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

GASTRITIS A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R EFERENCES J AMES N. P...

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GASTRITIS A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R EFERENCES

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

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright ©2003 by ICON Group International, Inc. Copyright ©2003 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., 1960Gastritis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83923-9 1. Gastritis-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 gastritis. 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 GASTRITIS.................................................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Gastritis ...................................................................................... 12 E-Journals: PubMed Central ....................................................................................................... 58 The National Library of Medicine: PubMed ................................................................................ 62 CHAPTER 2. NUTRITION AND GASTRITIS ...................................................................................... 109 Overview.................................................................................................................................... 109 Finding Nutrition Studies on Gastritis ..................................................................................... 109 Federal Resources on Nutrition ................................................................................................. 112 Additional Web Resources ......................................................................................................... 113 CHAPTER 3. ALTERNATIVE MEDICINE AND GASTRITIS ............................................................... 115 Overview.................................................................................................................................... 115 National Center for Complementary and Alternative Medicine................................................ 115 Additional Web Resources ......................................................................................................... 120 General References ..................................................................................................................... 124 CHAPTER 4. DISSERTATIONS ON GASTRITIS ................................................................................. 127 Overview.................................................................................................................................... 127 Dissertations on Gastritis .......................................................................................................... 127 Keeping Current ........................................................................................................................ 127 CHAPTER 5. PATENTS ON GASTRITIS ............................................................................................ 129 Overview.................................................................................................................................... 129 Patents on Gastritis ................................................................................................................... 129 Patent Applications on Gastritis................................................................................................ 147 Keeping Current ........................................................................................................................ 165 CHAPTER 6. BOOKS ON GASTRITIS ................................................................................................ 167 Overview.................................................................................................................................... 167 Book Summaries: Federal Agencies............................................................................................ 167 Book Summaries: Online Booksellers......................................................................................... 173 The National Library of Medicine Book Index ........................................................................... 174 Chapters on Gastritis ................................................................................................................. 174 Directories.................................................................................................................................. 177 CHAPTER 7. MULTIMEDIA ON GASTRITIS ..................................................................................... 179 Overview.................................................................................................................................... 179 Video Recordings ....................................................................................................................... 179 Bibliography: Multimedia on Gastritis ...................................................................................... 180 CHAPTER 8. PERIODICALS AND NEWS ON GASTRITIS .................................................................. 181 Overview.................................................................................................................................... 181 News Services and Press Releases.............................................................................................. 181 Newsletter Articles .................................................................................................................... 183 Academic Periodicals covering Gastritis.................................................................................... 186 CHAPTER 9. RESEARCHING MEDICATIONS .................................................................................. 187 Overview.................................................................................................................................... 187 U.S. Pharmacopeia..................................................................................................................... 187 Commercial Databases ............................................................................................................... 189 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 193 Overview.................................................................................................................................... 193 NIH Guidelines.......................................................................................................................... 193 NIH Databases........................................................................................................................... 195 Other Commercial Databases..................................................................................................... 198

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The Genome Project and Gastritis ............................................................................................. 198 APPENDIX B. PATIENT RESOURCES ............................................................................................... 203 Overview.................................................................................................................................... 203 Patient Guideline Sources.......................................................................................................... 203 Finding Associations.................................................................................................................. 206 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 209 Overview.................................................................................................................................... 209 Preparation................................................................................................................................. 209 Finding a Local Medical Library................................................................................................ 209 Medical Libraries in the U.S. and Canada ................................................................................. 209 ONLINE GLOSSARIES................................................................................................................ 215 Online Dictionary Directories ................................................................................................... 218 GASTRITIS DICTIONARY......................................................................................................... 219 INDEX .............................................................................................................................................. 303

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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 gastritis 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 gastritis, 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 gastritis, 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 gastritis. 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 gastritis, 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 gastritis. 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 GASTRITIS Overview In this chapter, we will show you how to locate peer-reviewed references and studies on gastritis.

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

Helicobacter Pylori Infection, Gastritis and Gastric Cancer: A Short-Term Eradication Therapy for Helicobacter Pylori Acute Gastritis Source: Journal of Gastroenterology and Hepatology. 15(12): 1377-1381. December 2000. Contact: Available from Blackwell Science. 54 University Street, Carlton South 3053, Victoria, Australia. +61393470300. Fax +61393475001. E-mail: [email protected]. Website: www.blackwell-science.com. Summary: Acute gastritis (stomach inflammation), caused by an initial infection of Helicobacter pylori, may resolve spontaneously, but the infection sometimes becomes chronic. The authors of this article examined the efficacy of a short term H. pylori eradication therapy on acute gastritis. Among the 15 patients with hemorrhage acute gastritis who were randomly allocated to group A (eradication therapy) or group B

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(lansoprazole), 10 of the patients started to receive treatment within 1 day after the disease onset. The other five patients began the eradication therapy 4 to 6 days after disease onset (group C). Eradication therapy consisted of a daily oral administration of each of 30 milligrams lansoprazole (LPZ) once a day; 400 milligrams clarithromycin, twice a day; 1000 milligrams amoxicillin, twice a day; and 300 milligrams rebamipide, three times a day, for one week. If the endoscopy was normal, medication was stopped for the following 4 weeks before gastric endoscopy was performed again in order to assess H. pylori eradication. All group A patients were cured after the 1 week treatment and, therefore, they became H. pylori negative. Group B and C patients had erosions or ulcers after the 1 week treatment and so received an additional 3 week administration of LPZ. Four weeks later, their gastritis was cured and except for one group B patient, they became H. pylori negative. The authors conclude that in patients with acute gastritis, caused by an initial H. pylori infection, eradication therapy was efficacious in achieving early healing. This therapy should therefore be started as soon as possible after disease onset. 1 table. 25 references. •

Trend Toward a Reduced Prevalence of Helicobacter Pylori Infection, Chronic Gastritis, and Gastric Cancer in Japan Source: Gastroenterology Clinics of North America. 29(3): 623-631. September 2000. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32821-9816. (800) 654-2452. Summary: Although there has been a remarkable decline in the prevalence and mortality (death) rates of gastric (stomach) cancer in developed countries, gastric cancer is one of the common malignancies in the world and is still the main cause of death in Japan. This article investigates the trends in Helicobacter pylori infection and gastritis in Japan over the past few decades. The author notes that it is important to investigate the relationship between H. pylori infection and gastric cancer and gastritis to understand better the mechanisms for carcinogenesis (the development of cancer) in the stomach. The author speculates that declines in H. pylori infection and gastritis over the past few decades may lead to a decline in gastric cancer in Japan, supplemented by excellent procedures for the early detection of gastric cancer. H. pylori infection rarely is acquired in adult life, so once it is eradicated, reinfection is not expected in adult patients. The author concludes that adequate treatment of H. pylori provides long term protection against gastric cancer.

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Gastritis: A Common Source of Acute Bleeding in the Upper Gastrointestinal Tract? Source: Southern Medical Journal. 83(7): 769-770. July 1990. Summary: Gastritis is commonly reported as a frequent cause of acute hemorrhage of the upper gastrointestinal tract. This article reviews the literature and also reports on 4 years clinical experience studying this phenomenon. The authors conclude, in contrast to conventional belief and in agreement with more recent publications, that even though gastritis is a relatively common endoscopic finding, it is a rare cause of acute bleeding in the upper gastrointestinal tract. This is clinically significant in that a clinical or presumptive diagnosis of gastritis as the cause of acute bleeding may be inaccurate, but may preclude the use of diagnostic and therapeutic endoscopy to locate the true source of the bleeding. 11 references.

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Improvement in Atrophic Gastritis and Intestinal Metaplasia in Patients in Whom Helicobacter Pylori Was Eradicated Source: Annals of Internal Medicine. 134(5): 380-386. March 6, 2001. Contact: Available from American College of Physicians. American Society of Internal Medicine. 190 North Independence Mall West, Philadelphia, PA 19106-1572. Website: www.acponline.org. Summary: Glandular atrophy and intestinal metaplasia (changes in the cells of the intestinal lining) are precancerous lesions; whether Helicobacter pylori infection or its eradication affects these lesions is controversial. This article reports on a study undertaken to determine whether eradication of H. pylori is associated with improvement in glandular atrophy and intestinal metaplasia after at least 1 year. The single blind prospective trial included 163 consecutive patients with dyspepsia and H. pylori infection, seen at an academic gastroenterology clinic in Japan. The intervention consisted of a 1 week course of a proton pump inhibitor and antibiotic therapy. In the 115 patients in whom H. pylori was eradicated, inflammation and mean neutrophil activity had decreased by 1 to 3 months, and both glandular atrophy in the corpus (the main body of the stomach) and intestinal metaplasia in the antrum had decreased by 12 to 15 months. Glandular atrophy in the corpus improved in 34 of 38 patients (89 percent) with atrophy before treatment, and intestinal metaplasia in the antrum improved in 28 of 46 patients (61 percent) who had metaplasia at baseline. In the 48 patients in whom eradication was unsuccessful, no significant histologic changes were observed. The authors conclude that in the year after successful H. pylori eradication, precancerous lesions improved in most patients. 1 figure. 1 table. 20 references.

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Helicobacter Pylori Infection and Atrophic Gastritis in Middle-Aged Japanese Residents of Sao Paulo and Lima Source: International Journal of Epidemiology. 28(3): 577-582. June 1999. Contact: Available from Oxford University Press. Journals Subscription Department, Great Clarendon Street, Oxford OX2 6DP, UK. 44 (0)1865 267907. Fax 44 (0)1865 267485. Summary: Helicobacter pylori infection and atrophic gastritis (AG) are markedly more prevalent in Japan than in other industrialized countries; however, the reasons for such a high prevalence are not fully understood. This article reports on a study to add to information on H. pylori infection and its association with AG, in which the authors studied Japanese persons living in less developed countries. Cross sectional surveys were conducted of randomly selected Japanese residents aged 40 to 59 years in Sao Paulo, Brazil and in Lima, Peru. Serum IgG antibody to H. pylori and pepsinogen I and II were measured as markers of AG. The prevalence of H. pylori infection was similar in both populations: 77 percent in Sao Paulo and 75 percent in Lima, and was within the range of five populations in Japan from the authors' previous study. However, the presence of AG was more prevalent among Japanese in Sao Paulo than Japanese in Lima. This difference was not explained by sex, age, generation, or H. pylori infection. The authors conclude that factors other than H. pylori infection are important in the development of AG among Japanese persons. 1 figure. 3 tables. 21 references.

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Long-Term Effects of Cure of Helicobacter Pylori Infection on Patients with Atrophic Body Gastritis Source: Alimentary Pharmacology and Therapeutics. 16(10): 1701-1708. October 2002.

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Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email: [email protected]. Website: www.blackwell-science.com. Summary: Helicobacter pylori infection induces atrophic body gastritis (chronic inflammation of the stomach, associated with degeneration of the stomach mucosa), but the long-term effect of its cure on body atrophy is unclear. This article reports on a study undertaken to investigate the long term effects of H. pylori cure on gastric (stomach) morpho-functional parameters in patients with atrophic body gastritis. Forty patients with atrophic body gastritis were cured of H. pylori infection. At eradication assessment (6 to 12 months), in eight of the 40 patients, body atrophy was no longer observed, whereas in 32 of the 40 it remained substantially unchanged. In the 8 patients with reversed body atrophy, gastrinemia decreased significantly with respect to pretreatment values, and basal and stimulated acid secretion increased significantly after cure. In the 32 patients still presenting body atrophy, gastrinemia was similar to pretreatment values. At follow up, the eight patients with revered body atrophy continued with normal gastrinemia, but in the 19 patients with continued atrophy, both corporal atrophy and intestinal metaplasia remained substantially unchanged. The authors conclude that following successful treatment in patients with atrophic body gastritis and H. pylori infection, long-term histological investigations are crucial in order to detect reversed body damage or to confirm continued body atrophy. 4 figures. 2 tables. 35 references. •

Gastritis and Helicobacter Pylori: Forty Years of Antibiotic Therapy Source: Digestion. 58(3): 203-210. May-June 1997. Contact: Available from S. Karger Publishers, Inc. 26 West Avon Road, P.O. Box 529, Farmington, CT 06085. Summary: Helicobacter pylori is now at the forefront of gastroenterology, particularly regarding its eradication as the treatment of gastroduodenal ulcer, whereas its role in gastritis is still widely ignored. The author notes that gastritis was the disease for which H. pylori was originally studied. This article reviews the 40 years of antibiotic therapy for gastrointestinal diseases, notably gastritis, and the application of this experience to present considerations for treatment. Forty years ago, it was shown for the first time that antibiotics can eliminate gastric ammonia production in humans; this suggested that this was due to eradication of bacterial urease activity. Researchers also found that the gastric juice ammonia concentration correlates with hypoacidity (low acid levels) or anacidity (no acid) in people with uremia and with mucosal inflammation in subjects with gastritis. In patients with nonalcoholic and alcoholic gastritis, the histology as well as the symptoms of gastritis were strikingly improved by antibiotic treatment. The beneficial effects of eradication of gastric urease activity and the resulting decreased ammonia production were also shown in patients with hepatic encephalopathy. The author concludes by emphasizing that broader studies and clinical applications of these earlier findings are now warranted. 7 figures. 62 references. (AA-M).

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Helicobacter Pylori Infection, Gastritis and Gastric Cancer: Helicobacter Pylori Infection Among Japanese Children Source: Journal of Gastroenterology and Hepatology. 15(12): 1382-1385. December 2000. Contact: Available from Blackwell Science. 54 University Street, Carlton South 3053, Victoria, Australia. +61393470300. Fax +61393475001. E-mail: [email protected]. Website: www.blackwell-science.com.

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Summary: In Japan, there are few reports describing Helicobacter pylori infection among young children. This article reports on a study undertaken to identify risk factors associated with H. pylori in school aged children in Japan. Subjects were first grade students of three elementary schools (n = 310) and second grade students of a junior high school (n = 300). Personal information, such as students' medical history, parents' history, family size, siblings, and household pets, was collected using a questionnaire. Saliva samples and personal information were collected twice. Among the children, factors related to Helicobacter antibody in saliva included spending a longer period of time in a nursery school or kindergarten and a maternal history of stomach disease. Birth order, sleeping situation, and number of siblings were not factors that were significantly related to Helicobacter antibody in the saliva. Chewing food for the infant, family size, rooms in the household, sharing a bedroom during childhood, pets, a past history, and a paternal history were not related to positivity. The results indicate that transmission is person to person, mainly through close contact with other children and intrafamilial infection. H. pylori infection seems to occur frequently early in life, probably before 6 years of age. 2 tables. 29 references. •

Detection of Helicobacter Pylori Colonization in Dental Plaques and Tongue Scrapings of Patients with Chronic Gastritis Source: Quintessence International. 32(2): 131-134. February 2001. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail: [email protected]. Website: www.quintpub.com. Summary: It has been suggested that the oral cavity (mouth) and dental plaque might be a reservoir for Helicobacter pylori (Hp). This article reports on a study in which the authors tried to detect the prevalence of Hp colonization in dental plaque and tongue scrapings of patients with chronic gastritis. The authors also investigated the effect of systemic treatment upon this colonization and eradication of Hp from the gastric (stomach) mucosa. The study included 81 patients (49 men, 32 women) in whom dental plaque and tongue scraping specimens were obtained and assessed with Campylobacter like organism (CLO) testing, prior to endoscopy examination. Chronic gastritis was diagnosed in 63 (77.7 percent) of the 81 patients. Dental plaque samples of 64 (79 percent) patients and tongue scraping samples of 48 (59.2 percent) patients were urease positive. Of the 63 patients with chronic gastritis, dental plaque and tongue scrapings were urease positive in 52 (83 percent) and 37 (59 percent) patients, respectively. After 14 days of triple drug therapy (omeprazole, clarithromycin, and amoxicillin), Hp was eradicated from the gastric mucosa of almost all of the patients, whereas no changes were detected in dental plaque and tongue scrapings by CLO test examination. The authors conclude that Hp colonization, which seemed to be high in dental plaque and on the tongue, might play an important role in the pathogenesis of the reinfection process. In order to eradicate Hp from both the oral cavity and the gastric mucosa, studies should be performed to assess the effects of plaque control procedures in addition to present treatment modalities. 6 figures. 27 references.

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Alteration of Histological Gastritis After Cure of Helicobacter Pylori Infection Source: Alimentary Pharmacology and Therapeutics. 16(11): 1923-1932. November 2002. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email: [email protected]. Website: www.blackwell-science.com.

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Summary: It is still disputed whether gastric (stomach) atrophy or intestinal metaplasia improves after the cure of Helicobacter pylori infection. If these condition improve, cure of the infection may reduce cancer risk. This article reports on a literature survey undertaken to clarify the histological changes after the cure of H. pylori infection. The authors reviewed 52 selected reports from 1,066 relevant articles. The extracted data were pooled according to histological parameters of gastritis based on the updated Sydney system. Activity improved more rapidly than inflammation. Eleven of 25 reports described significant improvement of atrophy. Atrophy was not improved in one of four studies with a large sample size (more than 100 samples) and in two of five studies with a long follow up period (longer than 12 months), suggesting that disagreement between the studies was not totally due to sample size or follow up period. Methodological flaws, such as patient selection, and statistical analysis based on the assumption that atrophy improves continuously and generally in all patients might be responsible for the inconsistent results. Five of 28 studies described significant improvement of intestinal metaplasia. The authors conclude that activity and inflammation were improved after the cure of H. pylori infection. Atrophy did not improve generally among all patients, but improved in certain patients. 5 tables. 65 references. •

Eradication of Helicobacter Pylori Increases Gastric Acidity in Patients with Atrophic Gastritis of the Corpus: Evaluation of 24-h pH Monitoring Source: Alimentary Pharmacology and Therapeutics. 13(2): 155-162. February 1999. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email: [email protected]. Website: www.blackwell-science.com. Summary: Recent studies have shown that the eradication of Helicobacter pylori results in a gastric acid secretion that decreases to normal levels in patients with duodenal ulcer disease. This article reports on a study undertaken to evaluate the effect of eradicating H. pylori in a 24 hour study of gastric acidity in patients with atrophic gastritis of the corpus. Intragastric acidity was measured by continuous 24 hour pH monitoring, and the histology of the gastric antrum and corpus were evaluated in 14 H. pylori positive patients (10 men, 4 women; mean age 57 years)with histologically proven atrophic gastritis of the corpus before and 1 year after anti H. pylori therapy. H. pylori was absent in 13 of 14 patients 1 year after treatment. Both gastritis and atrophy scores were significantly lower after eradication therapy. The 24 hour medical pH and the percentage of 24 hour pH readings above 4.0 units were significantly decreased after eradication therapy. The authors conclude that improving the histology of the gastric antrum and corpus may lead to the normalization of gastric acidity. 3 figures. 1 table. 45 references. (AA-M).

