal with respect to water-electrolyte balance. Fluids may be administered intravenously, orally, by intermittent gavage, or by hypodermoclysis. [NIH] Flumazenil: A potent benzodiazepine receptor antagonist. Since it reverses the sedative and other actions of benzodiazepines, it has been suggested as an antidote to benzodiazepine overdoses. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Forearm: The part between the elbow and the wrist. [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] 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] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored

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in the gallbladder. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastric Emptying: The evacuation of food from the stomach into the duodenum. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]

Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastritis: Inflammation of the stomach. [EU] Gastroduodenal: Pertaining to or communicating with the stomach and duodenum, as a gastroduodenal fistula. [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] Gastroparesis: Nerve or muscle damage in the stomach. Causes slow digestion and emptying, vomiting, nausea, or bloating. Also called delayed gastric emptying. [NIH] Gastrostomy: Creation of an artificial external opening into the stomach for nutritional support or gastrointestinal compression. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

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] Globus Pallidus: The representation of the phylogenetically oldest part of the corpus

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striatum called the paleostriatum. It forms the smaller, more medial part of the lentiform nucleus. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]

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] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]

Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Gluten: The protein of wheat and other grains which gives to the dough its tough elastic character. [EU] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]

Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] 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] Granule: A small pill made from sucrose. [EU]

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Granulomas: Small lumps in tissues caused by inflammation. [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] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartburn: Substernal pain or burning sensation, usually associated with regurgitation of gastric juice into the esophagus. [NIH] Helicobacter: A genus of gram-negative, spiral-shaped bacteria that is pathogenic and has been isolated from the intestinal tract of mammals, including humans. [NIH] Helicobacter pylori: A spiral bacterium active as a human gastric pathogen. It is a gramnegative, urease-positive, curved or slightly spiral organism initially isolated in 1982 from patients with lesions of gastritis or peptic ulcers in Western Australia. Helicobacter pylori was originally classified in the genus Campylobacter, but RNA sequencing, cellular fatty acid profiles, growth patterns, and other taxonomic characteristics indicate that the microorganism should be included in the genus Helicobacter. It has been officially transferred to Helicobacter gen. nov. (see Int J Syst Bacteriol 1989 Oct;39(4):297-405). [NIH] Hematology: A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues. [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] 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] 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] 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] Hepatic Artery: A branch of the celiac artery that distributes to the stomach, pancreas,

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duodenum, liver, gallbladder, and greater omentum. [NIH] Hepatic Duct, Common: Predominantly extrahepatic bile duct which is formed by the junction of the right and left hepatic ducts, which are predominantly intrahepatic, and, in turn, joins the cystic duct to form the common bile duct. [NIH] Hepatic Veins: Veins which drain 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] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocyte: A liver cell. [NIH] Hepatology: The field of medicine concerned with the functions and disorders of the liver. [NIH]

Hepatopulmonary Syndrome: A syndrome consisting of the triad of liver dysfunction, pulmonary vascular dilatation, and abnormal arterial oxygenation in the absence of detectable intrinsic disease of the lung and heart. [NIH] Hepatorenal Syndrome: Renal failure in those with liver disease, usually liver cirrhosis or obstructive jaundice. Historically called Heyd disease, urohepatic syndrome, or bile nephrosis. [NIH] Hepatotoxicity: How much damage a medicine or other substance does to the liver. [NIH] Hepatovirus: A genus of Picornaviridae causing infectious hepatitis naturally in humans and experimentally in other primates. It is transmitted through fecal contamination of food or water. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] 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] Hydrogenation: Specific method of reduction in which hydrogen is added to a substance by

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the direct use of gaseous hydrogen. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperammonemia: Metabolic disorder characterized by elevated level of ammonia in blood. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypersplenism: Condition characterized by splenomegaly, some reduction in the number of circulating blood cells in the presence of a normal or hyperactive bone marrow, and the potential for reversal by splenectomy. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthyroidism: Excessive functional activity of the thyroid gland. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypnotic: A drug that acts to induce sleep. [EU] 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] Hypokinesia: Slow or diminished movement of body musculature. It may be associated with basal ganglia diseases; mental disorders; prolonged inactivity due to illness; experimental protocols used to evaluate the physiologic effects of immobility; and other conditions. [NIH] Hypotension: Abnormally low blood pressure. [NIH] Hypothyroidism: Deficiency of thyroid activity. In adults, it is most common in women and is characterized by decrease in basal metabolic rate, tiredness and lethargy, sensitivity to cold, and menstrual disturbances. If untreated, it progresses to full-blown myxoedema. In infants, severe hypothyroidism leads to cretinism. In juveniles, the manifestations are intermediate, with less severe mental and developmental retardation and only mild symptoms of the adult form. When due to pituitary deficiency of thyrotropin secretion it is called secondary hypothyroidism. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Idiopathic: Describes a disease of unknown cause. [NIH] Ileostomy: Surgical creation of an external opening into the ileum for fecal diversion or drainage. Loop or tube procedures are most often employed. [NIH] Ileum: The lower end of the small intestine. [NIH] Ileus: Obstruction of the intestines. [EU] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience

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with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] 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] Indigestion: Poor digestion. Symptoms include heartburn, nausea, bloating, and gas. Also called dyspepsia. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] 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]

Inferior vena cava: A large vein that empties into the heart. It carries blood from the legs and feet, and from organs in the abdomen and pelvis. [NIH] 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]

Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called 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] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH]

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Inotropic: Affecting the force or energy of muscular contractions. [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] Insomnia: Difficulty in going to sleep or getting enough sleep. [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 and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interindividual: Occurring between two or more individuals. [EU] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] 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] Intracellular: Inside a cell. [NIH] Intracranial Pressure: Pressure within the cranial cavity. It is influenced by brain mass, the circulatory system, CSF dynamics, and skull rigidity. [NIH] Intrahepatic: Within the liver. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]

Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] 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] Irrigation: The washing of a body cavity or surface by flowing solution which is inserted and then removed. Any drug in the irrigation solution may be absorbed. [NIH] Irritable Bowel Syndrome: A disorder that comes and goes. Nerves that control the muscles in the GI tract are too active. The GI tract becomes sensitive to food, stool, gas, and stress.

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Causes abdominal pain, bloating, and constipation or diarrhea. Also called spastic colon or mucous colitis. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [NIH] Isoleucine: An essential branched-chain amino acid found in many proteins. It is an isomer of LEUCINE. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]

Jejunostomy: Surgical formation of an opening through the abdominal wall into the jejunum, usually for enteral hyperalimentation. [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] Kidney Cortex: The outer zone of the kidney, beneath the capsule, consisting of kidney glomerulus; kidney tubules, distal; and kidney tubules, proximal. [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] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactation: The period of the secretion of milk. [EU] Lactulose: A mild laxative. [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] Lassitude: Weakness; exhaustion. [EU]

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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]

Least-Squares Analysis: A principle of estimation in which the estimates of a set of parameters in a statistical model are those quantities minimizing the sum of squared differences between the observed values of a dependent variable and the values predicted by the model. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Likelihood Functions: Functions constructed from a statistical model and a set of observed data which give the probability of that data for various values of the unknown model parameters. Those parameter values that maximize the probability are the maximum likelihood estimates of the parameters. [NIH] Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] 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 Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Logistic Models: Statistical models which describe the relationship between a qualitative dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor. [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] 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]

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Lutein Cells: The cells of the corpus luteum which are derived from the granulosa cells and the theca cells of the Graafian follicle. [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] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [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] Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (magnetic resonance imaging). [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malabsorption Syndromes: General term for syndromes of malnutrition due to failure of normal intestinal absorption of nutrients. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Medial: Lying near the midsaggital plane of the body; opposed to lateral. [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] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH]

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Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Menopause: Permanent cessation of menstruation. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] Mesentery: A layer of the peritoneum which attaches the abdominal viscera to the abdominal wall and conveys their blood vessels and nerves. [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 disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metallothionein: A low-molecular-weight (approx. 10 kD) protein occurring in the cytoplasm of kidney cortex and liver. It is rich in cysteinyl residues and contains no aromatic amino acids. Metallothionein shows high affinity for bivalent heavy metals. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] 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] Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Midazolam: A short-acting compound, water-soluble at pH less than 4 and lipid-soluble at physiological pH. It is a hypnotic-sedative drug with anxiolytic and amnestic properties. It is used for sedation in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. Because of its short duration and cardiorespiratory stability, it is particularly useful in poor-risk, elderly, and cardiac patients. [NIH]

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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] Mitotic: Cell resulting from mitosis. [NIH] Mitotic inhibitors: Drugs that kill cancer cells by interfering with cell division (mitostis). [NIH]

Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] 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] Monoamine: Enzyme that breaks down dopamine in the astrocytes and microglia. [NIH] Monoamine Oxidase: An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] 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] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]

Multidrug resistance: Adaptation of tumor cells to anticancer drugs in ways that make the drugs less effective. [NIH] Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables. [NIH] 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] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH]

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Nasogastric: The process of passing a small, flexible plastic tube through the nose or mouth into the stomach or small intestine. [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] 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] Needle biopsy: The removal of tissue or fluid with a needle for examination under a microscope. Also called fine-needle aspiration. [NIH] Neomycin: Antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C. It acts by inhibiting translation during protein synthesis. [NIH] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] 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] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropeptides: Peptides released by neurons as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells. [NIH] Neuropsychological Tests: Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury. [NIH] Neurosis: Functional derangement due to disorders of the nervous system which does not affect the psychic personality of the patient. [NIH] Neurotic: 1. Pertaining to or characterized by neurosis. 2. A person affected with a neurosis. [EU]

Neurotoxicity: The tendency of some treatments to cause damage to the nervous system. [NIH]

Neurotoxin: A substance that is poisonous to nerve tissue. [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]

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Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophils: Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes. [NIH] Niacin: Water-soluble vitamin of the B complex occurring in various animal and plant tissues. Required by the body for the formation of coenzymes NAD and NADP. Has pellagra-curative, vasodilating, and antilipemic properties. [NIH] 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] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nosocomial: Pertaining to or originating in the hospital, said of an infection not present or incubating prior to admittance to the hospital, but generally occurring 72 hours after admittance; the term is usually used to refer to patient disease, but hospital personnel may also acquire nosocomial infection. [EU] 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] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritional Support: The administration of nutrients for assimilation and utilization by a patient by means other than normal eating. It does not include fluid therapy which normalizes body fluids to restore water-electrolyte balance. [NIH] Office Management: Planning, organizing, and administering activities in an office. [NIH] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH]

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Omentum: A fold of the peritoneum (the thin tissue that lines the abdomen) that surrounds the stomach and other organs in the abdomen. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Ornithine: An amino acid produced in the urea cycle by the splitting off of urea from arginine. [NIH] Osmolarity: The concentration of osmotically active particles expressed in terms of osmoles of solute per litre of solution. [EU] Osmoles: The standard unit of osmotic pressure. [NIH] 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] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxazepam: A benzodiazepine used in the treatment of anxiety, alcohol withdrawal, and insomnia. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]

Oxidative 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] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Paclitaxel: Antineoplastic agent isolated from the bark of the Pacific yew tree, Taxus brevifolia. Paclitaxel stabilizes microtubules in their polymerized form and thus mimics the action of the proto-oncogene proteins c-mos. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic Ducts: Ducts that collect pancreatic juice from the pancreas and supply it to the duodenum. [NIH] Pancreatic Fistula: Abnormal passage communicating with the pancreas. [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

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associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Papilla: A small nipple-shaped elevation. [NIH] Paradoxical: Occurring at variance with the normal rule. [EU] 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] Parasitic Diseases: Infections or infestations with parasitic organisms. They are often contracted through contact with an intermediate vector, but may occur as the result of direct exposure. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parenteral Nutrition: The administering of nutrients for assimilation and utilization by a patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously). [NIH] 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] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Particle: A tiny mass of material. [EU] Parturition: The act or process of given birth to a child. [EU] 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] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

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] Penicillin: An antibiotic drug used to treat infection. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: An ulceration of the mucous membrane of the esophagus, stomach or duodenum, caused by the action of the acid gastric juice. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of

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proteins. Peptides are combined to make proteins. [NIH] Peptide Chain Elongation: The process whereby an amino acid is joined through a substituted amide linkage to a chain of peptides. [NIH] 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] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [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] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness, constipation, vomiting, and moderate fever. [EU] P-Glycoprotein: A 170 kD transmembrane glycoprotein from the superfamily of ABC transporters. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many antineoplastic agents. Overexpression of this glycoprotein is associated with multidrug resistance. [NIH] Phantom: Used to absorb and/or scatter radiation equivalently to a patient, and hence to estimate radiation doses and test imaging systems without actually exposing a patient. It may be an anthropomorphic or a physical test object. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] 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] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [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

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teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [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] Pilot study: The initial study examining a new method or treatment. [NIH] Plantago: Three different species of Plantago or plantain, P. psyllium, P. ovata and P. indica. The seeds swell in water and are used as laxatives. [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: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [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] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]

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] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH]

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Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [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] Polytetrafluoroethylene: Homopolymer of tetrafluoroethylene. Nonflammable, tough, inert plastic tubing or sheeting; used to line vessels, insulate, protect or lubricate apparatus; also as filter, coating for surgical implants or as prosthetic material. Synonyms: Fluoroflex; Fluoroplast; Ftoroplast; Halon; Polyfene; PTFE; Tetron. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Portacaval: Surgical creation of an anastomosis between the portal and caval veins. [NIH] Portal Hypertension: High blood pressure in the portal vein. This vein carries blood into the liver. Portal hypertension is caused by a blood clot. This is a common complication of cirrhosis. [NIH] Portal Pressure: The venous pressure measured in the portal vein. [NIH] Portal System: A system of vessels in which blood, after passing through one capillary bed, is conveyed through a second set of capillaries before it returns to the systemic circulation. It pertains especially to the hepatic portal system. [NIH] Portosystemic Shunt: An operation to create an opening between the portal vein and other veins around the liver. [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] Postoperative: After surgery. [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] 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] Precipitation: The act or process of precipitating. [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]

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Preoperative: Preceding an operation. [EU] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary Biliary Cirrhosis: A chronic liver disease. Slowly destroys the bile ducts in the liver. This prevents release of bile. Long-term irritation of the liver may cause scarring and cirrhosis in later stages of the disease. [NIH] Primary Sclerosing Cholangitis: Irritation, scarring, and narrowing of the bile ducts inside and outside the liver. Bile builds up in the liver and may damage its cells. Many people with this condition also have ulcerative colitis. [NIH] Proctocolectomy: An operation to remove the colon and rectum. Also called coloproctectomy. [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] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should fertilization occur. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol is used in the treatment or prevention of many disorders including acute myocardial infarction, arrhythmias, angina pectoris, hypertension, hypertensive emergencies, hyperthyroidism, migraine, pheochromocytoma, menopause, and anxiety. [NIH] 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] 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 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

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acids determines the shape and function of the protein. [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] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. [NIH] Proto-Oncogene Proteins c-mos: Cellular proteins encoded by the c-mos genes. They function in the cell cycle to maintain maturation promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychometric testing: Psychological and mental testing and quantitative analysis of an individual's psychological traits or attitudes or mental processes. [NIH] Psychomotor: Pertaining to motor effects of cerebral or psychic activity. [EU] Psyllium: Dried, ripe seeds of Plantago psyllium, P. indica, and P. ovata (Plantaginaceae). Plantain seeds swell in water and are used as demulcents and bulk laxatives. [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 Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [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] 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] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [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.