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Cure of Helicobacter Pylori Infection in Atrophic Body Gastritis Patients Does Not Improve Mucosal Atrophy But Reduces Hypergastrinemia and Its Related Effects on Body ECL-Cell Hyperplasia Source: Alimentary Pharmacology and Therapeutics. 14(5): 625-634. May 2000. Contact: Available from Alimentary Pharmacology and Therapeutics. Blackwell Science Ltd., Osney Mead, Oxford OX2 OEL, UK. +44(0)1865 206206. Fax +44(0)1865 721205. Email: [email protected]. Website: www.blackwell-science.com. Summary: The effects of Helicobacter pylori eradication on atrophic body gastritis are controversial. This article reports on a study undertaken to investigate the effect of triple therapy on atrophic body gastritis in H. pylori positive patients and its effect on

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morphofunctional gastric parameters. Consecutive patients (n = 35) with atrophic body gastritis with histological or serological evidence of H. pylori infection were treated. Before and 6 and 12 months after H. pylori eradication the patients were evaluated for fasting gastrinemia and pepsinogen I, basal and peak acid output, and detailed histological assessment including the ECL cell proliferative patterns. Six months after treatment, 25 out of 32 patients were cured (78 percent). Cure of infection was associated with improvement in both basal and stimulated acid secretion, as well as with reduction in hypergastrinemia. In contrast, the eradication had no effect on body corporal atrophy and intestinal metaplasia, or pepsinogen I levels. These results were confirmed at 12 months after eradication. A statistical inverse correlation was obtained between the corporal chronic infiltrate score and peak acid output values. A total of 53 percent of atrophic body gastritis patients showed a regression in severity of body ECL cell hyperplastic change. The authors conclude that cure of H. pylori infection in patients with atrophic gastritis reverses some adverse effects on gastric function and ECL cell hyperplasia. 3 figures. 2 tables. 38 references. •

Favourable Effect of an Acidified Milk (LC-1) on Helicobacter Pylori Gastritis in Man Source: European Journal of Gastroenterology and Hepatology. 13(1): 25-29. January 2001. Contact: Available from Lippincott Williams and Wilkins. 241 Borough High Street, London SE1 1GB, UK 44(0)20-7940-7502. Fax: 44(0)20-7940-7574. Website: http://www.eurojgh.com/. Summary: The supernatant of Lactobacillus johnsonii La1 culture was shown to be bactericidal and to have a partial, acid independent suppressive effect on Helicobacter pylori in humans. This study investigated the effect of L. johnsonii La1 acidified milk (LC-1) on H. pylori infection in 53 volunteers infected with H. pylori. Volunteers were randomized to received either LC-1 or placebo 180 milliliters twice a day for 3 weeks. All subjects also received clarithromycin 500 milligrams twice a day (bid) during the last two weeks of acidified milk therapy. Esophagogastroduodenoscopy and biopsies were performed at inclusion and repeated 4 to 8 weeks after the end of the treatment. H. pylori infection was confirmed by urease test and histology. Results showed that LC-1 ingestion induced a decrease in H. pylori density in the antrum (the passage from the esophagus to the stomach, i.e., the first part of the stomach) and the corpus (the body of the stomach). LC-1 also reduced inflammation and gastritis activity in the antrum and of activity in the corpus. Clarithromycin eradicated H. pylori in 26 percent of the subjects; LC-1 did not improve the antibiotic effect. These results suggest that H. pylori infection and gastritis can be down regulated by LC-1. 4 tables. 33 references.

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Evaluation of New Anti-Infective Drugs for the Treatment of Gastritis and Peptic Ulcer Disease Associated with Infection by Helicobacter Pylori Source: Clinical Infectious Diseases. 15(Supplement 1): S268-S273. 1992. Summary: This article is one of a series of disease-specific guidelines that have been prepared to assist sponsors and investigators in the development, conduct, and analysis of studies of new anti-infective drugs. The article considers the evaluation of new antiinfective drugs for the treatment of gastritis and peptic ulcer disease associated with infection by Helicobacter pylori. Included is an introduction to the guideline, including standards of care, and six sections covering clinical definitions of the disease; information needed before conducting clinical trials; qualifications of investigators and institutions; design and implementation of phase 1, 2, and 3 clinical trials; elements to be

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considered in designed phase 2 and 3 clinical trials; and issues of informed consent. The authors note that a randomized, double-blind, placebo-controlled study design is recommended for evaluation of new therapies. Study participants should have their progress monitored by endoscopy performed at enrollment, at completion of therapy, and 3 months thereafter. Assessment of microbiological outcome is paramount for final evaluation of the patient. 1 table. 44 references. (AA-M). •

Surprise Cause of Gastritis Revolutionizes Ulcer Treatment Source: FDA Consumer. 28(10): 15-18. December 1994. Contact: Available from U.S. Public Health Service, Department of Health and Human Services, Food and Drug Administration. (HFI-40), 5600 Fishers Lane, Rockville, MD 20857. Summary: This article provides current information about the link between Helicobacter pylori and peptic ulcer disease. Topics include the symptoms and pathology of an ulcer; antibiotic therapy that can eradicate H. pylori infection; current drug therapy used to manage ulcers; discovering the infection connection; the conclusions of the National Institutes of Health's consensus development conference on this topic; diagnostic tests used to confirm H. pylori involvement; and treatment regimens of antibiotics. One sidebar discusses the possible role of H. pylori in the etiology of gastric cancer. 2 figures.

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Detection and Analysis of Helicobacter Pylori in Dental Plaque and Stomach of Gastritis Patients by PCR and PCR-SSCP Source: Chinese Journal of Dental Research. 5(2): 5-11. June 2002. Contact: Available from Quintessence Publishing Co, Inc. 551 Kimberly Drive, Carol Stream, IL 60188-9981. (800) 621-0387 or (630) 682-3223. Fax (630) 682-3288. E-mail: [email protected]. Website: www.quintpub.com. Summary: This article reports on a study undertaken to investigate the prevalence of Helicobacter pylori bacteria in the oral cavity of gastritis patients and to analyze the genotype similarity between H. pylori in the oral cavity and in the stomach. The study included 32 patients with chronic gastritis. Twelve supra and subgingival (above and below the gum) plaque samples were collected from 6 teeth in each subjects. Twentyseven patients (84.4 percent) had at least one H. pylori-positive plaque sample. The H. pylori positive rate was significantly higher in subgingival plaque (37 percent) than in supragingival plaque (21.9 percent). The data revealed that 3 out of 4 gastritis patients had the same strains of H. pylori found orally, and there was at least one identical genotype of H. pylori carried by these patients. The authors conclude that these results support the concept that oral H. pylori infection could be an important source of gastric infection. The cluster phenomenon and oral-oral transmission of H. pylori infection also exist. 3 figures. 2 tables. 27 references.

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Helicobacter Pylori Gastritis and Gastric Physiology Source: Gastroenterology Clinics of North America. 29(3): 687-703. September 2000. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32821-9816. (800) 654-2452. Summary: This article reviews Helicobacter pylori gastritis and gastric physiology. Helicobacter pylori gastritis (stomach inflammation) can alter stomach physiology, leading to increased or decreased acid secretion, depending on the pattern of gastritis

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present. These changes in physiology are related to the disease outcome, with increased acid secretion leading to duodenal ulcer disease and reduced acid secretion being a risk factor for gastric (stomach) cancer. Gastric acid secretion also affects the pattern of gastritis induced by the infection, with low acid secretion leading a pangastritis and possibly atrophy. This two way interaction between H. pylori gastritis and gastric acid secretion is important in understanding the role of H. pylori infection in the response to proton pump inhibitor therapy. This interaction explains the more profound control of gastric acid secretion in H. pylori positive patients and why rebound acid hypersecretion is confined to H. pylori negative subjects. 6 figures. 60 references. •

Community Acquired Acute Helicobacter Pylori Gastritis (editorial) Source: Journal of Gastroenterology and Hepatology. 15(12): 1353-1355. December 2000. Contact: Available from Blackwell Science. 54 University Street, Carlton South 3053, Victoria, Australia. +61393470300. Fax +61393475001. E-mail: [email protected]. Website: www.blackwell-science.com. Summary: This editorial comments on a study (printed in the same journal issue) that examined the efficacy of a short term Helicobacter pylori eradication therapy on acute gastritis. Among the 15 patients with hemorrhage acute gastritis who were randomly allocated to group A (eradication therapy) or group B (lansoprazole), 10 of the patients started to receive treatment within 1 day after the disease onset. The other five patients began the eradication therapy 4 to 6 days after disease onset (group C). All group A patients were cured after the 1 week treatment and therefore, they became H. pylori negative. Group B and C patients had erosions or ulcers after the 1 week treatment and so received an additional 3 week administration of LPZ. The authors of the research conclude that in patients with acute gastritis, caused by an initial H. pylori infection, eradication therapy was efficacious in achieving early healing. This therapy should therefore be started as soon as possible after disease onset. The editorial cautions that other factors need to be taken into consideration. The editorial notes that it is unclear whether the symptomatic response reported in the study was related to the therapy given, the natural history of the disease or both. The editorial also reminds readers that the spectrum of the initial presentation of H. pylori infection remains unknown. Most clinicians agree that the diagnosis of H. pylori infection should prompt therapy, but diagnosis is often not confirmed by endoscopy. For clinical purposes, this is unimportant, but the editorial stresses that the research presented in the accompanying article cannot support the conclusions the researchers made, without the confirmation of diagnosis through endoscopy. 29 references.

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Secretin Test in Achlorhydria-related Hypergastrinaemia: Further Data in Type A Chronic Atrophic Gastritis and in Gastric Carcinoid. (letter) Source: European Journal of Gastroenterology and Hepatology. 3(5): 423-424. May 1991. Summary: This letter briefly reports the experience of the authors in using gastrin provocative tests (such as secretin, calcium or glucagon). The data reported documents the use of the secretin test in achlorhydria-related hypergastrinemia. Preliminary data are also reported for three patients with chronic atrophic gastritis and for two with associated gastric carcinoid. The authors conclude that the results, even if preliminary, seem to lead to new considerations about specificity and reproducibility of the secretin test. 3 figures. 8 references.

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Helicobacter Pylori and the Risk and Management of Associated Diseases: Gastritis, Ulcer Disease, Atrophic Gastritis and Gastric Cancer Source: Alimentary Pharmacology and Therapeutics. 11(Supplement 1): 71-88. April 1997. Contact: Available from Mercury Airfreight International, Ltd. 2323 EF, Randolph Avenue, Avenel, NJ 07001. E-mail: [email protected]. Summary: This review article addresses the role of Helicobacter pylori and the effect of H. pylori eradication on gastritis, peptic ulcer disease, atrophic gastritis, and gastric cancer. The author emphasizes the various factors that influence the clinical course of this infection. H. pylori induces chronic gastritis in virtually all infected subjects. This inflammation can lead to peptic ulceration and atrophic gastritis in a considerable number of infected subjects. A minority eventually develops gastric cancer. The risk of such complications depends upon the severity of gastritis, which is determined by various host-and bacteria-related factors. Among bacterial factors, most of the evidence addresses the cagA pathogenicity island, the presence of which has been associated with more severe gastritis, peptic ulceration, atrophic gastritis, and gastric cancer. Among host factors, most of the evidence focuses on acid production in response to H. pylori infection. An increase in acid secretion limits H. pylori gastritis to the antrum at the risk of duodenal ulcer disease; a reduction allows more proximal inflammation at the risk of atrophic gastritis, gastric ulcer disease, and gastric cancer. Gastritis and atrophy negatively influence acid secretion. H. pylori eradication is required in peptic ulcer disease and may be advocated in patients on profound acid suppressive therapy; it has been shown to cure gastritis and prevent ulcer recurrence. The author concludes that further study is required to determine the efficacy of H. pylori eradication in the primary and secondary prevention of atrophic gastritis and gastric cancer. 3 figures. 193 references. (AA).

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Immunologic Basis for Celiac Disease, Inflammatory Bowel Disease, and Type B Chronic Gastritis Source: Current Opinion in Gastroenterology. 7(3): 450-462. June 1991. Summary: This review does not cover the entire field of gastrointestinal immunology, but focuses on relatively recent findings of immunopathologic interest in the gastrointestinal tract. The author discusses celiac disease, including mucosal T-cell alterations, mucosal T-cell activation, humoral immunity, and pathogenic events in celiac disease; inflammatory bowel disease, including mucosal T-cell properties, mucosal macrophages and dendritic cells, features of the prominent local IgG response, and the mucosal complement activation; type B chronic gastritis; and a common mechanism for induction of mucosal immunopathology. 3 figures. 97 annotated references. (AA-M).

Federally Funded Research on Gastritis The U.S. Government supports a variety of research studies relating to gastritis. 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 2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration

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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 gastritis. 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 gastritis. The following is typical of the type of information found when searching the CRISP database for gastritis: •

Project Title: ACETONE METABOLISM IN HELICOBACTER PYLORI Principal Investigator & Institution: Hoover, Timothy R.; Microbiology; University of Georgia 617 Boyd, Gsrc Athens, Ga 306027411 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2005 Summary: (provided by applicant): Helicobacter pylori is a major human pathogen that colonizes the gastric mucosa, leading to gastric inflammation that can progress to chronic gastritis, peptic ulcer, gastric cancer or mucosal-associated lymphoma. The ability of H. pylori to establish a chronic infection in the human stomach indicates that it is well adapted to acquire the nutrients it needs for growth in this unique environment. Complete genomic sequences for two unrelated H. pylori strains, 26695 and J99, have greatly aided the understanding of the physiology of this bacterium. Both sequenced strains were reported recently to have the genes for a potential acetone carboxylase, an enzyme that initiates the metabolism of acetone by converting it to acetoacetate. Acetone is produced in the body upon the spontaneous decarboxylation of acetoacetate, one of the ketone bodies produced by the liver and used as an energy source when glucose is not readily available. Ketones are always present in the blood, with up to 185 grams of ketone bodies produced per day by the liver of a healthy adult. This proposal will test the hypothesis that H. pylori utilizes acetone as an important energy source for the bacterium in the gastric mucosa. The first specific aim of the proposal is to verify that H. pylori has a functional acetone carboxylase by expressing the protein in Escherichia coli, purifying it, and examining its ability to catalyze the carboxylation of acetone. The second specific aim is to determine if this enzyme is needed by H. pylori to establish a chronic infection in the gastric mucosa. The operon encoding the H. pylori acetone carboxylase will be disrupted and the resulting mutant strain will be examined for its ability to colonize the stomachs of mice and Mongolian gerbils. The proposed studies will expand knowledge of metabolic pathways in H. pylori, which will lead to a better understanding of how this pathogen establishes infections in humans and may provide new strategies for the prevention or treatment of H. pylori infections. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ACID INDUCIBLE RESPONSES IN H PYLORI Principal Investigator & Institution: Mcgowan, Catherine C.; Medicine; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 01-JUL-1999; Project End 30-JUN-2004