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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] Reaction Time: The time from the onset of a stimulus until the organism responds. [NIH] 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] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Rectum: The last 8 to 10 inches of the large intestine. [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] Regression Analysis: Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see linear models) the relationship is constrained to be a straight line and least-squares analysis is used to determine the best fit. In logistic regression (see logistic models) the dependent variable is qualitative rather than continuously variable and likelihood functions are used to find the best relationship. In multiple regression the dependent variable is considered to depend on more than a single independent variable. [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] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Reperfusion: Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing reperfusion injury. [NIH] Reperfusion Injury: Functional, metabolic, or structural changes, including necrosis, in

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ischemic tissues thought to result from reperfusion to ischemic areas of the tissue. The most common instance is myocardial reperfusion injury. [NIH] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Salivation: 1. The secretion of saliva. 2. Ptyalism (= excessive flow of saliva). [EU] Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Screening: Checking for disease when there are no symptoms. [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] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] 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] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [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] 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] 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] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH]

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Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

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] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spastic: 1. Of the nature of or characterized by spasms. 2. Hypertonic, so that the muscles are stiff and the movements awkward. 3. A person exhibiting spasticity, such as occurs in spastic paralysis or in cerebral palsy. [EU] 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] 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] Sphincters: Any annular muscle closing an orifice. [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] 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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Standard therapy: A currently accepted and widely used treatment for a certain type of cancer, based on the results of past research. [NIH] Status Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [NIH] Steatosis: Fatty degeneration. [EU] Stenosis: Narrowing or stricture of a duct or canal. [EU] Stent: A device placed in a body structure (such as a blood vessel or the gastrointestinal tract) to provide support and keep the structure open. [NIH] Sterile: Unable to produce children. [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] Stool: The waste matter discharged in a bowel movement; feces. [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] Stricture: The abnormal narrowing of a body opening. Also called stenosis. [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] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substrate: A substance upon which an enzyme acts. [EU] Sulfotransferases: Enzymes which transfer sulfate groups to various acceptor molecules. They are involved in posttranslational sulfation of proteins and sulfate conjugation of exogenous chemicals and bile acids. EC 2.8.2. [NIH] Supplementation: Adding nutrients to the diet. [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] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]

Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic

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nervous system. Called also adrenergic. [EU] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Taurine: 2-Aminoethanesulfonic acid. A conditionally essential nutrient, important during mammalian development. It is present in milk but is isolated mostly from ox bile and strongly conjugates bile acids. [NIH] Telencephalon: Paired anteriolateral evaginations of the prosencephalon plus the lamina terminalis. The cerebral hemispheres are derived from it. Many authors consider cerebrum a synonymous term to telencephalon, though a minority include diencephalon as part of the cerebrum (Anthoney, 1994). [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] 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] Thromboplastin: Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation. [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] 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] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth

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of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [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] Tonic: 1. Producing and restoring the normal tone. 2. Characterized by continuous tension. 3. A term formerly used for a class of medicinal preparations believed to have the power of restoring normal tone to tissue. [EU] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] 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] Tracheoesophageal Fistula: Abnormal communication between the esophagus and the trachea, acquired or congenital, often associated with esophageal atresia. [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] 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] 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] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Tremor: Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of cerebellar

166


diseases, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of Parkinson disease. [NIH] Triad: Trivalent. [NIH] Trifluoperazine: A phenothiazine with actions similar to chlorpromazine. It is used as an antipsychotic and an antiemetic. [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] Tumor Lysis Syndrome: A syndrome resulting from cytotoxic therapy, occurring generally in aggressive, rapidly proliferating lymphoproliferative disorders. It is characterized by combinations of hyperuricemia, lactic acidosis, hyperkalemia, hyperphosphatemia and hypocalcemia. [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] Tyramine: An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] 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] 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] Urease: An enzyme that catalyzes the conversion of urea and water to carbon dioxide and ammonia. EC 3.5.1.5. [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,

Dictionary 167

and mental confusion. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [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] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [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]

Varices: Stretched veins such as those that form in the esophagus from cirrhosis. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] 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] Vena: A vessel conducting blood from the capillary bed to the heart. [NIH] Venlafaxine: An antidepressant drug that is being evaluated for the treatment of hot flashes in women who have breast cancer. [NIH] 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 Pressure: The blood pressure in a vein. It is usually measured to assess the filling pressure to the ventricle. [NIH] Ventricles: Fluid-filled cavities in the heart or brain. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villous: Of a surface, covered with villi. [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] 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] 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]

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Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [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] 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] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH]

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INDEX A Abdomen, 86, 121, 127, 137, 144, 145, 147, 153, 154, 155, 162, 163, 164 Abdominal, 78, 82, 121, 128, 133, 146, 149, 153, 154, 155, 166 Abdominal Pain, 78, 121, 146, 155, 166 Abscess, 83, 121 Acceptor, 121, 147, 153, 163 Acetaminophen, 7, 78, 82, 92, 121, 138 Acetylcholine, 121, 129, 151, 152 Acidosis, 121, 166 Acute renal, 5, 121 Adaptability, 121, 128 Adenocarcinoma, 121, 142 Adenosine, 121, 156 Adrenal Medulla, 121, 128, 136, 137, 152 Adrenergic, 121, 124, 135, 137, 158, 163, 166 Adverse Effect, 10, 121, 161 Aetiology, 28, 121 Afferent, 121, 132 Affinity, 121, 122, 125, 149, 162 Aggravation, 71, 122 Agmatine, 10, 122 Agonist, 122, 127, 135 Alanine, 10, 122 Albumin, 51, 53, 117, 122, 156 Alertness, 116, 122 Algorithms, 78, 122, 127 Alimentary, 30, 122, 136, 154 Alkaline, 121, 122, 123, 127 Alkalosis, 72, 107, 122 Allylamine, 122, 123 Alpha Particles, 122, 159 Alternative medicine, 88, 122 Ameliorating, 72, 122 Amine, 72, 123, 142 Ammonia, 3, 4, 5, 7, 8, 9, 11, 13, 15, 16, 33, 48, 56, 71, 73, 80, 86, 88, 119, 123, 140, 143, 166 Amnestic, 123, 149 Ampulla, 76, 79, 123, 129, 136 Anal, 123, 150 Analgesic, 121, 123 Anaphylatoxins, 123, 131 Anastomosis, 36, 123, 157 Anatomical, 123, 129, 134, 144, 149 Anesthesia, 123, 149