(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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Summary: (Adapted from the Applicant's Abstract): Helicobacter pylori are curved Gram-negative bacteria that are now recognized as the cause of chronic superficial gastritis in humans, and this organism plays an important etiologic role in the pathogenesis of peptic ulcer disease and distal gastric adenocarcinoma. H. pylori colonizes the mucus layer overlying the gastric epithelium, where it is exposed to a wide range of pH values. Urease activity is required for H. pylori survival at low pH, and its presence is essential for colonization. However, little else is known about the mechanisms which allow H. pylori to survive in acidic environments. In previous studies, the investigators have used the strategy of subtractive RNA hybridization to identify an acid-inducible gene in H. pylori, wbcJ, that is essential for O-antigen expression and which contributes to acid survival of the organism. The long-term goal of this study is to isolate and identify additional acid-inducible factors in H. pylori which are required for establishment and maintenance of infection. The hypothesis of this study is that H. pylori possesses a regulated, inducible acid stress response system. The specific aims are 1) to study the transcriptional regulation of the acid-inducible H. pylori gene, wbcJ and to characterize its role in LPS biosynthesis and structure, 2) to identify other H. pylori genes whose expression is increased in response to acidic pH, and 3) to isolate acid-inducible promoters in H. pylori. To accomplish the first objective, analyses will be done to characterize the promoter region and genetic organization of wbcJ and its co-transcribed genes. Transcriptional wbcJ fusions then will be constructed using xylE to examine the expression of wbcJ under different environmental conditions in vitro. The LPS structure of wbcJ mutants will be analyzed to determine the role of this gene in H. pylori LPS biosynthetic pathways. The method of subtractive RNA hybridization will be used to isolate H. pylori genes whose expression is increased during growth at acidic pH. Genes identified by this approach will be cloned and disrupted using insertional mutagenesis, which will permit the study of their role in H. pylori acid survival and colonization. As an alternate strategy to identifying acidregulated genes, we will employ the technique of differential fluorescence induction to enrich for promoters that are up-regulated following exposure to acidic pH, utilizing GFP and a fluorescence-activated cell sorter. The proposed work will further elucidate the mechanisms used by H. pylori to colonize and persist within the gastric environment and will lead to improved understanding of how H. pylori causes disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ACTIN REMODELING AND HCL SECRETION Principal Investigator & Institution: Ammar, David A.; Molecular and Cell Biology; University of California Berkeley Berkeley, Ca 94720 Timing: Fiscal Year 2001; Project Start 01-SEP-2001 Summary: Hydrochloric acid secretion by the gastric parietal cell involves major membrane rearrangements. Stimulation triggers translocation of the H+/K+-ATPase proton pump from the intracellular compartment of tubulovesicles, leading to fusion of the vesicles with the apical/canalicular membrane. While the exact pathway of activation is not known, protein kinases are believed to be involved. The overall object of this proposal is to elucidate the nature of the signaling events that occur in the early stages of parietal cell activation, and the manner in which these events effect, and are dependent upon, the actin cytoskeleton. Toward this goal, several parietal cell models will be employed that allow access to, or manipulation of, the intracellular contents of the parietal cell. The effects of certain protein kinase inhibitors actin binding substances on acid secretion and cytoskeletal rearrangement will be determined. Elucidating the control mechanisms of HC1 secretion is fundamental for treatment of medical

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conditions of the stomach. These conditions range from minor issues, such as dyspepsia and gastritis, to life-threatening conditions, such as gastric and esophageal cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ALCOHOL REDUCTION IN MEDICAL ILLNESSES:HCV AS PROTOTYPE Principal Investigator & Institution: Dawson, Neal V.; Medicine; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Alcohol use is discouraged or contraindicated for patients with a variety of medical illnesses. For many diseases directly caused by alcohol, the use of alcohol may be associated with recurrent symptoms shortly after its consumption, e.g., pancreatitis or gastritis, and the prohibition against alcohol is straightforward. However, for many chronic diseases, the use of alcohol is not associated with any short-term symptoms or sequelae. The course of these chronic diseases (or their treatments) among non-abusing/nondependent patients can be adversely affected by even moderate alcohol use, e.g., chronic hepatitis, (nonalcoholic) cirrhosis, severe diabetes, or the use of the 'blood thinner', warfarin. Chronic Hepatitis C virus (HCV) infection is a prototypical example of a disease in which alcohol use tends to cause no symptoms. Even moderate chronic alcohol use can be associated with an increased likelihood of cirrhosis and liver cancer. HCV infection rates and prognosis are related to alcohol use in multiple ways. Alcohol use during HCV treatment is associated with a decreased likelihood of viral clearance. Long-term alcohol use may increase the proliferation of HCV and the associated liver damage even with moderate alcohol consumption. Greatly reducing or eliminating alcohol use may importantly enhance the prognoses of patients, even if they are not candidates for specific HCV treatments. Despite having diagnoses that warrant abstinence from alcohol, many patients continue to drink alcohol. Little is known about why patients continue to consume alcohol in the face of diagnoses that warrant a reduction in use or abstinence. The current study is designed to determine factors that lead to continuing alcohol intake among alcohol nonabusing/nondependent patients who are advised to stop drinking by health care providers. In Phase 1, focus groups (patients and providers) will be used to discover issues that may be associated with continued drinking. In Phase 2, questionnaire items will be developed based on the data gleaned from Phase 1. The potential pool of items will be administered to 10 patients per item and factor analyzed. In Phase 3, the items retained from the pool of potential items will be used to create a questionnaire that will be tested for its ability to predict alcohol reduction or cessation. Since alcohol use is common in the U.S. and since most patients who currently have HCV are not candidates for treatment, abstinence from alcohol use represents a major opportunity to prevent a decline in the health and quality of life of patients with HCV and similar diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GENOTYPE

B12

ABSORPTION,

KINETICS

AND

TRANSCOBALAMIN

Principal Investigator & Institution: Miller, Joshua W.; Medical Pathology; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 95616 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-APR-2005 Summary: (provided by applicant): Vitamin B12 deficiency is common in older adults, as well as in children and young adults in developing countries. Potential consequences

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of B12 deficiency include megaloblastic anemia and neurological degeneration, as well as increased risk of degenerative disorders such as vascular disease, cancer, and loss of cognitive function. The primary cause of B12 deficiency is malabsorption due to pernicious anemia and atrophic gastritis. In preliminary studies, circumstantial evidence has been obtained suggesting that a common polymorphism (G775C) in the B12 transport protein, transcobalamin II, affects B12 absorption and delivery to the tissues. Consequently, this polymorphism may influence an individual's susceptibility to B 12 deficiency caused by malabsorption. The primary goal of the present study is to directly assess the influence of the G775C polymorphism on B12 absorption and the kinetics of B12 metabolism. To accomplish this goal, a major technological advance available through collaboration with the Lawrence Livermore National Laboratories, called Accelerator Mass Spectrometry (AMS), will be employed. AMS provides the capacity to detect levels of carbon-14 (14C) in biological samples at attomolar concentrations. The technology is thus uniquely suited to detect the appearance of 14C in the blood, urine, and feces after oral ingestion of even small, minimally radioactive substrates. The specific aim of this proposal is to exploit AMS to assess the absorption and metabolism of 14C-labelled B12 in healthy human subjects who differ by which polymorphic variant of transcobalamin II they possess. The results of these studies will provide important basic information about the biological handling of B12 and may ultimately provide insight into the contribution of B12 deficiency to the risk of degenerative disease. Moreover, it is anticipated that the AMS technology will provide the means to develop a sensitive and specific method for assessment of B12 absorptive capacity in humans suspected of B 12 malabsorption. This novel method would ultimately replace the Schilling test, the current gold standard, but flawed and cumbersome method for clinical assessment of B 12 absorptive capacity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BACTERIAL INDUCED COLITIS IN HLA-B27 RATS Principal Investigator & Institution: Dieleman, Levinus A.; Medicine; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2001; Project Start 10-MAY-1998; Project End 30-NOV-2002 Summary: (taken from application) Genetic and environmental factors are extremely important in the pathogenesis of the idiopathic chronic inflammatory bowel diseases (IBD), ulcerative colitis (UC) and Crohn's disease (CD). New rodent models of chronic intestinal inflammation have contributed substantially to our knowledge of the pathogenesis of IBD. One better characterized model is HLA-B27 transgenic rats, in which the overexpression of the gene for the MHC class I molecule HLA-B27 leads to the spontaneous development of colitis, gastroduodenitis, peripheral arthritis and spondylitis. Our hypothesis is that chronic colitis and gastritis is the result of an overly aggressive immune response to luminal bacteria in a genetically susceptible host. This T Iymphocyte-dominated immune response to specific luminal bacteria is regulated by antigen presenting cells (APC). This hypothesis will be evaluated in HLA-B27 transgenic rats, which develop progressive colitis, gastritis and arthritis when raised in specific pathogen-free environment or when colonized with Bacteroides vulgatus, but which have no clinical or histological disease when raised in a sterile environment or monoassociated with E. coli. However, the immunological mechanisms determining how these bacteria initiate and perpetuate a chronic immune response need to elucidated. The unraveling of these mechanisms will answer several fundamental questions concerning the pathogenesis of chronic inflammatory bowel diseases. We will address several fundamental questions of IBD pathogenesis in the following specific

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aims: 1) Determine which bacterial components induce gastrointestinal inflammation and conversely, whether certain resident luminal bacteria can prevent this inflammation. 2) Define the mechanisms by which T lymphocytes induce or prevent gastrointestinal inflammation. Successful completion of these specific aims will not only provide essential insights into the pathogenesis of experimental intestinal inflammation, but will also reveal pathogenetic mechanisms of IBD and suggest novel therapeutic approaches targeting etiologic mechanisms. This MD/PhD has considerable experience with various studies on the role of cytokines in several murine models of acute and chronic intestinal inflammation. The research project for this grant will enable the candidate to expand his knowledge in new areas of cellular immunology and gnotobiotic technology, which will be complemented by formal immunology/microbiology courses. This training experience will take place in a Digestive Disease Center focused on inflammation and fibrosis under the sponsorship of experts in animal studies, gnotobiotic research and cellular immunology. This expertise will foster the development of an independent investigator with skills in both clinical and basic science. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BETA2 INTEGRIN SIGNALING IN HUMAN NEUTROPHILS Principal Investigator & Institution: Takami, Mimi S.; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 15-MAY-1999; Project End 31-MAR-2004 Summary: A variety of gastrointestinal disorders, that include H. pylori, NSAID induced gastritis and inflammatory bowel disease, involve the recruitment of leukocytes from the circulation to the site of injury. The severity of the mucosal injury in these disease processes has been directly correlated with the extent of the neutrophil infiltration. In addition, the persistent neutrophil infiltrate which is the hallmark of chronic H. pylori infection, has been implicated as a possible mechanism facilitating malignant transformation in the gastric mucosa. Central to the modulation of adhesion and migration of leukocytes in inflammatory processes such as these, is a subfamily of cell surface receptors, the beta2 integrins. Adhesion through beta2 integrins is a complex process that involves activation of the integrin through an inside out signaling mechanism, triggered by the engagement of well characterized receptors such as the chemokine receptors, IL-8, C5a, and N-Formylmethionlleucyl- phenylalanine (FMLP), cytokine receptors, such as TNF, and activation of Protein Kinase C. Integrin activation results in enhanced binding to ligand, and subsequently, generation of an outside-in signal cascade that may lead to changes in gene expression and cytoskeletal rearrangement, enabling the leukocyte to migrate to sites of injury, and facilitating the physiologic response of the cell. Recent reports have identified Interleukin-8 as an important epithelial-derived inflammatory mediator in both IBD and H. pylori gastritis. In neutrophils, I1-8 has been shown to induce chemotaxis, respiratory burst and granule release, and to enhance cellular adhesion. However, the specific effects of IL-8 on beta2 integrin activation and ligand binding have not been closely examined. In addition, while recent reports indicate that IL-8 activates the MAPK pathway through Ras/Rafmediated events, the relationship of these events to beta2 integrin function has yet to be elucidated. Our goal, within this proposal, is to delineate the signal transduction cascades involved in beta2 integrin activation, with a particular focus on the physiologic stimulus at the chemokine receptor. In addition, we will examine post-ligand-binding events, including protein tyrosine phosphorylation and protein-protein interactions that are central to the outside-in signaling cascade initiated by engagement of beta2 integrins

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on human neutrophils. We will examine the relationship of these events to the complex shape changes involved in aggregation and transmigration. And, as a biological model, we will explore the way in which exposure to Helicobacter pylori, may impact these signals and affect neutrophil adhesion and migration on epithelial surfaces. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CHEMOPREVENTION OF GASTRIC DYSPLASIA-LONG TERM FOLLOW UP Principal Investigator & Institution: Fontham, Elizabeth Th.; Professor and Chairman; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2003; Project Start 08-JUL-2003; Project End 30-JUN-2008 Summary: (provided by applicant): While Helicobacter pylori is now established as a pivotal factor in gastric carcinogenesis, its mechanisms of action and timing in the premalignant process are the subject of research. This project builds upon a recently completed 6-year randomized chemoprevention trial in a high-risk region of Colombia. A significantly greater regression of premalignant lesions was observed in study participants who were treated and were cleared of H. pylori infection. Upon completion of the trial, participants who had not been in the anti-H. pylori treatment arm were offered standard triple therapy. Quarterly contact has been maintained with trial participants, and this project now proposes to evaluate the long-term effectiveness of anti-H. pylori treatment in an adult population in which the community prevalence of infection is greater than 90 percent. The specific aims of the study are to: 1. determine the proportion of subjects free of infection in 2002; 2. document the reinfection rates from 2002 to 2007 in subjects free of infection in 2002; 3. compare the H. pylori genotypes in persons receiving treatment and found to be free of infection during the follow-up phase with prior pre-treatment genotypes (1998); 4. determine the status of histopathologic lesions (progression; regression; no change) at the end of the follow-up phase (2006-7) in relation to their infection status over time and previous histopathology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CORE--GENETIC CHARACTERIZATION OF H PYLORIA STRAINS Principal Investigator & Institution: Schneider, Barbara A.; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2003; Project Start 08-JUL-2003; Project End 30-JUN-2008 Summary: (provided by applicant): Helicobacter pylori (H.p.) gastritis is the most common chronic infection worldwide, affecting about half the world's population. In most infected persons, the bacteria produce few ill effects, but in a minority, ulcers and gastric cancer are associated with infection. Factors affecting the severity of results of infection are poorly understood. One factor likely to be important in controlling severity of symptoms is the virulence of the strain of H.p. This core laboratory will perform genotyping of major virulence factors of H.p. strains for the other laboratories of the program project. One key virulence factor is vacA, a secreted cytotoxin, which resembles an ion channel or transport protein. When the toxin binds to gastric epithelial cells, it is taken into the cells in vacuoles (hence the name). Subsequently the cells lyse, and the cell debris contributes to inflammation. The vacA gene contains 2 portions, one coding for a signal peptide, or s portion, and one coding for the middle or m portion. Both s and m are present in multiple alleles (s1a, s1b, s1c, s2, m1, m2a, and m2b), some of which are associated with more severe pathology. In addition, some strains of H.p. produce a cagA

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protein, which is a marker for a pathogenicity island, a group of 40 genes, which encode proteins, which enhance the virulence of the strain. Another virulence determinant is babA, which encodes an adhesion, which binds the bacteria to the surface of the gastric epithelial cells. This core laboratory will genotype clinical strains of H.p. for cagA, s and m regions of vacA, and babA. The laboratory will culture and genotype clinical strains of H.p. isolated from Colombian and New Orleans patients, and will serve all projects in the application. Genotyping will be performed by the line probe assay (LiPA) and with PCR using radioactive primers. In addition, we have developed and will employ for project 3, a method for performing genotyping from stool samples, which will greatly expand our abilities to genotype strains found in asymptomatic persons. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CORE--HUMAN STUDIES Principal Investigator & Institution: Jensen, Dennis M.; Professor of Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-DEC-2000; Project End 30-NOV-2001 Summary: (Adapted from the application) The mission of the Human Studies Core is to provide shared resources, personnel, services, education, and consultation to CURE investigators, trainees, and their collaborators for the study of patients with selected digestive diseases. The primary goal of this core is to facilitate collaboration, education about, and performance of GI clinical trials, human physiological studies, and health service studies in digestive diseases. The traditional focus of the core has been the investigation of peptic diseases and upper GI physiology, including secretion, motility, and hormonal regulation. This focus has been broadened to include the study of other important gastrointestinal illnesses such as complicated ulcer disease, gastroesophageal reflux disease (GERD), Barrett's epithelium, GI hemorrhage, non-ulcer dyspepsia, Helicobacter pylori infection, pre-cancer conditions (gastritis, polyposis, and ulcerative colitis), and inflammatory bowel disease. An overriding theme of the core is the study of the physiology of visceral pain which may be associated with all of these disorders. The importance of this area in GI diseases is highlighted by the impact of GI symptoms on quality of life and demand for health care services. With this in mind, the core has greatly expanded the study of neuroenteric diseases such as irritable bowel syndrome (IBS), non-ulcer dyspepsia, and non-cardiac chest pain. The specific goals of this core are to provide CURE investigators, trainees, and their collaborators with access to: (1) a quality clinical research unit for performance of GI clinical research at a low cost, (2) utilization of fully equipped endoscopy units for GI clinical and physiologic research studies, (3) laboratory services for GI secretory tests, GI motility and pH testing, and H. pylori assessments (ELISA, C-14 breath testing, and histopathology), (4) teaching of clinical research techniques and consultation about study design, data management, statistical analysis, and routine outcomes, (5) tissue and clinical data banks of patients with selected GI diseases (the largest data bases are for GI hemorrhage and functional GI disease), (6) consultation about conducting health services research including design of studies, cost assessments, quality of life instruments, effectiveness studies, and modeling cost-effectiveness studies, (7) specialized equipment for GI studies (such as equipment for ablating Barrett's epithelium or endoscopic ultrasound instruments), (8) psychophysiology and GI motility laboratories for the study of neuroenteric diseases, and (9) utilization of a brain imaging unit for the study of neuroenteric diseases. The instruments and personnel required for these services and functions are expensive, so

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that sharing them among various investigators in a core is cost effective and promotes collaboration. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CYTOKINE IMMUNIZATION