Aneurysm, 123, 167 Angina, 123, 158 Angina Pectoris, 123, 158 Anions, 122, 123, 145 Antagonism, 17, 123 Antibacterial, 123, 162 Antibiotic, 123, 124, 129, 137, 151, 154, 162 Antibody, 122, 124, 130, 142, 143, 144, 148, 162 Antidote, 124, 138 Antiemetic, 124, 129, 166 Antigen, 122, 124, 130, 142, 144, 148, 149 Antigen-Antibody Complex, 124, 130 Anti-infective, 124, 128 Anti-inflammatory, 121, 124 Antineoplastic, 124, 153, 155 Antineoplastic Agents, 124, 155 Antioxidant, 124, 153 Antipruritic, 124, 128 Antipsychotic, 124, 129, 166 Antipyretic, 121, 124 Anus, 123, 125, 130, 136 Anxiety, 125, 153, 158 Anxiolytic, 125, 127, 149 Appendicitis, 78, 125 Aqueous, 70, 125, 133 Arginine, 10, 122, 123, 125, 152, 153 Arterial, 16, 38, 56, 122, 125, 128, 142, 143, 158, 164 Arteries, 125, 127, 128, 132, 146, 149, 150 Artery, 123, 125, 132, 136, 146, 160 Artifacts, 26, 125 Ascites, 4, 5, 6, 72, 75, 76, 77, 78, 79, 82, 83, 84, 86, 125 Aspartate, 9, 12, 47, 50, 125 Asterixis, 22, 42, 125 Astrocytes, 11, 125, 149, 150 Asymptomatic, 125, 153 Auditory, 16, 17, 125, 137 Autodigestion, 125, 153 Autoimmune Hepatitis, 77, 125 Autonomic, 121, 124, 125, 132, 152, 155 B Bacterial Infections, 53, 125 Bacteriophage, 125, 165 Bacteriostatic, 125, 137 Bacterium, 125, 131, 141 Basal Ganglia, 13, 19, 20, 124, 126, 143

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Basophils, 126, 147 Benign, 76, 79, 126 Benzene, 126 Benzodiazepines, 17, 31, 44, 126, 127, 138 Bilateral, 13, 126 Bile, 76, 78, 79, 86, 126, 129, 136, 138, 139, 142, 146, 147, 158, 163, 164 Bile Acids, 126, 139, 163, 164 Bile Acids and Salts, 126 Bile duct, 76, 78, 79, 126, 129, 136, 142, 158 Bile Pigments, 126, 146 Biliary, 33, 75, 76, 78, 83, 85, 126, 129, 142, 153 Biliary Tract, 76, 78, 79, 85, 126, 153 Bilirubin, 117, 122, 126, 143 Bioavailability, 6, 126 Biochemical, 12, 18, 22, 83, 126, 146, 161 Biomarkers, 8, 126 Biopsy, 75, 126 Bioreactors, 81, 126 Biotechnology, 13, 88, 101, 126 Bivalent, 127, 149 Bladder, 127, 144, 158, 167 Bloating, 127, 139, 144, 146 Blood Coagulation, 127, 164 Blood Platelets, 127, 161 Blood pressure, 82, 127, 143, 157, 162, 167 Blood vessel, 127, 128, 129, 136, 146, 148, 149, 155, 162, 163, 164, 167 Blood-Brain Barrier, 5, 71, 127 Body Fluids, 122, 126, 127, 135, 138, 152, 162, 166 Bone Marrow, 126, 127, 143, 148, 150 Bowel, 4, 85, 123, 127, 134, 136, 137, 144, 145, 147, 155, 163, 166 Bradykinin, 127, 152, 156 Bronchial, 127, 142 Buspirone, 7, 127 C Calcium, 127, 130 Camphor, 64, 128 Capillary, 127, 128, 157, 167 Carbohydrates, 86, 128 Carbon Dioxide, 128, 133, 139, 166, 167 Carcinogenic, 126, 128, 144 Carcinoma, 79, 128 Cardiac, 122, 128, 137, 149, 150 Cardiorespiratory, 128, 149 Cardioselective, 128, 158 Cardiovascular, 26, 34, 51, 119, 128, 161 Carnitine, 8, 40, 128 Case report, 49, 128

Catecholamine, 128, 134, 155 Catheter, 128, 136 Causal, 17, 128 Caustic, 78, 128 Celiac Artery, 128, 141 Celiac Disease, 77, 84, 128 Cell Death, 81, 128, 151 Cell Division, 125, 128, 148, 150, 156, 158 Cellulose, 128, 156 Central Nervous System, 4, 7, 8, 71, 73, 79, 83, 121, 122, 126, 128, 135, 137, 139, 140, 149, 151, 161 Cerebral, 5, 11, 12, 16, 20, 35, 40, 41, 55, 82, 126, 127, 129, 132, 133, 137, 159, 162, 164 Cerebrospinal, 15, 32, 56, 129, 161 Cerebrospinal fluid, 15, 32, 56, 129, 161 Cerebrum, 129, 164 Character, 84, 123, 129, 133, 140 Chemotactic Factors, 129, 131 Chin, 63, 72, 129, 149 Chlorpromazine, 129, 166 Cholangitis, 76, 79, 83, 85, 129 Cholecystectomy, 78, 129 Cholecystitis, 78, 83, 129 Choledocholithiasis, 83, 129 Cholelithiasis, 78, 83, 129 Cholestasis, 76, 79, 84, 129 Cholesterol, 126, 129 Choline, 41, 129 Cholinergic, 9, 124, 129 Chronic, 3, 4, 6, 8, 14, 15, 17, 18, 19, 23, 24, 26, 27, 28, 36, 37, 39, 41, 42, 44, 47, 48, 49, 52, 53, 55, 60, 64, 65, 71, 72, 76, 77, 78, 79, 81, 85, 106, 119, 129, 137, 144, 146, 153, 158, 163, 166 Chronic Disease, 76, 129 Circulatory system, 129, 145 Clarithromycin, 7, 129 Clinical Medicine, 130, 157 Clinical trial, 5, 101, 130, 132, 135, 150, 159 Cloning, 127, 130 Coenzymes, 71, 130, 152 Cofactor, 130, 158, 164 Colitis, 130, 146 Collagen, 123, 130, 139, 156 Collapse, 11, 130 Colloidal, 122, 130 Colon, 84, 130, 134, 144, 146, 158, 166 Colorectal, 77, 86, 130 Colorectal Cancer, 77, 130 Complement, 7, 123, 130, 131, 156

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Complementary and alternative medicine, 63, 67, 131 Complementary medicine, 63, 131 Computational Biology, 101, 131 Computed tomography, 75, 79, 131 Computerized axial tomography, 131 Computerized tomography, 131 Congestion, 71, 124, 131 Congestive heart failure, 9, 131 Conjugated, 126, 131, 133 Conjugation, 131, 163 Connective Tissue, 127, 130, 132, 138, 139 Consciousness, 71, 82, 106, 116, 123, 132, 133, 134, 163 Constipation, 78, 84, 86, 107, 124, 132, 146, 155 Constriction, 82, 132, 146 Contamination, 132, 142 Contraindications, ii, 132 Control group, 11, 132 Controlled study, 14, 29, 132 Convulsions, 42, 132, 143 Coronary, 123, 132, 149, 150 Coronary Thrombosis, 132, 149, 150 Corpus, 132, 139, 148, 158 Corpus Striatum, 132, 140 Cortex, 9, 132, 137, 158 Cortical, 14, 22, 42, 132, 161 Cortisol, 122, 132 Cranial, 72, 132, 145, 155 Cranial Nerves, 72, 132 Curative, 132, 152, 164 Cyanosis, 132, 137 Cyclic, 71, 133, 141, 152 Cysteinyl, 133, 149 Cytochrome, 6, 133 Cytoplasm, 126, 133, 136, 137, 148, 149, 150, 152 Cytotoxic, 9, 133, 166 D Deamination, 133, 150, 166 Decarboxylation, 133, 142 Degenerative, 133, 142 Delirium, 25, 115, 124, 133 Dendrites, 133, 151 Density, 15, 36, 133, 153 Detoxification, 8, 18, 28, 79, 133 Diabetes Mellitus, 64, 133, 140, 141 Diagnostic procedure, 69, 88, 133 Diaphragm, 133, 156 Diarrhea, 133, 146 Diastolic, 133, 143