RESPONSES

TO

H

PYLORI

INFECTION

OR

Principal Investigator & Institution: Ernst, Peter B.; Professor; Internal Medicine; University of Virginia Charlottesville Box 400195 Charlottesville, Va 22904 Timing: Fiscal Year 2001; Project Start 01-SEP-1997; Project End 31-MAY-2003 Summary: (Adapted from the applicant's abstract): H. pylori causes gastritis and can contribute to recurrent peptic ulceration. However, investigations have shown that family members can express different manifestations of gastric disease even though they are infected with genetically identical strains of H. pylori. This and other evidence suggest that virulence factors of H. pylori interact with other elements within the gastric milieu to cause the more severe sequelae observed in a subset of infected patients. The immune system is one element that can contribute to the pathogenesis and prevention of disease associated with H. pylori infection. Control of the local immune response to luminal flora depends on the balance of helper T cell subsets. Helper T cells are implicated in the pathogenesis of gastritis and peptic ulceration since, during infection, gastric T cells are markedly increased in numbers and skewed toward a Th1 phenotype and cell-mediated immune responses. Moreover, patients receiving T cell-derived cytokines as immunotherapy can develop gastric ulceration. H. pylori is relatively noninvasive so T cells enhancing cell-mediated immune responses may promote inflammation and, in susceptible individuals, contribute to epithelial damage. This leads to our hypothesis that a relative imbalance in helper T cell subsets favors the stimulation of inflammation and epithelial damage in response to persistent infection with H. pylori. More specifically, Th1 responses increase during natural infection and contribute to epithelial damage, while Th2 cells will favor tissue integrity and immunity. The following specific aims will be addressed to test the hypothesis: 1) characterize the helper T cell subsets which develop in response to H. pylori, 2) elucidate the mechanisms of epithelial damage by Th1 cells, 3) compare the differential effects of Th1 and Th2 cells on the function of gastric epithelium, and 4) characterize the expression of IL-10 receptors on gastric epithelium. In summary, this proposal addresses unanswered questions regarding the molecular basis for the gastric T cell response and defines the mechanisms by which an imbalance in helper T cells modulates inflammation and epithelial damage. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DETERMINANTS OF H PYLORI INFECTION IN THE RHESUS MONKEY Principal Investigator & Institution: Solnick, Jay V.; Associate Professor of Medicine; Internal Medicine; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 95616 Timing: Fiscal Year 2001; Project Start 01-DEC-1997; Project End 30-NOV-2002 Summary: (Adapted from the applicant's abstract): Infection with Helicobacter pylori causes a histological gastritis that in some individuals is associated with the development of peptic ulcer disease or gastric malignancy. H. pylori infection may be more common than infection with any other bacterial agent. Yet despite what must be repeated exposures, some individuals do not become infected. What accounts for the

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fact that some individuals become persistently infected while others remain uninfected, and perhaps still others have a transient infection? Presumably, bacterial as well as host variables are important. Because experimental infection of humans with H. pylori is not possible, the investigators propose to use the rhesus monkey as a model of H. pylori infection to address this question. They hypothesize that inoculation of human H. pylori in rhesus monkeys will result in diverse outcomes that will be associated with conditions of bacterial inoculation as well as host variables. A type strain of human H. pylori will be selected by in vitro characterization and in vivo passage through rhesus monkeys. The effects on infection of inoculum size, gastric acid suppression, and bacterial growth phase will be examined. Animals will be orogastrically inoculated with a standard dose of the type strain and acute and chronic infection will be studied. The outcome of infection will be determined by serial endoscopy, urea breath test, and examination of bacterial shedding in saliva and feces by culture and PCR. The host immune response will be assessed by immunophenotyping of gastric lymphocytes and peripheral blood mononuclear cells, immunohistochemistry of gastric mucosal inflammation, T cell proliferative responses from peripheral blood and gastric mucosa, and cytokine secretion by T cells. Gastric physiology will be examined by assay of serum gastrin levels and gastric basal acid output. The results will be compared in juvenile and adult animals. These studies will further understanding of the host-pathogen relationship in acute and chronic H. pylori infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DEVELOPMENT OF GASTRIC HCL SECRETION Principal Investigator & Institution: Forte, John G.; Professor of Physiology; Molecular and Cell Biology; University of California Berkeley Berkeley, Ca 94720 Timing: Fiscal Year 2001; Project Start 01-JUL-1987; Project End 31-MAR-2005 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: DIFFERENTIAL TRANSCRIPTION FACTOR ACTIVATION BY H PYLORI Principal Investigator & Institution: Smoot, Duane T.; Associate Professor of Medicine; Medicine; Howard University 2400 6Th St Nw Washington, Dc 20059 Timing: Fiscal Year 2001; Project Start 30-SEP-1997; Project End 29-SEP-2002 Summary: (taken from the application) H. pylori infection of the stomach causes chronic gastritis, and epidemiological studies have demonstrated that H. pylori is an independent risk factor for gastric cancer. However, the mechanisms by which H. pylori causes epithelial cell injury, or leads to the development of gastric cancer is not well understood. People infected with H. pylori have a 3 to 9 fold higher risk of developing gastric cancer than non-infected persons. Progression from superficial gastritis caused by H. pylori to atrophic gastritis with intestinal metaplasia is felt to be a precursor to gastric cancer development. Investigators have postulated that the natural progression of H. pylori-associated chronic gastritis is to atrophic gastritis, which may be prolonged or shortened by bacterial factors that can modulate gastric epithelial defense mechanisms. H. pylori strains that possess the cag pathogenicity island are more strongly associated with gastric cancer, than those that do not (cagA-negative strains). H. pylori has been shown to induce oxidative bursts from macrophages and there is increased iNOS and peroxynitrite in the gastric mucosa in infected persons, along with less vitamin C. We postulate that H. pylori may increase the risk of gastric cancer by

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interacting with specific transcription factors (NF-kappaB, p53) resulting in a relative resistance to apoptosis with cagA positive strains. This grant is part of an interactive R01/R29 grant proposal to elucidate interactions between H. pylori and transcription factors NF- kB and p53, in vitro and in vivo, which may impact negatively on apoptosis and lead to increased cancer risk from exposure to chemical carcinogens and reactive oxygen species. The specific aims of this proposal are: (1) to determine if the differential regulation of p53 by cagA-positive as opposed to cagA-negative strains results in arresting cells at different phases of the cell cycle; (2) To determine if activation of NF-kB by cagA-positive strains is associated with decreased apoptosis in response to H. pylori cell injury, and whether or not this involves inhibition of p53 dependent pathways of apoptosis and/or stimulation of bc1-2. Studies will also look at the potential impact of iNOS stimulation in preventing apoptosis in this setting. Our experiments will utilize human gastric epithelial cells and include primary cultures of normal human gastric epithelial cells and an SV-40 transformed non-malignant human gastric epithelial cell line. In vivo studies will be performed as part of this interactive R01/R29 proposal by Dr. Peek, who will use established animal models which can be infected with H. pylori. These studies will elucidate pathways within gastric cells which can be altered by H. pylori and show potential mechanisms by which this bacteria may increase the susceptibility of gastric epithelial cells to DNA damage from carcinogens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ETIOLOGICAL STUDIES OF GASTRIC CARCINOMA Principal Investigator & Institution: Correa, Pelayo; Boyd Professor; Pathology; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2003; Project Start 01-JUN-1981; Project End 30-JUN-2008 Summary: (provided by applicant): The goal of this Program Project has been and continues to be the multi-disciplinary study of the etiology of gastric cancer. This neoplastic disease is second only to lung cancer in incidence and mortality worldwide. In the United States gastric cancer rates have decreased considerably. There are, however, high-risk groups, especially African Americans, Amerindians, and immigrants from Asia, Northern/Eastern Europe and Latin America. It has become increasingly clear that a major etiologic factor is chronic infection with Helicobacter pylori. About one half of today.s world population is infected, especially groups of lower socioeconomic status. The International Agency for research on Cancer has classified Helicobacter infection as a class 1 carcinogen. There are great differences in the outcome of the infection. Most infections are mild and subclinical. Clinical infections may lead to duodenal ulcer accompanied by non-atrophic gastritis, which does not increase gastric cancer risk, or to multifocal atrophic gastritis, which may lead to gastric ulcer and gastric cancer. Our general hypothesis is that the immune and inflammatory responses determine the outcome of the infection. Our Program Project explores the dynamics of the response with immunologic and histopathologic techniques in adults and children (Project 1,2 and 3). Two epidemiologic projects are also proposed: 1) follow-up of the chemoprevention cohort, which explores the natural history of infection after eradication attempts (Project 1); and 2) study of the dynamics of infection and reinfection in children of a hyper-endemic area in search for answers to the critical events in initiating the possible carcinogenesis pathway, namely persistence of infection in childhood. (Project 3). COLLABORATING INSTITUTION(S): Delft laboratories, The Netherlands Emory University Medical Center Atlanta, GA University del Valle, Cali, Colombia University de Narino, Colombia University de Antioquia, Medellin, Colombia University of Texas School of Public Health, Houston TX APR NOTE: This Program

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Project Grant has addressed the etiology of gastric cancer for 20 years and is in the fifth cycle of funding. This competitive renewal application continues the unique and multidisciplinary study of gastric cancer. The general hypothesis put forward by this Program Project is that the immune and inflammatory responses determine the outcome of the Helicobacter pylori infection leading to gastric ulcer or gastric cancer. The Program includes 3 Projects and 4 Cores. It was felt at the accelerated review that the investigators had resolved all the problems identified in the last review. The Program Project has continued to build on the broad clinical, pathological, and molecular experience accumulated by the Principal Investigator and his program project staff. Two unique populations of H. pylori-infected individuals located in Colombia are being studied. In one population non-atrophic gastritis (NAG) is more common along with low gastric cancer rates and in the second population multi-focal atrophic gastritis (MAG) is more common with a much higher gastric cancer rate. A major strength of this research and the Program Project is the investigators' matchless understanding of the etiology of gastric cancer in these unique and well-characterized populations. These two populations (a major world-wide resource for studying H. pylori pathogenesis) constitute the major strength of this application along with the more than 18 years of study of this gastric cancer problem by the Principal Investigator in a program project environment. In a previous review there were problems with some of the work not being adequately described for an accurate assessment of its feasibility, but these deficiencies have been eliminated. The program is totally unique, has been highly successful in the past, and should make substantial progress in this new funding period. The recommended merit scores of all three projects was 1.4. Three of the cores, Histopathology, Administrative and Field Activites, and Genetic Characterization are rated superior, and the Administrative and Data Management Core is rated satisfactory. The Program is highly integrated and in a very special way makes the whole more valuable than the parts. This was a unanimous observation by the reviewers. The Program is recommended for 5 years of funding. Project 1, "Chemoprevention of gastric Dysplasia", is led by Elizabeth Fontham, Ph.D. The focus of this project continues to be an important population from Colombia who are at high risk for gastric cancer and who have been the focus of this program project since its inception. A unique cohort of subjects with MAG from this population were the subjects of an interventional study in the 1990's to examine the effect of beta carotene and Vitamin C and/or eradication of H. pylori on the progression of gastric precancerous histological lesions. Contact has been maintained with these subjects, around half of who are now H. pylori-negative. This project will continue to follow these subjects closely by endoscopy and clinical evaluation to determine whether the continuing natural history of progression in gastric preneoplasia is altered by the persistent eradication of H. pylori. A secondary aim will be to determine whether those subjects who become reinfected by H. pylori are infected by less virulent strains, as suggested by preliminary data. The project has many strengths, including its focus on a unique and well-defined clinically relevant population, and the expertise of the clinicians and pathologists, who have proven their ability to work cohesively under the supervision of Drs Correa and Fontham over many years. This project received an average merit rating of 1.4. Project 2. "Immune Response to H. pylori in Non-atrophic Gastritis and Multifocal Gastritis" is led by Augusto Ochoa, M.D. It has continued to improve since the first review. One major exception was the validation of using PBL responses to reflect the immune and inflammatory status of leukocytes in the gastric mucosa. This was addressed satisfactorily in the accelerated peer review. The investigators responded by stating that for the first third of the patients analyzed (numbering 20), in vitro PBL responses will be compared with in situ gastric tissue responses. If concordance is observed, the remaining patients in the study will be followed as initially proposed, with concentration of efforts on PBL analysis. If, on the

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other hand, concordance between the PBL vs. in situ tissue analysis is not observed, the investigators will be able to adjust their analysis to include both PBL's and in situ analysis of all remaining subjects. This response is entirely appropriate and alleviates the biggest uncertainty in the approach taken in Project 2 during the previous submission. The greatest strengths of this project include the unique patient resources available and the previous productivity of the investigators. The overall goal of defining differences in the host immune response between H. pylori-infected patients at risk of developing gastric cancer versus duodenal ulcers is very worthwhile, and within the capability of the investigators. The project has the potential to help dissect the relative contributions of host and bacteria to the development of gastric cancer. This project received an average merit rating of 1.4. Project 3, "Community Intervention-Follow-up of Colombian Children" is led by Karen Goodman in a consortium arrangement with The University of Texas School of Public Health. This project addresses important questions in an appropriate fashion. In the previous version of this project, a clerical effort resulting in the reviewers not seeing the final draft. This problem has been resolved with many of the perceived scientific problems also being clarified. The 3-drug therapy chosen was identified by the reviewers as "a peculiar combination". In the most recent submission, Metronidazole has been added to create a 4-drug therapy. This regimen is consistent with contemporary medical practices. This project received a merit rating of 1.4 Core A, Histopathology, is led by the Principal Investigator, Dr. Pelayo Correa. This laboratory will perform all the histological and histochemical processing and evaluation of the numerous biopsies taken from each of the projects. It is a critically important core for this program project. It will be essential for all three projects, especially Project 1. This laboratory has proven over many years that it is ideally equipped for these purposes, and Dr Correa, the Core director, has an unequalled expertise in the interpretation of gastric pathology. This is a superior core. Core B, "Genetic Characterization of H. pylori Strains" led by Barbara Schneider, Ph.D., provides resources for genotypic characterization of three putative virulence genes in H. pylori strains. The LiPA assay for this purpose is well validated and supported by the experience of its inventor, Dr. van Doorn, who will serve as a consultant. The highthroughput advantages of the LiPA assay will be exploited in Projects 1 and 2. It is not clear whether babA typing will also be done by LiPA or by other, independent PCR's. In addition development of non-invasive genotyping methods using fecal samples is proposed. This core received a superior rating. Core C, "Administrative and Data Management (New Orleans)" is led by Dr. Pelayo Correa, M.D. who is also the Principal Investigator of this grant application. This administrative effort has been quite successful in the past and is very well organized and efficient. This Core had the deficiency during the last review of an underpowered statistical analysis effort. Dr. Correa has addressed this deficiency, and both Ms. Du and Ms. Camargo have been assigned to work under Dr. Mera. The question during the last review was regarding the amount of time Dr. Mera could devote to this Program Project. His credentials are perfectly matched for this Program Project, but his time available was considered inadequate because of the large amount of statistical analysis needed by this Program Project. To satisfy this criticism, two new faculty were recruited the biostatistics area. One of these individuals, Dr. Velasco, is Spanish speaking and could help the program project and reports to Dr. Fontham, the Project Leader of Project 1. Most importantly, the new head of the Cancer Center Statistical Department (just hired the week of the current review at the full professor level) will give 15 percent of his time to this Program. This individual is highly qualified and very experienced with the types of statistical problems that will occur in these studies. Thus, the program project statistical effort is going to be run 25 percent time by Dr. Mera and 15% by the new senior faculty member with 2 capable support people at LSU. This is a strong addition to the Core and

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resolves the major statistical problem from the last review. This core received a satisfactory rating. Core D, "Administrative and Field Activities (Colombia)" is led by Luis Eduardo Bravo, M.D. As was stated previously this is an outstanding core. The cost effectiveness of this effort is remarkable. Past history of this effort and the intact staff from the previous funding period make this core effort convincing and very workable. Some of the details missing about data flow and quality assurance from the previous review were not entirely provided in this new submission, but the effort is still superior, as the overall coordination between the various units in Colombia and between Colombia and the US look strong. This core received a superior rating. Commentary related to Progress in the current funding period, Integrated Effort, Principal Investigator, Support to be negotiated for replacement and Human Subjects are unchanged from the previous review. REVISION NOTE: Modified to include review panel roster. INDIVIDUAL PROJECTS AND CORES PROJECT 1: Chemoprevention of Gastric Dysplasia: Long-term follow-up of a cohort treatment for H. pylori infection (Elizabeth T.H. Fontham, Dr. Ph.H., 15 percent effort) Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EVALUATION OF BOTANICALS FOR H.PYLORI INFECTIONS Principal Investigator & Institution: Mahady, Gail B.; Assistant Professor; Prog/Collab Res/Pharmactl Scis; University of Illinois at Chicago 1737 West Polk Street Chicago, Il 60612 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-DEC-2002 Summary: (Applicant's Abstract): After more than a decade of research and controversy, it has been conclusively demonstrated that Helicobacter pylori is the main cause of peptic ulcer disease. High infection rates around the world pose serious health and economic problems. In the U. S. alone, 500,000 new cases, and 4 million recurrences are reported annually, at a cost of $3 to $4 billion dollars. Current therapies for H. pylori infections consist of combinations of antibiotics, and H2 blockers. However, due to the serious adverse reactions, patient compliance is low, leading to the development of antibiotic resistance. Thus, new approaches to the treatment H. pylori infections are urgently needed. For thousand of years traditional systems of medicine have successfully used botanicals (plant-based medicines) for the treatment of dyspepsia, gastritis and peptic ulcers. However, most of these botanicals have not been systematically screened for anti-H. pylori activity. This proposal describes an international, multidisciplinary approach to investigating botanical extracts for the treatment and prevention of H. pylori infections. The work is designed to generate sufficient preliminary data to serve as the basis of more definitive studies. The major goal of the project is to identify and standardize botanical extracts and combinations of extracts for the treatment of H. pylori infections. To accomplish this goal, the project involves (1) selection and procurement of botanicals to be tested (2) extraction of the source materials, (3) short-term in vitro and fn vivo testing biological studies to determine activity and mechanistic information (4) in vivo evaluations to establish safety and efficacy, and (5) determination of the major chemical constituents for standardization of the active extracts. Over the two-year period, approximately 60 new botanicals will be selected and evaluated for antibacterial activity against H. pylori. The list of high priority botanicals for testing will be generated based on data analysis from the Napralertsm database, Medline, German Commission E Monographs and other data sources. The success of this method for plant selection is seen in our preliminary results where an initial testing of 25 identified botanicals led to 13 active extracts. In this project, the botanicals will be procured and extracts prepared. The botanical extracts will be

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subjected to in vitro bioassay protocols using 15 H. pylori strains. Active extracts will be utilized for in vivo studies. The long-term objectives are to develop safe and effective botanical extracts for the treatment and prevention of H. pylori infections. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EXPERIMENTAL NEUROPATHY (AM

MODELS

OF

ACUTE

MOTOR

AXONAL

Principal Investigator & Institution: Sheikh, Kazim A.; Assistant Professor; None; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 03-JUL-2002; Project End 30-JUN-2006 Summary: (provided by applicant): Guillain-Barre syndrome (GBS), an autoimmune post-infectious neuropathy, is the most frequent cause of acute flaccid paralysis since the eradication of polio. It is now widely accepted that there are two major forms of the disease, acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Molecular mimicry has been proposed as a pathogenic mechanism for AMAN because it mostly follows Campylobacter jejuni infection, the LPS of AMAN associated C. jejuni contain ganglioside-like moieties, patients with AMAN have specific IgG anti-ganglioside antibodies including those against GD1a, and pathological studies demonstrate deposition of IgG and complement on motor axons and specific motor fiber injury. However, a direct relationship between anti-ganglioside antibodies and nerve fiber injury has not been established. Further, in vitro or animal models of antibody mediated motor axonal injury are not available. This largely reflects difficulties in generating high affinity IgG complement fixing antiganglioside antibodies similar to those seen in AMAN. We propose to use mice lacking complex gangliosides, which are immune naive to complex gangliosides, to generate the desired monoclonal (mAb) anti-ganglioside antibodies. These mAbs will be used to reproduce motor axonal injury in passive transfer animal models and in an in vitro spinal cord culture system. mAbs will also be used for localization and biochemical studies to probe the basis of the preferential motor axonal damage seen in AMAN. The ganglioside nature of antigens targeted by anti-ganglioside antibodies will be established by genetic and or pharmacologic manipulation of ganglioside expression in in vitro and animal models. An in vitro system will also be used to investigate the components of complement cascade involved in antibody-mediated axonal degeneration. Finally, affinity purified anti-ganglioside antibodies from patients with AMAN will be used in parallel to establish the causal relationship between the human antibodies and motor axonal degeneration. These studies will prove the hypothesis of molecular mimicry as an underlying mechanism for the pathogenesis of AMAN. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GDNF IN THE ENTERIC NERVOUS SYSTEM Principal Investigator & Institution: Xia, Yun; Anesthesiology; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 30-JUN-2008 Summary: (provided by applicant): This is a proposal for a KO8 Mentored Clinical Scientist Development Award for a physician scientist who holds an M.D. and Ph.D. in Physiology. The applicant aims to acquire the skills and conceptual knowledge necessary for conducting research on the nervous system of the digestive tract. This requires advanced training in electrophysiological methods, fluorescent immunohistochemistry and molecular biology to be obtained during the 5-year tenure

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of the Award. A lifelong career as a clinician scientist in an academic medical center is the applicant's goal. The proposed research is in the new and rapidly developing field of neurogastroenterology. The focus in this proposal on the enteric nervous system as a "brain-in-the-gut" addresses an important aspect of neurogastroenterology that is related to functional gastrointestinal disorders. Functional gastrointestinal disorders are believed to reflect neuropathic changes in the enteric nervous system that may be manifest as the irritable bowel syndrome (IBS), nonulcer dyspepsia or non-cardiac chest pain. The research is directed to understanding the role of glial derived neurotropic factor (GDNF) in the enteric nervous system. GDNF came to scientific and clinical life as a promising treatment to reverse neuronal degenerative changes in the brain that lead to Parkinson's disease. GDNF is a protective factor for neurons in the brain and peripheral nervous system. Mutations in the GDNF gene leads to Hirschsprung's disease in animals and humans. Parkinsonian patients in recombinant GDNF therapy trials experienced IBS-like diarrhea and cramping abdominal pain. Human trials showed evidence of a prokinetic action on gastrointestinal transit. The general scientific aim of the proposed work is to understand how GDNF works in the "brain-in-the-gut" to alter motility and secretory functions. The investigative work is based on results of pilot/feasibility studies that show significant actions of applied GDNF on both neuronal excitability and neurotransmission. Experimental protocols are designed to: 1) determine the action of GDNF on electrical and synaptic behavior of neurons in the enteric nervous system; 2) identify the morphological types of enteric neurons on which GDNF acts; 3) determine the localization and distribution of GDNF receptors in the enteric nervous system; 4) identify subtype/s of GDNF receptors that mediate its action on enteric neurons; 5) investigate factors that influence gene expression for the GDNF receptors in enteric neurons. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENE TRANSFECTION ENDOTHELIAL CELL FUNCTION

TO

ENHANCE

DENDRITIC

AND

Principal Investigator & Institution: Lotze, Michael T.; Professor/ Chief; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2001 Summary: We have evaluated the systemic administration of Interleukin-4 (IL-4) alone and then in combination with IL-2 to patients with cancer. Responses were only observed in patients treated with both cytokines and included patients with melanoma and renal cell cancer as well as in a single patient with breast carcinoma. Synergistic toxicity was also observed, primarily that ascribed to a vascular leak syndrome but also including a major sensation of nasal congestion and gastritis and frank gastric ulceration on occasion. Evaluation of rejecting allografts and sites of tumor associated with an immune response consistently have demonstrated the presence of IL-4 message or protein, making it perhaps the most frequent cytokine observed at such sites. The local production of IL-4 at the site of tumor vaccine has in five separate murine studies been associated with the induction of protective immunity and regression of the transfected tumor as well as, in some studies, established metastic cancer. IL-4 is a pleiotropic cytokine that activates vascular endothelial cells, monocytes, dendritic cells and lymphocytes. It induces the local endothelium to express the vascular cell adhesion molecule, VCAM. This facilitates trafficking of macrophages, eosinophils and lymphocytes to sites of inflammation. GM-CSF and IL-4 are potent costimulators of murine and human dendritic cell proliferation, enhancing effective tumor derived peptide vaccination in vivo and in vitro respectively. IL-4 promotes T-cell growth

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following appropriate activation by mitogen or antigen and synergizes with IL-2 in the growth of tumor infiltrating lymphocytes. Although it decreases the production of proinflammatory cytokines by macrophages, it enhances antigen presentation. We have begun a clinical gene therapy protocol and enlisted 15 patients to date. The specific aims of this project are to: 1: Evaluate the effects of IL-4 gene therapy on dendritic cell activation and stimulation of T-helper cells. Patients with cancer will be assessed for evidence of systemic immune response at draining lymph node and distant sites following local delivery of IL-4; 2: Determine the immunologic effects and therapeutic efficacy of systemic cytokine (IL-2, IL-10 or IL- 12) delivered in conjunction with this tumor vaccine, first in murine models and then in patients with cancer. Engineered fibroblasts will be tested for their ability to enhance an immune response in combination with systemic cytokine administration and 3: Determine the most effective combination of IL-4 gene therapy with other expressed gene products as components of a tumor vaccine. The use of IL-4 in combination with IL-1, GM-CSF, hepatocyte growth factor and the herpes thymidine kinase gene will be tested in murine models. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETIC AND CELLULAR BASIS OF H. PYLORI PATHOGENESIS Principal Investigator & Institution: Tompkins, Lucy S.; Professor; Microbiology and Immunology; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 01-MAY-1996; Project End 28-FEB-2006 Summary: (Adapted from the Applicant's Abstract): The goal of the proposed research is to understand better the interaction between H. pylori and its human host. H. pylori is the causative agent of gastritis and ulcer disease, and infection is an important risk factor for the development of gastric cancer. In previous studies, these investigators have shown that H. pylori CagA is transported into the host cell, and is then phosphorylated on tyrosine residues by host cell kinase activity. The insertion of CagA into host cells and its subsequent phosphorylation is associated with reorganization of the host cell cytoskeleton, as well as a dramatic change in host cell morphology. The investigators propose to examine the insertion of CagA into host cells and the sequence of events following CagA insertion. In addition, they propose to alter the structure of CagA by mutagenesis to determine the role of specific protein domains in bringing about cellular changes. In a second phase of work, these investigators have obtained DNA arrays of the H. pylori genome and host gene arrays of both human and mouse genes. They propose to use the H. pylori DNA array to examine the genotype of clinical isolates from well-defined epidemiological studies to determine whether particular genes or groups of genes are associated with discrete clinical syndromes like ulcer disease or malignancy. The major thrust of the proposed work will focus on the use of DNA arrays to follow gene transcription of both bacterial and host genes during infection of polarized cultures of human epithelial cells. They hypothesize that this will permit the identification of new classes of virulence genes. The sequence of the host response as measured by gene transcription is suggested to permit better understanding of the host cell pathways that are exploited by the bacteria during infection. Finally, a method called microarray transposon tagged H. pylori (MATT) will be used, which permits the identification of specific classes of mutation from selective environments, including infected cell cultures and animals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GNOTOBIOTIC TRANSGENIC MODELS OF THE GASTRIC ECOSYSTEM Principal Investigator & Institution: Gordon, Jeffrey I.; Professor and Head; Molecular Biol & Pharmacology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-DEC-2005 Summary: (Adapted from the Applicant's Abstract): This proposal examines 2 questions. (1) What are the molecular features of gastric epithelial lineage progenitors and how are they affected by parietal cell loss? (2) What role does attachment of Helicobacter pylori to these progenitors play in defining the outcome of H. pylori infection? These investigators have developed a transgenic mouse (toxl 76) where ablation of parietal cells leads to progressive amplification of these progenitors. The progenitors produce NeuAcalpha2,3Galbeta 1,4-glycans that serve as receptors for H. pylori adhesins in vivo. These glycans are also found in human gastric Ca and its precursors. The results suggest that when the relationship between host and H. pylori results in loss of parietal cells, as in chronic atrophic gastritis (CAG), H. pylori tropism to lineage progenitors may occur if there is a matching of H. pylori adhesin and host receptor production. Binding to amplified progenitor cells may then help facilitate initiation and/or progression of tumorigenesis. The investigators will explore this hypothesis using gnotobiotic toxl 76 mice and test its clinical relevance using materials from a completed Swedish case control study of H. pylori-infected patients with Ca + CAG. There are 3 related aims: 1). Obtain a molecular signature of lineage progenitors and of parietal cells. Identify parietal cell factors that affect the progenitors. Lectin panning will be used to recover these cells. Cellular RNA will be probed with Affymetrix GeneChips to identify (i) a panel of molecular markers of these cell types; and (ii) genes expressed in parietal cells that may affect the proliferative status/census of progenitors. The effects of candidates selected from (ii) will be tested directly by gene knockout. 2). Determine the molecular responses of the host when H. pylori interacts with NeuAc-alpha2,3Gal-beta1,4+ progenitors. Germ-free normal and toxl76 mice will be colonized with an H. pylori isolate that produces adhesins that bind to NeuAcalpha2,3Gal-beta1,4+ progenitors. GeneChips will be used to profile host gene expression before and after colonization. The role of mucosal immune cells in the host response will be examined by gene expression profiling of gnotobiotic Ragl-/normal + toxl76 mice. The impact of manipulating expression of the adhesin responsible for progenitor cell attachment will be tested. 3). H. pylori isolates from the case control study will be used to characterize H. pylori genes that affect host responses. Isolates will be tested for their binding to NeuAc-alpha2,3Gal-beta 1,4 glycans. Whole genome genotyping of binding isolates from cases with Ca + CAG, and from controls + CAG will be performed using DNA arrays containing 1661 amplified OREs from the sequenced H. pylori 26695 and J99 strains. Isolates with representative genotypes associated with CAG and Ca will be selected from the panel (or genetically engineered), introduced into toxl76 mice, and host responses defined. These studies should yield new insights about H. pylori pathogenesis plus markers for identifying patients at risk for severe pathology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: H PYLORI INDUCED OXIDATIVE DNA DAMAGE Principal Investigator & Institution: Groopman, John D.; Associate Director of Cancer Prevention; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 13-JUL-2001; Project End 30-APR-2006

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Summary: The discovery of Helicobacter pylori (H. pylori) infection has greatly changed our understanding of upper G.I. tract, diseases, including peptic ulcer disease and stomach cancer. Antibiotics are first-line treatment for ulcer patients which are infected with this bacterium. Also, the World Health Organization has classified H. pylori as a group I or definite carcinogen. People infected with H. pylori have a 3 to 6 fold higher risk of developing gastric cancer than non-infected persons. Progression from superficial gastritis caused by H. pylori to atrophic gastritis with intestinal metaplasia is felt to be a precursor to gastric cancer development. Investigators have postulated that the natural progression of H. pylori-associated chronic gastritis is to atrophic gastritis, which may be prolonged or shortened by dietary factors. A diet rich in fruits and vegetables and low in starch and salt is associated with a decreased risk of developing gastric cancer. The presence of antioxidants in this diet has been postulate to be responsible for the decrease in cancer risk. We postulate that H. pylori increases the susceptibility of gastric cells to injury from reactive oxygen species, in part by generating the production of intracellular reactive oxygen species. The specific aims of this grant are to (1) determine the ability of H. pylori exposure (live bacteria vs. bacterial proteins) to induce related DNA damage in gastric epithelial cell lines; and elucidate the spectrum and repair course of oxidant related DNA adducts formed after exposure to H. pylori. (2) identify the types of reactive oxygen species that are generated by exposure to H. pylori (live bacteria vs. bacterial proteins) using fluorescent microscopy, fluorometer and lucigeninand luminol-derived chemiluminescence, and determine whether or not cytochrome p450s and/or mitochondria are important in the generation of reactive oxygen species after exposure to H. pylori. (3) Further evaluate the role of glutathione peroxidase and catalase in the detoxification of intracellular reactive oxygen species, and their association with oxidant induced DNA adducts and cell injury. These studies will demonstrate the potential significant role for bacteria in stimulating oxidative cell injury and DNA damage which may increase the susceptibility of lining epithelial cells to carcinogenic conversion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: H. PYLORI INFECTION AND GI DISEASE IN ALASKA NATIVES Principal Investigator & Institution: Berg, Douglas E.; Professor; Molecular Microbiology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 29-SEP-2004 Summary: (Adapted from the Applicant's Abstract): Helicobacter pylori (Hp), one of the most genetically diverse of bacterial species, chronically infects the gastric mucosa of more than half of all persons world wide. It is the major cause of severe gastritis and peptic ulcers, and a risk factor for gastric cancer, although most infections are asymptomatic. Infection is more common in Alaska Natives than in mainstream US populations, and the spectrum of associated diseases is distinct. Most striking is an Hpassociated hemorrhagic gastritis and iron deficiency anemia that is common only in Alaska Natives. Here the investigators propose to study the genetics of Hp from Alaska natives. First, they will seek to define the population genetic structure of Hp in Alaska Natives. In these experiments they will (a) test the view that the Alaska Native Hp gene pool is far less diverse than that in other human populations, (b) learn whether Hp from some regions or linguistic/ethnic groups of Alaska Natives differs significantly from that in others, and (c) test the idea that Hp lineages in this population are far more nearly clonal (less scrambled by recombination) than has been seen in other human populations. They propose that recombination is important, assuming that Hp colonization of individual hosts is often associated with considerable adaptation on the