Dietetics, 84, 134 Dietitian, 86, 134 Digestion, 86, 122, 126, 127, 134, 135, 139, 144, 145, 147, 154, 163 Digestive system, 134, 139 Digestive tract, 134, 162 Dilatation, Pathologic, 134, 167 Dilation, 127, 134, 167 Direct, iii, 8, 72, 91, 130, 134, 135, 143, 154, 160, 164 Disaccharides, 29, 46, 134 Disorientation, 133, 134 Disposition, 7, 24, 81, 134 Dissociation, 31, 122, 134 Dissociative Disorders, 134 Distal, 28, 134, 139, 146 Diuretic, 51, 134 Diverticula, 134 Diverticulitis, 134 Diverticulosis, 84, 134 Docetaxel, 65, 134 Dopamine, 15, 72, 124, 129, 134, 150, 151, 155 Double-blind, 25, 27, 29, 30, 39, 40, 41, 47, 65, 135 Drive, ii, vi, 6, 43, 59, 77, 78, 79, 81, 82, 135 Drug Interactions, 82, 94, 135 Drug Tolerance, 135, 165 Duct, 123, 135, 136, 138, 142, 163 Duodenum, 126, 135, 136, 139, 142, 153, 154, 163 Dyspepsia, 77, 135, 144 Dysphagia, 84, 135 Dyspnea, 135, 137 E Eating Disorders, 78, 135 Edema, 4, 9, 18, 21, 82, 116, 135, 166 Effector, 121, 130, 135 Efferent, 132, 135 Efficacy, 5, 21, 26, 27, 127, 135 Elastic, 135, 140, 163 Electrolyte, 79, 133, 135, 138, 146, 152, 157, 162, 166 Electrons, 124, 135, 145, 148, 153, 159 Electrophysiological, 9, 26, 135 Elementary Particles, 135, 148, 152, 159 Emboli, 26, 27, 34, 136 Embolization, 26, 27, 34, 136 Embryology, 79, 136 Endogenous, 15, 22, 134, 136 Endorphins, 136, 151 Endoscope, 136

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Endoscopic, 6, 78, 85, 136, 149 Endoscopic retrograde cholangiopancreatography, 78, 86, 136 Endoscopy, 76, 78, 79, 136 Endothelial cell, 127, 136 Endothelium, 136, 152 Endothelium-derived, 136, 152 Endotoxins, 131, 136 Enema, 35, 136 Enkephalins, 136, 151 Enteral Nutrition, 27, 48, 65, 136 Enteritis, 84, 136 Enterocolitis, 136, 137 Environmental Health, 100, 102, 137 Enzymatic, 123, 127, 131, 137, 142 Enzyme, 72, 126, 130, 133, 135, 137, 141, 149, 150, 154, 156, 159, 163, 166, 168 Eosinophils, 137, 147 Epigastric, 137, 153 Epinephrine, 121, 134, 137, 151, 152, 166 Ergot, 122, 137 Erythromycin, 7, 93, 129, 137 Esophageal, 78, 84, 85, 137, 139, 165 Esophageal Atresia, 78, 137, 165 Esophageal Motility Disorders, 78, 137 Esophagitis, 137, 139 Esophagus, 86, 134, 137, 139, 141, 147, 154, 155, 160, 163, 165, 167 Estrogen, 137, 158 Ethanolamine, 55, 137 Evacuation, 132, 137, 139, 147 Evoked Potentials, 16, 50, 52, 56, 137 Excitation, 138, 151 Excrete, 138, 146 Exhaustion, 123, 138, 146 Exocrine, 138, 153 Exogenous, 25, 136, 138, 163 Extracellular, 9, 10, 125, 132, 138, 162 Extrapyramidal, 124, 134, 138 F Failure to Thrive, 78, 138 Family Planning, 101, 138 Fat, 86, 126, 127, 136, 138, 147, 157, 163 Fatigue, 138, 141 Fatty Liver, 77, 83, 84, 86, 138 Feces, 132, 138, 163 Fibrosis, 78, 83, 122, 138 Fine-needle aspiration, 138, 151 Fistula, 138, 139 Flatus, 138, 139 Fluid Therapy, 138, 152 Flumazenil, 4, 11, 29, 30, 35, 138

Fold, 138, 149, 153 Forearm, 127, 138 Free Radicals, 124, 134, 138 Fulminant Hepatic Failure, 11, 40, 77, 78, 79, 82, 83, 138 G Gallbladder, 76, 78, 79, 82, 121, 126, 129, 134, 136, 138, 139, 142 Ganglia, 121, 139, 151, 155 Gas, 10, 92, 123, 128, 137, 138, 139, 142, 144, 145, 152, 167 Gas exchange, 139, 167 Gastric, 41, 85, 125, 128, 137, 139, 141, 142, 154 Gastric Acid, 137, 139 Gastric Emptying, 85, 139 Gastric Juices, 139, 154 Gastrin, 139, 142 Gastritis, 78, 139, 141 Gastroduodenal, 85, 139 Gastroesophageal Reflux, 77, 78, 139 Gastroesophageal Reflux Disease, 77, 139 Gastrointestinal, 31, 48, 76, 77, 78, 79, 81, 82, 83, 84, 85, 107, 127, 136, 137, 139, 161, 163, 166 Gastrointestinal Hemorrhage, 77, 139 Gastrointestinal tract, 76, 77, 139, 161, 163, 166 Gastroparesis, 85, 139 Gastrostomy, 136, 139 Gelatin, 139, 140, 164 Gene, 127, 139 Gland, 121, 139, 153, 158, 161, 163, 164, 165 Globus Pallidus, 37, 45, 132, 139 Glomerular, 140, 146, 160 Glucose, 9, 13, 128, 133, 140, 141, 143, 144 Glucose Intolerance, 133, 140 Glutamate, 8, 12, 27, 140 Glutamic Acid, 140, 151 Glutamine, 8, 10, 12, 32, 41, 49, 140 Gluten, 77, 128, 140 Glycine, 123, 126, 140, 151 Glycogen, 32, 86, 140 Glycoprotein, 7, 140, 155, 166 Glycoside, 134, 140 Governing Board, 140, 157 Grade, 22, 29, 41, 140 Grading, 5, 77, 140 Graft, 38, 140 Gram-negative, 140, 141 Granule, 72, 140

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Granulomas, 76, 141 Guanylate Cyclase, 141, 152 H Habitual, 129, 141 Health Education, 86, 141 Heart failure, 77, 141 Heartburn, 92, 141, 144 Helicobacter, 15, 33, 51, 77, 85, 141 Helicobacter pylori, 15, 33, 51, 77, 85, 141 Hematology, 75, 78, 141 Heme, 126, 133, 141 Hemochromatosis, 77, 78, 141 Hemodialysis, 141, 146 Hemoglobin, 132, 141, 146, 147 Hemostasis, 141, 161 Hepatic Artery, 76, 79, 141 Hepatic Duct, Common, 136, 142 Hepatic Veins, 79, 142 Hepatitis, 6, 71, 72, 76, 77, 78, 79, 82, 83, 84, 86, 106, 138, 142, 167 Hepatitis A, 71, 72, 76, 142 Hepatobiliary, 79, 83, 142 Hepatocellular, 21, 75, 77, 142 Hepatocellular carcinoma, 77, 142 Hepatocyte, 81, 129, 142 Hepatopulmonary Syndrome, 83, 142 Hepatorenal Syndrome, 5, 76, 77, 82, 142 Hepatotoxicity, 64, 82, 142 Hepatovirus, 142 Histamine, 36, 123, 124, 142 Histidine, 142 Homeostasis, 10, 142 Homologous, 127, 142, 164 Hormonal, 10, 142 Hormone, 32, 132, 137, 139, 142, 158, 164 Hydrogen, 121, 123, 128, 142, 147, 150, 152, 153, 159 Hydrogenation, 126, 142 Hydroxyproline, 123, 130, 143 Hyperammonemia, 8, 11, 19, 20, 42, 46, 51, 71, 80, 143 Hyperbilirubinemia, 143, 146 Hypersplenism, 79, 143 Hypertension, 6, 77, 82, 83, 143, 157, 158, 166 Hyperthyroidism, 143, 158 Hyperuricemia, 143, 166 Hypnotic, 143, 149 Hypoglycaemia, 133, 143 Hypoglycemia, 82, 143 Hypokinesia, 143, 154 Hypotension, 124, 132, 143

Hypothyroidism, 49, 143 Hypoxia, 133, 143 I Idiopathic, 53, 143 Ileostomy, 60, 143 Ileum, 143 Ileus, 83, 143 Immune response, 124, 143, 163, 167 Immune system, 86, 125, 143 Immunologic, 83, 129, 143 Impairment, 45, 81, 86, 117, 129, 133, 144 In vitro, 8, 12, 144 In vivo, 6, 8, 10, 11, 20, 23, 36, 144 Incompetence, 139, 144 Incontinence, 78, 144 Indigestion, 77, 144 Induction, 124, 144, 158 Infancy, 76, 79, 144 Infarction, 144, 160 Infection, 15, 33, 37, 51, 77, 78, 82, 107, 129, 133, 144, 148, 152, 154, 163 Inferior vena cava, 27, 144 Inflammatory bowel disease, 5, 78, 84, 144 Infusion, 26, 37, 51, 70, 144 Ingestion, 64, 78, 144, 156 Inhalation, 144, 156 Initiation, 71, 144 Inositol, 9, 12, 144 Inotropic, 135, 145 Insight, 4, 145 Insomnia, 145, 153 Intensive Care, 29, 81, 82, 145 Interferon, 85, 145 Interferon-alpha, 145 Interindividual, 53, 145 Interstitial, 145, 160 Intestinal, 6, 40, 84, 128, 137, 141, 145, 148 Intestinal Mucosa, 128, 137, 145 Intestine, 3, 71, 126, 127, 130, 136, 145, 146 Intoxication, 133, 145, 168 Intracellular, 7, 144, 145, 152, 157, 160 Intracranial Pressure, 36, 50, 145 Intrahepatic, 6, 10, 34, 45, 51, 142, 145 Intramuscular, 145, 154 Intravenous, 38, 119, 144, 145, 154 Intrinsic, 122, 142, 145 Invasive, 145, 148 Ion Channels, 125, 145 Ions, 134, 135, 142, 145 Irrigation, 48, 145 Irritable Bowel Syndrome, 77, 145 Ischemia, 123, 146, 160

174


Ischemic stroke, 9, 146 Isoleucine, 70, 146 J Jaundice, 76, 78, 79, 82, 117, 142, 143, 146 Jejunostomy, 136, 146 K Kb, 100, 146 Kidney Cortex, 146, 149 Kidney Failure, 82, 107, 146 Kidney Failure, Acute, 146 Kidney Failure, Chronic, 146 L Labile, 130, 146 Lactation, 146, 158 Lactulose, 4, 21, 25, 26, 35, 39, 40, 41, 48, 51, 54, 60, 73, 146 Large Intestine, 130, 134, 145, 146, 160, 162 Lassitude, 72, 146 Latent, 17, 28, 29, 50, 147 Laxative, 146, 147 Least-Squares Analysis, 147, 160 Lesion, 147, 166 Lethargy, 143, 147 Leucine, 70, 147 Leukocytes, 32, 126, 127, 129, 137, 145, 147, 150, 152, 166 Ligands, 17, 24, 47, 147 Ligation, 7, 147 Likelihood Functions, 147, 160 Linear Models, 147, 160 Lipid, 129, 147, 149, 153 Lipid Peroxidation, 147, 153 Liver cancer, 63, 147 Liver Cirrhosis, 19, 20, 24, 34, 43, 50, 56, 65, 66, 142, 147 Liver Transplantation, 4, 11, 25, 35, 43, 44, 49, 52, 76, 77, 78, 81, 82, 85, 86, 147 Localized, 12, 41, 121, 144, 147, 150, 156, 166 Logistic Models, 147, 160 Loop, 60, 143, 147 Lower Esophageal Sphincter, 137, 139, 147 Lutein Cells, 148, 158 Lymphatic, 136, 144, 148, 162 Lymphatic system, 148, 162 Lymphocytes, 124, 147, 148, 162 Lymphoproliferative, 148, 166 M Magnetic Resonance Imaging, 36, 37, 50, 75, 79, 148 Magnetic Resonance Spectroscopy, 20, 21, 36, 55, 60, 148

Malabsorption, 78, 84, 128, 148 Malabsorption Syndromes, 78, 148 Malignant, 76, 121, 124, 147, 148 Malnutrition, 37, 86, 122, 148 Medial, 140, 148 Mediate, 134, 148 Mediator, 148, 161 MEDLINE, 101, 148 Meiosis, 127, 148, 164 Melanin, 148, 155, 166 Membrane, 11, 125, 131, 140, 145, 148, 150, 153, 154, 155, 156, 157 Memory, 117, 133, 148 Meninges, 128, 149 Menopause, 149, 158 Mental, iv, 3, 4, 5, 84, 86, 100, 102, 106, 116, 129, 133, 134, 138, 143, 144, 148, 149, 159, 166, 167 Mental Processes, 134, 149, 159 Mentors, 11, 149 Mesenteric, 27, 149 Mesentery, 149, 155 Meta-Analysis, 30, 39, 149 Metabolic disorder, 4, 48, 60, 143, 149 Metallothionein, 80, 149 MI, 120, 149 Microbe, 149, 165 Microcirculation, 147, 149 Microglia, 125, 149, 150 Micro-organism, 141, 149 Microtubules, 149, 153 Midazolam, 6, 149 Mitochondrial Swelling, 150, 151 Mitotic, 134, 150 Mitotic inhibitors, 134, 150 Modification, 123, 150, 159 Molecular, 4, 49, 72, 101, 103, 127, 131, 149, 150, 158, 160, 165, 166 Molecule, 124, 130, 132, 134, 135, 136, 138, 140, 150, 153, 160, 167 Monoamine, 36, 150, 166 Monoamine Oxidase, 36, 150, 166 Monocytes, 147, 150 Mononuclear, 150, 166 Morphological, 12, 150 Morphology, 84, 141, 150 Motility, 84, 150, 161 Motor Activity, 132, 150 Mucosa, 150, 158 Mucus, 150, 166 Multicenter study, 38, 150 Multidrug resistance, 150, 155