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part of the bacterium to that given person, and that the formation of recombinants during even transiently mixed infection can markedly speed this process. These tests will entail arbitrarily primed PCR (RAPD) typing of several hundred Hp isolates from Alaska Natives, and then multilocus DNA sequence typing (MLST) of informative gene loci from many representative strains. The data will also help assess whether much or any significant portion of the Hp gene pool of Alaska Natives is of Asian origin, as defined by studies of Hp isolates from Eastern China and Japan, and as might be expected if the ancestors of current Alaska Natives carried Hp with them when they migrated from Asia many millennia ago. Second, they will search for previously unknown genes affecting Hp virulence, with special interest in genes affecting the risk of hemorrhagic gastritis or iron deficiency anemia. This will be based on new subtractive hybridization and DNA microarray-based comparative genomic methods. Third, they will search for genes or alleles of divergent gene families that may contribute to the growth of individual strains in particular human hosts. This will entail analyses of recombinant derivatives of individual strains that emerge in Alaska Native populations, often, they postulate, as the result of selection for a gene or allele that may have been transferred from an unrelated Hp strain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: H.PYLORI ARGINASE MODULATION OF ULCERS AND CANCER Principal Investigator & Institution: Mcgee, David J.; Assistant Professor; Microbiology and Immunology; University of South Alabama Mobile, Al 366880002 Timing: Fiscal Year 2003; Project Start 18-JUL-2003; Project End 30-JUN-2008 Summary: (provided by applicant): Helicobacter pylori infects approximately 50% of the human population, causing severe gastric diseases including gastritis, peptic ulcers, and gastric cancer. H. pylori exerts an enormous amount of cellular energy on nitrogen metabolism including the urease enzyme. Therefore, the critical role of urease in virulence has been a major research focus. However, H. pylori has a substantial number of other nitrogen metabolizing proteins, whose role in virulence and maintaining nitrogen balance are poorly understood. Here, the focus is arginase, an enzyme metabolically upstream of urease that converts arginine to urea and ornithine. Polyamines (produced from ornithine) and arginase are elevated in the gastric mucosa of gastric cancer patients. Preliminary data demonstrate arginase is critical for H. pylori survival from acid and nitric oxide (NO), two innate host defenses. Furthermore, gerbils infected with wild type H. pylori develop gastritis and ulcers, whereas no pathologies are observed in gerbils infected with the isogenic arginase mutant. The central hypothesis of this proposal is that H. pylori arginase inhibits host NO, elevates polyamines, and contributes to gastritis, ulcers and cancer. To test this hypothesis, there are two specific aims: 1) Determine roles of H. pylori arginase in virulence in tissue culture models and 2) Determine the roles of H. pylori arginase in virulence using gerbils. In aim 1, levels of arginase needed to inhibit macrophage NO and elevate polyamines will be assessed. Arginase-dependent cytokine profiles will be identified. In aim 2 the role of arginase in virulence in the gerbil model will be assessed by determining whether arginase contributes to gastric cancer or ulcer development, induces an immune response, affects host NO, arginase or polyamine levels, and protects gerbils from H. pylori challenge. The proposed experiments will significantly enhance our understanding of the roles of H. pylori arginase in protection from innate defenses as well as roles in ulcer and cancer development and optimization of nitrogen levels in vivo. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: H.PYLORI GASTRIC PROLIFERATION & INFLAMMATORY CYTOKINES Principal Investigator & Institution: Peterson, Richard A.; Veterinary Biosciences; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2001; Project Start 01-MAR-2001 Summary: The central hypothesis of this research is i) that gastric epithelial hyperplasia Helicobacter pylori infected mice is due to an imbalance, and ii) that this imbalance is mediated by pro-inflammatory cytokines (ie. IFN-gamma, IL-1 and TNF-alpha). This hypothesis is based upon four observations. First, both apoptosis and proliferation are increased in H. pylori-infected mice is dependent on an intact T-cell immune response. Finally, in-vitro data support the proposed relationship between apoptosis, hyperplasia and inflammatory cytokines. Preliminary data have shown that IFN-gamma increases apoptosis in cultured gastric epithelial cells, but conditioned media (which contain IFNgamma) induce proliferation. Taken together, these data suggests that pre-neoplastic proliferation due to H. pylori is host-mediated, and that both proliferative and apoptotic mechanisms contribute. The initial aim of the study is to confirm the presence and relative quantity of IFN-gamma, IL-1, and TNF-alpha mRNA and protein in gastric tissue and conditioned media from gastric LPL of infected mice. Aim 2 will evaluate the functional effect of these cytokines on gastric epithelial cell culture and will address the presence and up/down regulation of cytokine receptor mRNA and protein in the cells. Aim 3 will address apoptosis in chronic H. pylori infection focusing on the Fas and TRAIL mechanisms. Compensatory hyperplasia secondary to the apoptosis will be evaluated. The final aim will be to evaluate the role of gastric somal and epithelial cells in gastric proliferation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: HB-EGF'S ROLE IN ATROPHIC GASTRITIS AND GASTRIC CANCER Principal Investigator & Institution: Koh, Theodore J.; Medicine; Univ of Massachusetts Med Sch Worcester Office of Research Funding Worcester, Ma 01655 Timing: Fiscal Year 2001; Project Start 15-FEB-2001; Project End 30-NOV-2002 Summary: We have found that gastrin is important in the growth of the colon, with gastrin deficiency resulting in decreased colonic proliferation, and over- expression of glycine-extended gastrin resulting in increased colonic proliferation and colonic mucosal hypertrophy. We have further demonstrated that gastrin appears to be a downstream target of the beta- catenin/Tcf-4 signaling pathway that mediates growth of intestinal polyps. Gastrin is also important in the development of the stomach. Gastrin deficiency results in a marked decreased in parietal cell number which can be rescued by short-term infusions of gastrin. With long term infusion however, parietal cell atrophy occurs. We have shown that transgenic mice that overexpress amidated gastrin also have initial hyperplasia, followed by parietal cell atrophy, foveolar hyperplasia, and eventually invasive gastric cancer. At the time when parietal cell atrophy develops, there is an up-regulation of heparin binding epidermal-like growth factor (HB-EGF). We have shown that gastrin can directly up- regulate HB-EGF expression through a PKC-dependent pathway. From these findings we hypothesize that gastrin can directly influence the gastric stem cell to differentiate towards the parietal cell partway, but with time it causes up-regulation of HB-EGF in parietal cells which in a negative feedback loop inhibits differentiation towards parietal cells and promotes differentiation into pit cells. The aims are to test this hypothesis: 1. Determine

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the cis-acting regulatory elements involved in gastrin's regulation of the HB-EGF promoter. 2. Determine the role of HB-EGF expression in gastric parietal cells on gastric mucosal differentiation by creating transgenic mice that over-expression HB-EGF in parietal cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HEAT PATHOGENESIS

SHOCK

PROTEINS

AND

HELICOBACTER

PYLORI

Principal Investigator & Institution: Kurt-Jones, Evelyn A.; Associate Professor; Medicine; Univ of Massachusetts Med Sch Worcester Office of Research Funding Worcester, Ma 01655 Timing: Fiscal Year 2002; Project Start 15-MAY-2002; Project End 30-APR-2007 Summary: (provided by applicant): Helicobacter pylori infection causes gastritis, peptic ulcer disease, gastric atrophy and gastric cancer. The World Health Organization has classified H. pylori as a Class I carcinogen. In animal models, the progression of H. pylori disease from superficial gastritis to gastric cancer is related to the severity of the host inflammatory response. The identification of H. pylori components and host factors that contribute to the inflammatory response may lead to important insights into the mechanism of peptic ulcer disease and/or gastric malignancy. Heat shock proteins are potent activators of inflammatory cytokine production. Heat shock proteins produced by bacteria and endogenous heat shock proteins produced by damaged tissue cell accumulate in foci of infection and inflammation. Our recent data indicate that Toll-like receptors and CD14 are important in the innate immune response to bacterial heat shock proteins. In this proposal we will investigate the role of Toll-like receptors in the recognition of bacterial heat shock proteins and in the control of bacterial infection and inflammation. Specifically, we will use in vitro and in vivo approaches to investigate the role of heat shock proteins in H. pylori infection and pathogenesis and development of tumors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HELICOBACTER HOST INTERACTIONS IN ANIMAL MODELS Principal Investigator & Institution: Falkow, Stanley; Professor; Microbiology and Immunology; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2005 Summary: (provided by applicant): Helicobacter pylori infection is causally associated with gastritis and peptic ulcer, as well as two gastric malignancies, gastric carcinoma and B-cell-mucosa-associated lymphoid tissue (MALT) lymphoma. Our proposed research focuses on the application of genetic and molecular tools to manipulate the H. pylori chromosome and the use of DNA microarray technology to monitor both the host and the pathogen in H. pylori animal models of infection and disease. Specifically, we propose to examine the H. pylori infection of mice and Mongolian gerbil. While none of the cell culture models or the animal models we propose to use can fully reflect what is seen in humans, the mouse model of infection can be used to productively investigate how H. pylori colonizes the stomach. We wish to follow long-term infection of the mouse and the host cell response to long-term H. pylori carriage measured by transcriptional profile changes as compared to uninfected littermates. Also, the mouse infection model is useful to study one form of malignancy caused by H. pylori, MALT lymphoma, and we propose to study this feature of long-term H. pylori murine infection by both bacterial transcription profiling and by the use of a mouse DNA

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microarray to follow the host response and changes that occur in the malignant transformation. We also propose to identify bacterial genes essential for gastric colonization and persistence in the stomach using a method developed in our laboratory called MicroArray Transposon Tagging (MATT) strategy. H. pylori infection reflects a particularly intriguing example of a host-pathogen interaction. The microbe serves as a tool to understand host cell biology and malignancy. The response of the bacterium to the host cell environment allows us to understand the essence of bacterial pathogenicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HELICOBACTER PYLORI AND GASTROINTESTINAL BIOLOGY Principal Investigator & Institution: Peek, Richard M.; Associate Professor; Medicine; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 30-JUN-2006 Summary: (provided by applicant): Persistent H. pylori infection is a risk factor for atrophic gastritis and distal gastric adenocarcinoma; however, only a small percentage of colonized persons develop neoplasia. Enhanced cancer risk may be related to differences in expression of specific bacterial products, to differences in host response to the bacteria, or to the specific interactions between host and microbe. H. pylori strains that possess the cag pathogenicity island induce more severe gastritis and are associated with an additional risk for developing atrophy and gastric cancer. A specific mechanism by which cagA+ strains may lower the threshold for carcinogenesis is by altering epithelial cell proliferation and apoptosis, processes that can be regulated by host inflammatory mediators such as prostaglandin products of cyclooxygenase-2 (COX-2). Over-expression of COX-2 in vitro inhibits apoptosis, and COX-2 is up-regulated within H. pylori-induced gastritis, atrophic gastritis, and gastric adenocarcinoma specimens. In vitro, H. pylori cagA+ strains stimulate COX-2 expression in gastric epithelial cells. Since we and others have shown that cagA+ strains are associated with increased gastric epithelial cell proliferation but attenuated apoptosis in vivo, induction of COX-2 by strain-specific microbial factors may represent a specific mechanism by which certain H. pylori strains heighten the risk for gastric adenocarcinoma. The long-term objective of this proposal is to examine the molecular mechanisms by which H. pylori strains selectively affect COX-2 regulated epithelial cellular turnover in vitro and in vivo. To address this, we will first determine whether H. pylori or secreted bacterial products alter COX-2-dependent apoptosis in a novel in vitro model of bacterial:gastric epithelial cell interaction (conditionally immortalized gastric epithelial cells). COX-2 expression will also be examined in myofibroblasts co-cultured with H. pylori and epithelial cells to more closely approximate events occurring within native gastric mucosa. Second, we will determine whether H. pylori infection affects COX-2-dependent cellular turnover in wild-type and COX-2 deficient mice. Third, we will investigate the role of specific H. pylori determinants on COX-2-regulated cellular responses by inactivating strainspecific genes identified by H. pylori whole genome microarray. H. pylori parental and isogenic mutant strains will then be co-incubated with conditionally immortalized cells and infected into mice. The effects of strain-specific bacterial factors and COX-2 generated products also will be investigated in a murine model of gastric carcinogenesis, INS-GAS hypergastrinemic mice. Systematic studies of each of these variables in vitro and in animal systems that reflect H. pylori pathogenesis in humans should help elucidate their relative importance, direct the course of future intervention and prevention strategies, and potentially provide a model of carcinogenesis arising within the context of chronic mucosal inflammation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: IDENTIFICATION OF HELICOBACTER PYLORI VIRULENCE GENES Principal Investigator & Institution: Holland, Michael J.; Professor; Biological Chemistry; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 95616 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2005 Summary: (Adapted from the Applicant's Abstract): H. pylori chronically infects gastric mucosa and is implicated in the pathogenesis of human gastritis, peptic ulcer disease, and gastric cancer. This proposal outlines a functional genomics-based approach designed to identify and characterize H. pylori virulence genes associated with human gastric disease. The proposed experiments will provide a functional map of the H. pylori genome which complements the complete sequences of two fully sequenced H. pylori genomes. A method termed "kinetically monitored reverse transcriptase-initiated PCR"; (kRT-PCR) forms the basis for the experimental plan. This method was developed in the laboratory of the principal investigator, and permits high throughput transcript quantitation. Genome-wide transcript profiling is proposed for H. pylori in certain benchmark states. The effects of growth phase, pH shift, iron, and human epithelial cells on H. pylori gene expression will be analyzed. These growth conditions, as well as knockout mutations within the cag pathogenicity island and within specific transcription factor genes, will be tested for their effects on the H. pylori transcriptome. Candidate virulence genes identified from the genome sequence include those involved in molecular mimicry, LPS biosynthesis, outer membrane proteins, candidate "phase variation" genes, and several hundred H. pylori-specific genes identified by comparisons of H. pylori genome sequences with those of other pathogenic and nonpathogenic bacteria. The H. pylori transcriptome will be organized into operons. Operon structures and coordinate expression profiles should reveal potential functions for unknown ORFs. Gene expression profiles for H. pylori in vivo will be obtained using a non-human primate model. Transcript profiles obtained under a variety of in vitro conditions will be organized into relational data sets and analyzed to reveal transcriptional paths and networks operative in H. pylori. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: IMMUNE RESPONSE TO H PYLORI GASTRITIS Principal Investigator & Institution: Ochoa, Augusto C.; Associate Professor; Louisiana State Univ Hsc New Orleans New Orleans, La 70112 Timing: Fiscal Year 2003; Project Start 08-JUL-2003; Project End 30-JUN-2008 Summary: (provided by applicant): Helicobacter pylori (H. pylori) infects over half of the world's population and is associated with multiple disease states ranging from gastritis and duodenal ulcer to gastric cancer and lymphomas. The mechanisms leading from infection to malignancy are not clearly established, but are prominently associated with the type of inflammatory response to the bacteria. In addition to inducing an antibody response, H. pylori causes a T cell response which initially appears to be a Th1 type with the production of IL2, IFNgamma, and TNFalpha and the development of gastritis. The type of gastritis has been divided into two major categories by its histologic appearance, non-atrophic gastritis (NAG), generally associated with duodenal ulcer disease, and Multi-focal atrophic gastritis (MAG), associated with gastric ulcers, epithelial dysplasia and gastric cancer. Most of the previous work has studied the immune response on patients with NAG, while little is known on patients with MAG. Our preliminary data comparing both groups of patients shows an increased infiltration by B cells and an enhanced expression of HLA-DR expression in patients with NAG, which markedly decreases in patients with MAG. In contrast the peripheral

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blood lymphocytes of patients with MAG show a significantly increased production of IFNgamma, IL5 and IL10 after stimulation with H. pylori antigens. However, our data also shows that H. pylori can impair the T cell response by diminishing the proliferation to mitogens, altering the expression of signal transduction proteins and, in patients with MAG, increasing the production of arginase, an enzyme known to diminish the T cell response. Therefore our hypothesis is that the immune response to H. pylori antigens differs in patients with NAG and MAG and therefore plays a central role in determining the type of gastritis developed by the host and its possible progression to gastric malignancy. To test this hypothesis we have developed the following specific aims: 1. To Compare the local inflammatory response in the gastric mucosa of patients with Nonatrophic antral gastritis (NAG) and patients with Multi-focal atrophic gastritis (MAG) using histopathology, immunohistochemistry and in situ hybridization techniques. 2. To compare the cellular immune response of peripheral blood lymphocytes and gastric mucosa lymphocytes to H. pylori antigens in patients with NAG and MAG. 3. To identify the mechanisms by which H. pylori impairs T cell signal transduction and T cell function in patients with H. pylori induced gastritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMMUNOBIOLOGY AND PREVENTION OF H PYLORI DISEASE Principal Investigator & Institution: Smith, Phillip D.; Professor of Medicine; Medicine; University of Alabama at Birmingham Uab Station Birmingham, Al 35294 Timing: Fiscal Year 2001; Project Start 30-SEP-1998; Project End 31-AUG-2003 Summary: Worldwide, the most common bacterial pathogen of the gastrointestinal tract among humans is Helicobacter pylori. Chronic infection with this noninvasive organism is the leading cause of gastritis, gastroduodenal ulcer and gastric carcinoma. In the U.S., the cohort prevalence of H. pylori increases approximately 10 percent per decade, whereas in developing countries, such as Chile, up to 80 percent of school-age children are already infected. Prolonged infection and its attendent inflammation predispose the gastric mucosa to malignant transformation, causing gastric cancer to be the leading cause of death in many developing countries. Since therapeutic eradication of H. pylori is expensive and unlikely in many countries, an effective vaccine is highly desirable, but its development will require elucidation of the mechanism(s) by which H. pylori causes mucosal inflammation. Accordingly, we hypothesize that: 1) After colonization of gastric mucosa, H. pylori releases antigens that are absorbed Into the lamina propria where they stimulate T helper type 1 (Th1) mucosal lymphocytes to produce cytokines that promote a cellular inflammatory response. 2) H. pylori antigens, such as urease, can be delivered in novel vaccines to induce protection against infection. 3) Along with the antigen, regulatory cytokines can be delivered in the vaccine to direct the local response from a Th1 inflammatory response to a Th2 humoral response. These hypotheses will be tested with the following four specific aims: 1) Determine whether human H. pylori gastritis in geographically diverse populations is associated predominantly with Th1 CD4+ lymphocytes, which promote a delayed hypersensitivity response, or with Th2 CD4+ lymphocytes, which promote a humoral B cell response. 2) Determine which H. pylori products stimulate purified primary mucosal cells to produce the cytokines associated with H. pylori gastritis (Specific Aim 1). 3) Characterize the cytokine response in mice infected with H. pylori in order to identify the dominant antigens that induce gastric inflammation and the Th cytokines (Specific Aim 2). 4) Using two new vaccine strategies readily adaptable to the human, determine whether oral vaccination with the dominant H. Pylori antigen(s) (Specific Aim 3) and immunoregulatory cytokines (Specific Aims 1 and 2) protect mice against challenge infection.