175

Multivariate Analysis, 28, 150 Myocardial infarction, 132, 149, 150, 158 Myocardium, 123, 149, 150 N Nasogastric, 136, 151 Nausea, 124, 139, 144, 151, 166 Necrosis, 81, 144, 149, 150, 151, 160 Needle biopsy, 78, 138, 151 Neomycin, 25, 44, 67, 93, 151 Nephrosis, 142, 151 Nerve, 8, 121, 123, 129, 133, 135, 139, 148, 150, 151, 163, 165 Neural, 9, 11, 121, 149, 150, 151 Neuroblastoma, 9, 151 Neurologic, 7, 34, 151 Neuromuscular, 3, 106, 121, 151, 166 Neuronal, 7, 9, 45, 80, 151 Neurons, 7, 9, 133, 139, 151, 164 Neuropeptides, 85, 151 Neuropsychological Tests, 11, 21, 151 Neurosis, 151 Neurotic, 73, 151 Neurotoxicity, 4, 11, 151 Neurotoxin, 11, 151 Neurotransmitter, 8, 11, 12, 15, 35, 46, 70, 72, 121, 123, 127, 134, 140, 142, 145, 151, 152, 163, 166 Neutrons, 122, 152, 159 Neutrophils, 147, 152 Niacin, 152, 166 Nitric Oxide, 10, 12, 33, 45, 152 Nitrogen, 10, 73, 80, 123, 140, 146, 152, 166 Norepinephrine, 72, 121, 134, 151, 152 Nosocomial, 78, 152 Nuclear, 10, 19, 126, 131, 135, 151, 152 Nuclei, 122, 131, 135, 148, 152, 159 Nucleic acid, 152 Nucleus, 126, 132, 133, 135, 137, 140, 148, 150, 152, 158, 159 Nutritional Support, 5, 139, 152 O Office Management, 83, 152 Oliguria, 146, 152 Omentum, 142, 153 Opacity, 133, 153 Ornithine, 47, 50, 67, 71, 153 Osmolarity, 9, 153 Osmoles, 153 Osmotic, 122, 150, 153 Overdose, 82, 119, 138, 153 Ovum, 153, 158 Oxazepam, 32, 153

Oxidation, 121, 124, 133, 147, 153 Oxidative Stress, 11, 153 Oxygenation, 142, 153 P Paclitaxel, 63, 64, 153 Palliative, 153, 164 Pancreas, 76, 78, 79, 82, 84, 121, 126, 134, 139, 141, 153, 166 Pancreatic, 33, 53, 78, 85, 128, 136, 139, 153 Pancreatic Ducts, 136, 153 Pancreatic Fistula, 78, 153 Pancreatic Juice, 139, 153 Pancreatitis, 77, 78, 85, 153 Papilla, 136, 154 Paradoxical, 80, 154 Parasite, 154 Parasitic, 78, 79, 154 Parasitic Diseases, 78, 154 Parenteral, 4, 5, 48, 65, 70, 78, 84, 154 Parenteral Nutrition, 4, 5, 78, 154 Parietal, 154, 155, 156 Parkinsonism, 49, 124, 154 Particle, 154, 165 Parturition, 154, 158 Pathogen, 141, 154 Pathogenesis, 3, 4, 5, 11, 14, 15, 18, 27, 34, 35, 48, 49, 51, 79, 81, 106, 154 Pathologic, 42, 121, 126, 132, 143, 154 Pathologies, 12, 154 Pathophysiology, 53, 83, 85, 154 Patient Education, 106, 110, 112, 120, 154 Pelvis, 121, 144, 154 Penicillamine, 80, 154 Penicillin, 123, 154, 167 Pepsin, 154 Peptic, 78, 85, 141, 154 Peptic Ulcer, 78, 85, 141, 154 Peptide, 123, 130, 154, 155, 157, 158, 159, 164 Peptide Chain Elongation, 130, 155 Perfusion, 10, 35, 38, 126, 143, 155 Pericarditis, 22, 155 Peripheral Nervous System, 136, 151, 155, 163 Peritoneal, 125, 155 Peritoneal Cavity, 125, 155 Peritoneum, 149, 153, 155 Peritonitis, 76, 77, 82, 83, 155 P-Glycoprotein, 7, 155 Phantom, 12, 155 Pharmacologic, 123, 155, 165 Pharmacotherapy, 30, 72, 155

176


Pharynx, 139, 155 Phenylalanine, 70, 72, 155, 166 Phospholipids, 138, 144, 155 Phosphorus, 20, 127, 155 Physiologic, 122, 143, 156, 160, 165 Physiology, 7, 8, 10, 78, 84, 86, 135, 139, 141, 156 Pilot study, 50, 156 Plantago, 64, 156, 159 Plants, 128, 129, 140, 150, 152, 156, 157, 165 Plasma, 9, 15, 23, 26, 33, 49, 65, 70, 73, 79, 88, 122, 139, 140, 141, 146, 156 Plasma protein, 122, 156 Plasmapheresis, 55, 156 Platelet Aggregation, 123, 152, 156 Platelets, 152, 156, 164 Platinum, 147, 156 Pleura, 156 Pleural, 72, 156 Pleural cavity, 156 Pleural Effusion, 72, 156 Pneumonia, 132, 156 Poisoning, 71, 133, 137, 145, 151, 156 Pollen, 122, 157 Polypeptide, 123, 130, 157, 158 Polyposis, 130, 157 Polytetrafluoroethylene, 38, 157 Polyunsaturated fat, 65, 157 Portacaval, 36, 60, 157 Portal Hypertension, 4, 6, 47, 53, 76, 77, 78, 79, 82, 157 Portal Pressure, 38, 157 Portal System, 47, 157 Portosystemic Shunt, 6, 10, 38, 44, 45, 51, 82, 157 Posterior, 123, 153, 157 Postoperative, 38, 77, 157 Potassium, 26, 31, 157 Practice Guidelines, 102, 157 Precipitating Factors, 4, 107, 157 Precipitation, 10, 37, 157 Precursor, 8, 10, 129, 134, 135, 136, 137, 152, 155, 157, 166, 167 Preoperative, 49, 158 Presynaptic, 151, 158 Prevalence, 17, 49, 158 Primary Biliary Cirrhosis, 76, 77, 79, 158 Primary Sclerosing Cholangitis, 77, 78, 158 Proctocolectomy, 77, 158 Progesterone, 158

Progression, 8, 37, 158 Progressive, 129, 135, 146, 151, 158, 160 Projection, 152, 158 Prolactin, 38, 158 Prophase, 127, 158, 164 Prophylaxis, 48, 158 Propranolol, 21, 56, 158 Prostate, 126, 158, 166 Protein C, 122, 125, 158, 166 Protein S, 127, 130, 137, 151, 158 Proteolytic, 130, 159 Protons, 122, 142, 148, 159 Proto-Oncogene Proteins, 153, 159 Proto-Oncogene Proteins c-mos, 153, 159 Psychic, 149, 151, 159, 161 Psychology, 134, 159 Psychometric testing, 26, 50, 159 Psychomotor, 133, 159 Psyllium, 64, 156, 159 Public Policy, 101, 159 Publishing, 13, 76, 77, 82, 159 Pulmonary, 83, 127, 142, 146, 159, 163 Pulmonary Artery, 127, 159 Pulmonary Edema, 146, 159 Q Quality of Life, 37, 159, 163 R Radiation, 84, 123, 136, 138, 155, 159, 168 Radiology, 12, 26, 34, 41, 44, 50, 51, 60, 76, 79, 159 Randomized, 6, 25, 27, 29, 30, 38, 39, 40, 41, 48, 64, 135, 159 Randomized clinical trial, 6, 25, 48, 159 Reaction Time, 17, 160 Reactive Oxygen Species, 12, 160 Reagent, 137, 160 Receptor, 4, 9, 11, 15, 17, 20, 28, 47, 124, 127, 134, 137, 138, 160, 161 Receptors, Serotonin, 160, 161 Recombinant, 126, 160, 167 Rectum, 125, 130, 134, 138, 139, 144, 146, 158, 160 Refer, 1, 130, 136, 152, 160, 165 Reflux, 137, 139, 160 Refraction, 160, 162 Refractory, 26, 50, 160 Regeneration, 81, 84, 160 Regimen, 135, 155, 160 Regression Analysis, 13, 160 Regurgitation, 137, 139, 141, 160 Renal failure, 79, 82, 133, 142, 160, 166 Reperfusion, 60, 160

177

Reperfusion Injury, 160 Resection, 76, 161 Retrograde, 34, 41, 55, 161 Risk factor, 15, 33, 134, 147, 161 S Salivation, 137, 161 Scatter, 155, 161 Screening, 52, 77, 130, 161 Secretion, 32, 142, 143, 146, 149, 150, 161 Sedative, 54, 119, 138, 149, 161 Seizures, 117, 133, 161, 163 Semisynthetic, 129, 161 Sensor, 7, 161 Sepsis, 7, 10, 161 Sequencing, 141, 161 Serotonin, 11, 124, 127, 150, 151, 155, 160, 161, 166 Serous, 82, 136, 156, 161 Serum, 26, 31, 32, 38, 41, 52, 56, 122, 123, 130, 146, 155, 161, 166 Shock, 119, 161, 165 Shunt, 4, 10, 24, 28, 33, 34, 36, 39, 55, 60, 161 Side effect, 72, 91, 95, 121, 124, 143, 161, 163, 165 Signs and Symptoms, 83, 161, 166 Skeleton, 162 Skull, 9, 145, 162 Small intestine, 4, 84, 135, 136, 142, 143, 145, 151, 162 Smooth muscle, 122, 123, 142, 162, 163 Social Environment, 159, 162 Sodium, 5, 84, 162 Somatic, 132, 148, 155, 162 Soybean Oil, 157, 162 Spastic, 146, 162 Specialist, 108, 134, 162 Species, 137, 148, 154, 156, 160, 162, 165, 167 Specificity, 7, 122, 162 Spectroscopic, 12, 36, 60, 148, 162 Spectrum, 76, 149, 162 Sperm, 122, 157, 162 Sphincters, 137, 162 Spinal cord, 125, 128, 129, 149, 151, 155, 162 Spleen, 79, 148, 162 Splenectomy, 143, 162 Splenomegaly, 143, 162 Standard therapy, 4, 163 Status Epilepticus, 30, 163 Steatosis, 138, 163

Stenosis, 163 Stent, 38, 51, 163 Sterile, 70, 163 Stimulant, 142, 163, 167 Stimulus, 135, 137, 138, 145, 160, 163, 164 Stomach, 84, 121, 125, 134, 137, 139, 141, 142, 147, 151, 153, 154, 155, 160, 162, 163 Stool, 130, 144, 145, 146, 163 Stress, 128, 132, 145, 151, 153, 163 Stricture, 76, 79, 163 Stroke, 100, 146, 163 Subacute, 10, 80, 144, 163 Subclinical, 4, 5, 17, 20, 21, 23, 26, 33, 39, 45, 49, 50, 51, 52, 53, 54, 55, 71, 144, 161, 163 Subcutaneous, 135, 154, 163 Substance P, 137, 161, 163 Substrate, 6, 10, 163, 166 Sulfotransferases, 7, 163 Supplementation, 64, 65, 163 Supportive care, 82, 163 Surfactant, 137, 163 Sympathomimetic, 135, 137, 152, 163, 166 Symptomatic, 153, 164 Synapse, 121, 158, 164, 165 Synaptic, 8, 151, 164 Synergistic, 158, 164 Systemic, 4, 24, 26, 39, 64, 76, 77, 79, 92, 93, 94, 127, 133, 137, 144, 157, 164 Systemic disease, 76, 77, 79, 164 Systolic, 143, 164 T Taurine, 9, 13, 126, 164 Telencephalon, 126, 164 Therapeutics, 30, 73, 94, 150, 164 Thermal, 134, 152, 164 Thorax, 121, 164 Threonine, 13, 159, 164 Threshold, 143, 164 Thromboplastin, 118, 164 Thrombosis, 19, 158, 163, 164 Thrombus, 132, 144, 146, 156, 164 Thyroid, 143, 164, 165, 166 Thyroid Gland, 143, 164, 165 Thyrotropin, 143, 164 Thyroxine, 41, 122, 155, 165 Tolerance, 8, 121, 140, 165 Tomography, 11, 148, 165 Tonic, 137, 165 Toxic, iv, 71, 73, 77, 126, 132, 165 Toxicity, 5, 42, 63, 78, 135, 165 Toxicology, 102, 118, 165

178


Toxin, 71, 165 Trace element, 52, 165 Tracheoesophageal Fistula, 137, 165 Transduction, 9, 144, 165 Transfection, 127, 165 Translation, 123, 137, 151, 165 Translocation, 130, 137, 165 Transmitter, 121, 125, 134, 145, 148, 152, 165, 166 Transplantation, 4, 10, 30, 35, 49, 52, 76, 77, 78, 79, 81, 83, 146, 165 Trauma, 9, 76, 79, 133, 137, 151, 154, 165 Tremor, 154, 165 Triad, 142, 166 Trifluoperazine, 12, 166 Tryptophan, 19, 45, 53, 54, 130, 161, 166 Tumor Lysis Syndrome, 28, 166 Tumor marker, 126, 166 Tumor Necrosis Factor, 27, 52, 166 Tyramine, 150, 166 Tyrosine, 70, 134, 166 U Ulcer, 77, 166 Ulceration, 154, 166 Ulcerative colitis, 77, 144, 158, 166 Uraemia, 154, 166 Urea, 7, 10, 71, 93, 146, 153, 166 Urease, 141, 166 Uremia, 146, 160, 166 Urethra, 158, 167 Urinary, 55, 80, 144, 152, 166, 167 Urine, 56, 127, 134, 144, 146, 152, 167

V Vaccines, 167 Valine, 70, 72, 154, 167 Varices, 6, 41, 167 Vascular, 41, 50, 77, 122, 136, 142, 144, 147, 149, 152, 164, 167 Vasculitis, 154, 167 Vasodilation, 83, 167 Vasodilator, 127, 135, 142, 167 Vector, 154, 165, 167 Vein, 19, 27, 71, 76, 123, 144, 145, 152, 157, 167 Vena, 167 Venlafaxine, 24, 167 Venous, 33, 34, 56, 76, 79, 82, 157, 158, 167 Venous blood, 56, 167 Venous Pressure, 157, 167 Ventricles, 129, 167 Veterinary Medicine, 101, 167 Villous, 128, 167 Viral, 76, 77, 78, 83, 165, 167 Viral Hepatitis, 76, 77, 78, 83, 167 Virulence, 165, 167 Virus, 76, 79, 125, 145, 165, 167 Visceral, 132, 155, 168 Vitamin A, 144, 168 Vitro, 168 Vivo, 10, 12, 168 W Wakefulness, 133, 168 Withdrawal, 133, 153, 168 X X-ray, 131, 136, 152, 159, 168

179

180


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