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

Project Title: GASTRITIS

IMMUNOMODULATORY

STRATEGIES

IN

AUTOIMMUNE

Principal Investigator & Institution: Kosiewicz, Michele M.; Assistant Professor; Microbiology and Immunology; University of Louisville University of Louisville Louisville, Ky 40292 Timing: Fiscal Year 2001; Project Start 15-AUG-1999; Project End 31-JUL-2003 Summary: Many autoimmune diseases appear to be mediated by antigen-specific T cells that produce the pro-inflammatory cytokines, IFNgamma and TNFalpha. It would be of great value to develop a strategy to specifically downregulate or eliminate these autoreactive T cells without interfering with other immune functions. The goal of this grant proposal is to study the mechanisms that are involved in two strategies designed to specifically downregulate the activity of antigen-specific T cells and to test these strategies in a well-characterized murine model of autoimmune disease. Previous studies have demonstrated that antigen presenting cells (APCs) pulsed with antigen in the presence of TGFbeta2 transmit a potent tolerance-inducing signal to the peripheral immune system when injected intravenously into naive mice. Accumulating evidence suggests that CD4 and CD8 regulatory T cells are induced and mediate antigen-specific tolerance in this system. The goal of the first specific aim is to understand the mechanisms involved in tolerance induced by TGFbeta-treated APCs. In this aim, the role that regulatory T cells play in this system of tolerance as well as their general mechanism(s) of action will be examined in in vivo studies using knock-out mice, neutralizing antibodies and a TCR transgenic T cell transfer system. Further studies will involve in vitro analyses of the precise mechanisms utilized by regulatory T cells to downregulate effector T cell function. The goal of the second specific aim is to investigate the therapeutic potential of TGFbeta-treated APCs using a murine model of autoimmune gastritis. Neonatal thymectomy (Tx-3) in BALB/c mice induces an autoimmune gastritis that markedly resembles human pernicious anemia. Tile T cell response has been well characterized in this model and is Th1-type cytokine-mediated and targeted to the alpha and beta subunits of H/K ATPase of parietal cells. This aim is designed to determine whether treatment of Tx-3 mice with ATPase-pulsed TGFbetatreated APCs can "cure" or ameliorate autoimmune gastritis and to characterize the T cell response that is associated with this treatment. The goal of the third specific aim is to explore the ability of FasL-expressing APCs to treat autoimmune disease either independently or as a supplement to treatment with TGFbeta-treated APCs. This aim is designed to characterize the T cell response after activated T cells have been targeted for elimination in vivo by treatment with antigen-pulsed APCs genetically engineered to express FasL. This strategy may be used in conjunction with TGFbeta-treated APCs to successfully treat established autoimmune disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMMUNOPREVENTION OF H. PYLORI GASTRITIS Principal Investigator & Institution: Cummins, Joseph M.; Amarillo Bioscience, Inc. 800 W 9Th Ave Amarillo, Tx 79101 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 29-SEP-2002 Summary: (provided by applicant): Helicobacter pylori (Hp) gastric infection is a common and serious infectious disease of humans. Current therapeutic regimens, while successful in 80 percent of the instances of infection, are complicated by expense,

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duration of treatment, emergence of resistant strains of Hp and lack of patient compliance. An ideal alternative to antimicrobial therapy is prophylactic or therapeutic vaccination for Hp. In this phase I SBIR, we will test the hypothesis that proteolytic digests of Hp incorporated into a novel adjuvant formulation will prevent manifestations of bacterial gastritis and promote gastric bacterial clearance in Hpinfected gnotobiotic piglets, an established animal model of this disease. Piglets will be parenterally immunized with Hp digests prior to and after established gastric infection. Evidence for protection (reduced/absent bacterial cfu, local and systemic immunity, etc) will be sought. Protection will be correlated to patterns of Western blot immunoreactivity of convalescent immune sera and isolated leukocyte in vitro responses to putative bacterial antigen(s). Reactive peptides will be isolated by HPLC, sequenced and identified. From these data, the feasibility of parenteral vaccination for Hp will be determined in this nonrodent model of bacterial gastritis and a phase II SBIR will be prepared if the protection data are positive. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IMPAIRED TUMOR IMMUNITY DURING H PYLORI INFECTION Principal Investigator & Institution: Reyes, Victor E.; Professor; Pediatrics; University of Texas Medical Br Galveston 301 University Blvd Galveston, Tx 77555 Timing: Fiscal Year 2001; Project Start 01-JUN-1995; Project End 31-MAY-2004 Summary: Helicobacter pylori is an important pathogen which plays the major role in chronic gastritis, gastric and duodenal ulcers and gastric carcinomas. Although H pylori infection of the gastric epithelium elicits immune responses, insight into the mechanisms that regulate the development of those responses is limited. Recent studies have suggested that mucosal epithelial cells are active participants in immune responses to mucosal pathogens. The antral gastric epithelium constitutively expresses class II MHC molecules, and our cells have shown that these epithelial cells express other important markers which are required by antigen presenting cells. We noted that gastric epithelial cells in vitro and in vivo expressed the CD86 co-stimulatory molecule and this expression increased in parallel with the rise of local CD4+ T cell numbers and epithelial class II MHC expression increased in parallel with the rise of local CD4+ T cell numbers and epithelial c;ass II MHC expression during infection with H. pylori. Our most recent studies suggest that H pylori antigens are endocytosed by gastric epithelial cells and transported into endosomes that contain HLA-DM, a molecule which is essential in class II MHC-mediated antigen presentation and immunity to pathogens. Thus, gastric epithelial cells possess key functional elements of antigen presenting cells. Since antigen processing and presentation are pivotal events in the development of an immune response, our observations have led us to hypothesize that gastric epithelial cells are central regulators of the inflammatory and immunologic responses during H. pylori infection and that the nature of those responses is influenced by the bacteria. To examine this hypothesis we will address the following specific aims, as natural extensions of the studies performed during the initial period of funding. 1) Characterize the mechanisms of antigen internalization by gastric epithelial cells. In this aim we will (a) characterize the H. pylori antigens that are selectively internalized by human gastric epithelial cells and the mechanisms that promote their uptake; (b) define how internalized H. pylori antigens may alter various steps in the normal antigen processing (steps) and (c) identify the H. pylori peptides that are selective for presentation to T cells by gastric epithelial cells. 2) Characterize the mechanisms that allow gastric epithelial cells to influence CD4+ T cell function. In this aim we will (a) define the distribution of class II

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MHC in polarized gastric epithelial cells and (b) characterize the expression and function of Ii-CS, an essential co- receptor for CD44 on T cells, by human gastric epithelial cells. The overall goal of these studies is to better understand the interactions between H. pylori, the gastric epithelium and immune cells that determine the outcome of the infection. The studies may help explain why H. pylori infection persists and whether mechanisms that allow H. pylori to evade immune defenses may also permit the associated neoplasms to evade immune surveillance. Understanding the molecular basis for the regulation of the local immune response to natural infection will also facilitate the development of therapeutic or prophylactic vaccines against this clinically important pathogen. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: IN VIVO PATHOGENESIS OF HELICOBACTER PYLORI Principal Investigator & Institution: Fox, James G.; Director and Professor; Div of Comparative Medicine; Massachusetts Institute of Technology Cambridge, Ma 02139 Timing: Fiscal Year 2001; Project Start 01-SEP-1996; Project End 31-AUG-2005 Summary: (Adapted from the Applicant's Abstract): H. pylon, an infection approaching 100 percent in developing countries, has been strongly linked epidemiologically to gastric cancer, but the mechanism and cofactors required for gastric cancer are poorly understood. Furthermore, it is not known at what stage in progression to gastric cancer that eradication of H. pylon would interrupt the carcinogenic process. Polyparasitism is also ubiquitous in developing populations where H. pylori is endemic. The investigators have developed a C57BL/6 mouse model of chronic H. pylori/felis gastritis that is characterized by the progressive development of gastric atrophy, intestinal metaplasia and invasive gastric cancer. The mechanism of lesion development appears to involve increased apoptosis, mucus neck proliferation, intestinal metaplasia leading to altered cellular differentiation and changes in mucin phenotype and progression of invasive cancer in submucosal vasculature. They have also investigated bacterial and environmental factors that influence disease pathogenesis by generating isogenic mutants lacking specific candidate virulence determinants and by maintaining Helicobacter infected animals on diets high in salt. They have recently shown that in mice coinfected with helicobacter and a helminth infection, H. polygyrus, the gastric cytokine Thl/Th2 profile switches and the gastric phenotype changes from a Thl to a Th2 type gastritis. They now propose to explore the effects of specific genetic alterations, environmental influences and coinfections on the mucosal response and progression of Helicobacter associated gastric lesions. Specifically, they will ask whether 1) progression of H. pylon gastritis can be interrupted at critical points in the disease by antimicrobials or therapeutic vaccination to prevent development of premalignant lesions and gastric adenocarcinoma in the gerbil and/or mouse model 2) Alternatively, do environmental factors such as dietary salt, accelerate or otherwise alter the carcinogenic process, and importantly does the strain of H. pylon (with and without specified pathogenic determinants) influence the outcome of gastric disease in the mouse and gerbil model 3) Does modulation of the Thl/Th2 axis of the immune system by various helminth infections influence the severity and progression of gastritis in rodent models. Overall, these rodent models of Helicobacter infection will be used to study the mechanism by which Helicobacter contributes to neoplasia, and the factors (host, bacteria, dietary or co-infections) which confer susceptibility and/or resistance to premalignant lesions and gastric cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: INTERACTIONS OF HELICOBACTER WITH THE GASTRIC MUCOSA Principal Investigator & Institution: Guiney, Donald G.; Professor; Medicine; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2001; Project Start 30-SEP-1997; Project End 29-SEP-2002 Summary: (taken from the application) Helicobacter pylori is responsible for chronic inflammation in the gastric mucosa. We propose that a long-term carrier state is the result of a balance of pro-inflammatory mediators and regulatory elements that maintain mucosal integrity. Mucosal damage results from a disruption of this balance, leading to sequelae such as ulceration, MALT, and adenocarcinoma. Our aim is to investigate the role of NO, prostaglandin E2, and cytokines in mediating both mucosal protection and damage during Helicobacter infections. We have preliminary data indicating that H. pylori interacts with gastric epithelial cells to induce both interleukin8 and nitric oxide synthesis. In addition, NO has an effect on growth and morphology of H. pylori. The IL-8 induction in gastric epithelial cells is dependent on the expression of the cag pathogenicity in H. pylori, which encodes numerous proteins potentially involved in the secretion of virulence factors. Therefore, we will study isogenic mutants in this pathogenicity island with respect to their ability to induce inflammatory mediators in gastric epithelial cells. We have established a mouse model of infection with H. pylori, and propose to study iNOS induction, cox-2 induction, and cytokine profiles in infected mice. In addition, gastric epithelial cell lines will be used to optimize conditions and give preliminary data. Finally, iNOS, IL-4, IL-10 and IFN-g knockout mice will also be used to determine the importance of these enzymes and cytokines in H. pylon-induced gastritis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LACTOFERRIN AND MUCOSAL IMMUNITY Principal Investigator & Institution: Thomas, Larry L.; Associate Professor; RushPresbyterian-St Lukes Medical Ctr Chicago, Il 60612 Timing: Fiscal Year 2001; Project Start 01-SEP-2000; Project End 31-AUG-2003 Summary: (Adapted from applicant's abstract): The important role of lactoferrin in innate mucosal immunity is well described. Neutrophils, which are the most abundant and rapidly mobilized immune cell within the circulation, constitute along with glandular epithelial cells the sole source of lactoferrin in vivo. Neutrophils, however, also are well recognized as pro-inflammatory cells, due in part to the release of proteases such as elastase and matrix metalloproteinase-9 (MMP-9). Neutrophils also are directly implicated in the pathogenesis of various mucosal-related diseases, including inflammatory bowel disease, gastritis, cystic fibrosis, and periodontal disease. Although lactoferrin is a distinguishing component of neutrophil secondary granules, results obtained by the Principal Investigator demonstrate that lactoferrin is also constitutively present on the surface of resting neutrophils. In addition, results suggest that neutrophil activation by chemoattractants induces a conformational change in the surfaceassociated lactoferrin. These observations, together with the demonstrated lactoferrinbinding activity of several bacterial pathogens associated with mucosal infection, suggest that the surface-associated lactoferrin may either directly mediate neutrophil activation or may contribute to the regulation of neutrophil function by lactoferrinbinding organisms. As such, lactoferrin- mediated activation and resultant degranulation of the neutrophils would amplify the mucosal host defense response but, at the same time, also trigger mucosal damage and potentially lead to inflammatory

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pathogenesis. Alternatively, lactoferrin-mediated induction of neutrophil apoptosis could provide a survival benefit to lactoferrin binding organisms by limiting neutrophil activation and subsequent release of the various host defense mediators. Accordingly, this proposal has two specific aims. (1) Does surface-associated lactoferrin mediate neutrophil activation and/or regulate neutrophil function?; (2) Does neutrophil activation by chemoattractants alter the capacity of surface-associated lactoferrin to mediate or regulate neutrophil function? It is proposed that the results of this study will identify a new mechanism for the activation or regulation of neutrophil function with direct implications for mucosal immunity and pathogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISMS OF COLITIS INDUCED BY DEFINED BACTERIAL FLORA Principal Investigator & Institution: Sartor, Ryan B.; Professor; Medicine; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2001; Project Start 01-FEB-1989; Project End 14-SEP-2005 Summary: The etiology of IBD is unknown, but both genetic and environmental factors are involved. In the current funding period of this grant experimentally-induced and genetically engineered rodent models have been used to provide convincing evidence that the normal endogenous enteric bacterial flora is essential to the development of chronic colitis, gastritis and arthritis in genetically susceptible rodents. Very importantly, the use of HLA-B27/beta2 transgenic (TG) rats has demonstrated that all components of the resident bacterial flora are not equal in their capacity to induce inflammation: some are aggressive (B. vulgatus), some are neutral (E. coli) and some are protective (Lactobacillus sp). B. vulgatus from several sources causes more aggressive colitis in B27 TG rats than B. distasonis isolated from normal rats. Chronic intestinal inflammation in these models is mediated by activated T lymphocytes which are induced by normal luminal bacteria. These data support the hypothesis that chronic intestinal inflammation in genetically susceptible hosts is the result of an overly aggressive cellular immune response to a subset of ubiquitous luminal bacterial constituents. Genetic susceptibility is determined by defective downregulation of inflammatory responses or defective mucosal barrier function. This clinically relevant hypothesis will be tested by the following specific aims: 1) determine mechanisms by which B. vulgatus selectively induces colitis in HLA-B27 TG rats; 2) identify the mechanisms of immunologically determined susceptibility to B. vulgatus and other resident enteric bacterial components in HLA-B27 TG rats versus nontransgenic littermates. A NIH-funded Core Center for Gastrointestinal Biology and Disease at UNC supports a barrier-intact gnotobiotic rodent facility, providing the investigators with a unique environment to selectively colonize germ-free rats with defined luminal bacterial species. These studies will generate novel insights into the pathogenesis of IBD and open new opportunities for novel therapeutic interventions to block induction of antigen-specific immune response to luminal bacteria. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MECHANISMS OF GROWTH INHIBITION BY HELICOBACTER PYLORI Principal Investigator & Institution: Ashktorab, Hassan; Medicine; Howard University 2400 6Th St Nw Washington, Dc 20059 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2003

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Summary: (provided by applicant): The discovery that H. pylori is an important factor in the development of peptic ulcers has dramatically changed the way ulcer patients are treated. Ulcers heal faster in persons treated with antibiotics in addition to acid medication. One possible explanation for this observation is that cell generation is impaired by H. pylori; thus, ulcer healing occurs more rapidly in the absence of H. pylori infection. Epidemiological studies have strongly associated H. pylori with gastric carcinogenesis. These data led the World Health Organization to designate H. pylori a Class I carcinogen. It is felt that at least half of all gastric cancers are attributed to infection with this bacterium. However, there is little known as to how H. pylori may directly effect gastric cells to cause gastric cancer. Epidemiological data supports this bacterium as a cofactor because it causes chronic gastritis which may progress to atrophic gastritis, a precursor lesion for intestinal type gastric cancer. However, this bacterium is also strongly linked to diffuse gastric cancer which occurs in otherwise normal (non-atrophic) gastric mucosa, where the bacterial infection is present at the time the cancer occurs. In vivo studies show that some bacterial strains cause significant cell injury in the absence of a rise in gastric apoptosis. One explanation is that the bacterium, while causing cell injury, is able to down regulate apoptosis. The decrease in apoptosis in injured gastric cells is one possible mechanism by which this bacterium might directly increase the susceptibility of gastric cells to carcinogenic conversion. This grant proposes to evaluate the direct effects of H. pylori on the cell death in gastric epithelial cells. The Specific Aims of this project are: 1)To better elucidate the involvement of the p53 pathway in H. pylori induced apoptosis by determining the extent of phosphorylation of p53 in cells exposed to H. pylori strains and the importance of phosphorylation at serine-15,-20 and-46 in regard to apoptosis. Also, to evaluate p53 phosphorylation in response to ROS species in the absence of H. pylori and in the presence of H. pylori and antioxidants. 2)To determine the involvement and significance of activation of p53AIPl, which is activated by phosphorylating p53 at serine-46. The mechnism of bacterial exposure on the gastric epithelial cell death has not been studied in regard to p53. These studies are important to elucidate specific p53 pathways that are modulated by exposure to this bacterium, resulting in an regulating cell death. Specifically, whether or not stimulation of reactive oxygen species (ROS) by H. pylori is essential for p53 phosphorylation leading to apoptosis. These studies will help to establish how bacteria can increase apoptosis possibly through generation of ROS and in specific circumstances this may alter one's risk of developing cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MICROARRAYS OF INTERMEDIATE ENDPOINTS OF GASTRIC CANCER Principal Investigator & Institution: Parsonnet, Julie; Associate Professor; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2003; Project Start 20-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): Helicobacter pylori (H. pylori) infection causes gastric adenocarcinoma, the second leading cause of cancer mortality worldwide. Screening and treatment of H. pylori could be a cost-effective way of preventing cancer, but whether H. pylori eradication can stop progression of gastric carcinogenesis remains unknown. Several studies have been completed that indicate incomplete regression of gastric preneoplastic conditions with H. pylori eradication. Using preneoplastic conditions as surrogate markers, however, is problematic in that regressions of surrogates may not signify regressions in cancer risk. To know the meaning of microscopic regression, one must look at the molecular underpinnings of the observed

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phenotypic changes. We hypothesize that the histologic regression observed with H. pylori eradication reflects molecular changes. To determine if this is the case we will dissect the role that H. pylori plays in molecular pathways of gastric preneoplasia. cDNA microarray will be used to assess gene expression profiles of archived tissues from a randomized placebo-control trial of H. pylori eradication conducted in Mexico. A total of 90 subjects (45 from the treatment arm and 45 from the placebo arm) with preneoplastic conditions (gastritis, atrophy, and metaplasia) will be selected from the original trial. For each of the 90 subjects, a pair of pre- and post-treatment gastric tissues will be used for cDNA microarray. The resulting gene expression data will be analyzed by hierarchical clustering and Significant Analysis of Microarrays (SAM). In addition to the data on patients with preneoplastic lesions, we also have access to gene expression profiles of 90 gastric cancer tissues and 22 normal gastric tissues from investigators at our institution. Our data can then bridge the gap between different carcinogenetic stages between normal and cancer. In summary, the primary aims of this study are: 1) to assess the changes of global gene expression patterns associated with H. pylori eradication and identify reversible, molecular "intermediate biomarkers" for gastric cancer, 2) to compare the results from gene expression studies to those from pathologic diagnoses, and 3) to compare the results from gene expression studies in normal, preneoplastic, and malignant tissues. This proposed study will not only help elucidate the poorly understood molecular mechanisms of gastric carcinogenesis, but also help delineate the role of H. pylori infection in this process. Despite National Institutes of Health (NIH) guidelines to the contrary, H. pylori screening and eradication therapy is being widely used by primary care practitioners in the hope that it will prevent cancer in high-risk populations. We hope our results will provide impetus for more rational screening and treatment policies, particularly for the minority populations in the United States and people in developing countries who suffer most from this highly fatal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MODIFICATION OF HELICOBACTER PYLORI LIPID A Principal Investigator & Institution: Trent, Michael S.; Microbiology; East Tennessee State University Box 70565 Johnson City, Tn 37601 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2005 Summary: (provided by applicant): The outer membrane of Gram-negative bacteria consists of a unique molecule known as lipid A that serves as the membrane anchor for lipopolysaccharide (LPS). Lipid A (endotoxin) is the component of LPS responsible for the stimulation of the host innate immune system involved in Gram- negative sepsis. The lipid A of Escherchia coli is a hexa-acylated disaccharide of glucosamine that is substituted at the 1- and 4'- positions with phosphate and glycosylated at the 6' position with two Kdo (3-deoxy-D-manno-octulosonic acid) moieties. Nine enzymes are required for biosynthesis of Kdo2- lipid A, the minimal LPS required for E. coli growth under normal laboratory conditions. Since lipid A is required for bacterial growth, it has become an interesting target for the design of novel antibacterial agents. Although single copies of the lipid A biosynthetic genes are found in nearly all Gram-negative bacterial genomes including those of Helicobacter pylori, the lipid A of the latter is underacylated with the phosphate groups either absent or modified. The primary focus of the present study is the identification of novel enzymes required for the modification of H. plyori lipid A and initial studies to evaluate the importance of such modifications during infection. Secondly, the lipid A structure of Helicobacter heilmannii will be investigated. H. pylori is now considered the causative agent of gastric and duodenal ulcers and H. heilmannii has recently been found associated with human gastritis. The

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specific aims of the current proposal are: (I) characterization and cloning of lipid A deacylases of H. pylori; (II) characterization and cloning of genes required for modification of the phosphates of H. pylori lipid A; (III) relevance of H. pylori lipid A modifications during infection; and (IV) isolation, purification, and structural characterization of key lipid A species of H. heilmannii. The completion of these aims will not only further the understanding of the lipid A biosynthetic pathway in H. pylori and H. heihnannii but also lay the foundation for new molecular insights into the pathogenesis of these unique organisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MOLECULAR PATHOGENESIS OF DIGESTIVE DISEASES Principal Investigator & Institution: Omary, M Bishr.; Professor of Medicine; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 01-MAY-2001; Project End 28-FEB-2006 Summary: OVERALL (Adapted from the application) The Digestive Disease Center at Stanford University was established in 1987 and has two major areas of focus. The first deals with studying host-pathogen interactions, and the mechanism and signals that target leukocytes to specific digestive organs and pathogens. Infections under study include hepatitis A-D, H. pylori, and the diarrheal agents rotavirus, salmonella, E-coli, cholera and astrovirus. It also addresses mucosal immunity and targeting of immunocytes to the intestine and liver in normal and disease states including inflammatory bowel disease, viral hepatitis, and H. pylori-induced gastritis. The second focus addresses the cell and molecular biology of digestive epithelia with emphasis on normal and abnormal cell growth, differentiation, development, polarity, and the nature and role of signaling pathways and the cytoskeleton in facilitating these processes. This focus targets several digestive diseases including esophageal, pancreatic and colorectal cancer; cryptogenic liver disease; pancreatitis and Barrett?s esophagus. The Center consists of 29 established investigators who blend several clinical and basic science departments. Five core facilities are administered by the Center and they provide several important technologies and services. The Administrative Core offers the Pilot and Feasibility Program which provides one year funding ($20,000/year) to junior investigators or those with a collaborative project, the Named Investigator Program which provides a two year 20-25% effort/year support to a promising junior faculty, and a Collaborative Trainee Program that specifically funds trainees who work with two or more Center investigators. The Fluorescence Activated Cell Sorting/Immunoprobe Core offers an array of services that allow studying single cells. The Cell Imaging Core offers state of the art imaging tools including confocal and electron microscopy. The Microarray/DNA Sequencing Core offers the ability to identify disease-associated regulatory changes in multiple genes, and as such provides potential means to develop diagnostic and therapeutic modalities. Cell Biology & Signaling Core offers expertise and services in cell culture methods, characterizing protein-protein interaction, dissecting signaling pathway and characterizing regulatory modifications such as phosphorylation. In the aggregate, this Center brings together an accomplished group of investigators, creates a highly interactive environment, and makes available state of the art technologies to address important digestive diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MUCOSAL IMMUNOLOGY OF HELICOBACTER INDUCED GASTRITIS Principal Investigator & Institution: Czinn, Steven J.; Professor; Pediatrics; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 15-DEC-1993; Project End 30-NOV-2002 Summary: (Adapted from the applicant's abstract): Since the rediscovery of Helicobacter pylori (H. pylori) in the early 1980's, studies have now demonstrated that H. pylori plays an etiologic role in the development of gastritis, peptic ulcer disease, and gastric cancer. The investigators have previously demonstrated the importance of the host as a factor in disease outcome following gastric Helicobacter infection. A related issue, is whether the host immune response contributes to the pathogenesis or acts to protect the host from infection. Using the H.felis/mouse model, the investigators have demonstrated that the T-cell mediated immune response to Helicobacter infection can contribute either to the pathogenesis or act in concert with the humoral immune response to clear this infection. Specifically, the results of studies funded during the previous granting period indicate the Helicobacter infection activates antigen specific cell-mediated immune responses in immunized or infected hosts. These responses have a phenotype which is either pro-inflammatory in nature (TH1) or protective in nature (TH2). Adoptive transfer of Helicobacter-specific TH1 lymphocytes exacerbates gastric inflammation in recipients. However, transfer of a TH2 cell line from immunized/protected mice decreases the magnitude of infection in the recipients. There continues to be a number of unanswered questions, however, which are the focus of this proposal. Using the recently developed H. pylori/mouse model, a number of contemporary techniques, such as the use of knock-out or transgenic mice, recombinant cytokine therapy, and adoptive transfer studies, will be used to further investigate the role of the host immune response in preventing or promoting chronic H. pylori gastroduodenal disease. the investigators will specifically assess the contribution of the humoral immune system in preventing H. pylori gastroduodenal disease following immunization as well as assess the contribution of the host cellular immune response in preventing or promoting H. pylori gastroduodenal disease. An in-depth understanding of the pro-inflammatory mechanisms employed by the host in this model will contribute to our general understanding of immune regulation and the pathogenesis of infectious disease. Finally, these aims are a logical extension of the work previously performed in their laboratory and may ultimately allow them to develop a safe and efficacious subunit vaccine to prevent morbidity and potential long-term consequences of Helicobacter infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: NEURAL PATHWAYS & MEDIATORS OF VISCRAL SENSITIVITY IN NONULCER DYSPEPSIA Principal Investigator & Institution: Ladabaum, Uri; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: NONINVASIVE TEST FOR MANAGEMENT OF NONULCER DYSPEPSIA Principal Investigator & Institution: Craine, Brian L.; Western Research Company, Inc. 2127 E Speedway, Ste 209 Tucson, Az 85719 Timing: Fiscal Year 2002; Project Start 01-NOV-1999; Project End 31-JUL-2004 Summary: (Applicant's abstract): Nonulcer dyspepsia is a highly prevalent medical condition affecting up to 30 percent of the Western population, accounting for 2-5 percent of all visits to primary care physicians and leads to over one billion dollars worth of upper endoscopy procedures per year. In an attempt to lower this tremendous burden on the health care system the general practice currently is to attempt to avoid endoscopy in the majority of patients, which are low risk, by an initial empiric trial of medication. Endoscopy can then be performed on those that fail initial therapy. Unfortunately, empiric treatment is only effective in about 40-50 percent of cases since it is difficult to determine in advance the most effective treatment. Consequently the high cost of endoscopy continues to be a problem. The overall goal of this project is to develop an inexpensive, non-invasive test for the objective and quantitative categorization of nonulcer dyspepsia patients with the purpose of providing the most effective initial treatment. The effectiveness of objective patient categorization will be tested with respect to ability to predict which patients will be responders to acid suppression therapy and which will be responsive to prokinetic treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: OXIDATIVE DAMAGE TO GASTRIC EPITHELIAL CELLS BY H PYLORI Principal Investigator & Institution: Crowe, Sheila E.; Associate Professor; Internal Medicine; University of Virginia Charlottesville Box 400195 Charlottesville, Va 22904 Timing: Fiscal Year 2001; Project Start 21-SEP-2001; Project End 31-AUG-2006 Summary: Helicobacter pylori is a chronic infection that affects 50% of the world's population causing gastritis in all infected while only a subset develop disease of the epithelium in the form of ulceration or adenocarcinoma. Both bacterial and host factors appear to play a role in the pathogenesis of these human diseases but the specific mechanisms remain unclear. H. pylori and cytokines known to be increased in H. pylori infection, induce alterations of gastric epithelial cell growth such as the induction of programmed cell death. Phagocytic leukocytes recruited to the gastric mucosa during infection become activated, generating reactive oxygen species (ROS) that we have shown to alter gastric epithelial cell growth and induce apoptosis. Infection with H. pylori also induces the accumulation of ROS in gastric epithelial cells that may be dependent on bacterial genotype. Gastric epithelial cells respond to oxidative stress with the initial generation of ROS and subsequent activation of a redox-sensitive signaling pathway which has been shown to control the transcription of genes that regulate cell growth, repair and death processes. Of particular interest is ROS-induced activation of apurinic/apyrimidinic endonuclease-1 (AP endonuclease), a multifunctional protein that is the rate-limiting enzyme in the DNA base excision repair pathway of oxidative lesions, which also activates transcription factors including activator protein (AP)-1, and p53. Thus, the general hypothesis underlying this proposal is that oxidative stress contributes to the epithelial cell injury that occurs during H. pylori infection. The specific hypothesis that H. pylori infection stimulates redox-sensitive signaling through AP endonuclease that leads to apoptosis in gastric epithelial cells will be examined in the following specific aims: Aim 1. Evaluate oxidative stress in gastric epithelial cell

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injury (apoptosis) during H. pylori infection; Aim 2 Determine if H. pylori regulates the expression and function of AP endonuclease in gastric epithelial cells; Aim 3. Define how AP endonuclease regulates apoptosis and the transcription of pro-apoptotic genes. These studies in cultured human cell lines and human tissue will address unanswered questions regarding the effect of oxidative stress on gastric epithelial cell injury. The molecular mechanisms governing the epithelial response to oxidative stress will also be defined. This new knowledge will improve our understanding of the pathogenesis of epithelial cell damage associated with H. pylori infection and help identify strategies for the prevention and treatment of human gastric disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OXIDATIVE STRESS AND SURVIVAL OF HELICOBACTER PYLORI Principal Investigator & Institution: Maier, Robert J.; Microbiology; University of Georgia 617 Boyd, Gsrc Athens, Ga 306027411 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2006 Summary: (provided by the applicant): Helicobacter pylori is a spiral bacterium that colonizes the gastric mucosa of humans, leading to a variety of inflammatory gastric diseases that include peptic ulcers, chronic gastritis, adenocarcinoma of the lower stomach, and MALToma (mucosal-associated lymphoma). The severity of the inflammatory-based disease is related to the persistent nature of the pathogen, and chronic infection is the predominant pre-disposing factor for carcinoma. The persistence is attributed to the pathogens' stringent adaptation to the harsh environment of the human stomach, which must include avoiding acidity and combating host defense mechanisms. The battery of host-produced partially reduced oxygen species and other reactive molecules that damage the bacterial cellular components needed for survival of the pathogen are in turn counteracted by enzymes produced by the successful pathogen. The goal is to identify and characterize the antioxidant enzymes produced by H pylori to combat oxidative stress and maintain virulence (stomach colonization). This will be approached by targeted mutagenesis of five specific antioxidant genes. Then each mutant will be characterized for its ability to withstand oxidative stresses, to acquire spontaneous mutations, to survive air-exposure, and to colonize mouse stomachs. The environmental host-related signals (such as iron, oxygen, mucin, pH, and oxidizing agent) that may regulate each of the five genes will be determined, and some of the antioxidant activities will be characterized. In addition to the five targeted antioxidant activities, global approaches involving proteomics and DNA microarray will be used to determine the number and nature of proteins that are expressed upon adaptation of H pylori to oxidative stress conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PATHOGENIC MECHANISMS OF HELICOBACTER PYLORI GASTRITIS Principal Investigator & Institution: Kelly, Ciaran P.; Associate Professor; Beth Israel Deaconess Medical Center St 1005 Boston, Ma 02215 Timing: Fiscal Year 2001; Project Start 01-MAY-1998; Project End 30-APR-2003 Summary: Strains of Helicobacter pylori which carry the cag (cytotoxin-associated gene) region upregulate production of the neutrophil-activating chemokine IL-8 in gastric epithelial cells. cag+ strains are more frequently isolated from patients with peptic ulceration and gastric adenocarcinoma. Cag strains are less potent in up-regulating IL-8 production and are more frequently isolated from asymptomatic subjects. Thus

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activation of an inflammatory response in gastric epithelial cells by cag+ H. pylori may be a critical step in the pathogenesis of H.pylori-associated gastroduodenal disease. This proposal examines the hypothesis that differences in the virulence of H.pylori strains are correlated to their ability to induce epithelial cell activation and differentially regulate epithelial cell chemokine production. Infection with cag+ H.pylori activate the transcription factors NF- kappaB and AP-1 in gastric epithelial cells. These factors then up- regulate IL-8 gene transcription. ENA-78 is an epithelial cell-derived chemokine structurally and functionally similar to IL-8. Cag+ H. Pylori block cytokine-stimulated ENA-78 production in the gastric epithelial cell. The ability of H. pylori to inhibit ENA78 release may be a virulence mechanism which allows the bacterium to balance immune activation with immune evasion and thereby achieve chronic indolent infection of its host. Aim 1 will define the molecular mechanisms whereby cag+ H.pylori upregulate IL-8 gene expression in AGS gastric epithelial cells using IL-8 reporter gene transfections and electrophoretic mobility shift analysis of transcription factor activation. It will also test the importance of NF-kappaB activation in the pathogenesis of H.pylori gastritis in mice treated with p65 NF-kappaB antisense oligonucleotides. Aim 2 will identify specific genes in the H.pylori cag region which participate in upregulating IL-8 expression by the host epithelial cell using isogenic cag gene mutants. Aim 3 will determine the molecular mechanisms whereby cag+ H.pylori block ENA-78 expression in IL-1beta- stimulated AGS cells and will examine the contribution of specific H. Pylori cag region genes to this effect. It will also attempt to isolate and characterize the H.pylori-derived factor responsible for ENA-78 repression. Identifying H.pylori virulence factors which modulate host immune and inflammatory responses and determining their mechanisms of action are key to targeting new management strategies for this highly prevalent pathogen. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PATHOLOGIC INFLUENCES MODULATING GASTRIC EPITHELIAL DIFFERENTIATION Principal Investigator & Institution: Merchant, Juanita L.; Professor; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: (provided by applicant): Chronic inflammation of the gastric mucosa (chronic gastritis) may occur from Helicobacter pylori infection or bacterial overgrowth in the hypochlorhydric stomach. The central question posed in this Subproject is how does reduced stomach acid trigger the reversion of the gastric epithelium to cells with small bowel characteristics? Recently, we have confirmed in a hypochlorhydric mouse model that reduced stomach acid coincides with bacterial overgrowth and changes in the epithelium reminiscent of H. pylori infection in patients. Since bacterial colonization of the stomach induces an inflammatory response, it is difficult to study the contribution from bacterial gene products versus the inflammation. Therefore to distinguish between these two components of chronic gastritis, we will study transgenic mice expressing the H. pylori gene product CagA and wild type mice treated with the pro-inflammatory cytokine interferon gamma (INF-gamma). INF-gamma was selected since it is the major Th1 cytokine secreted during H. pylori infection. Recently, CagA was shown to translocate into the cytoplasm of human gastric cells suggesting that this event may be one signal triggering the cascade of events. However, the role of a specific bacterial virulence factor on the pathogenesis that is observed has not been studied. Over time, the inflammatory process progresses and alteration of the epithelial cell population occurs which includes gradual loss of parietal cells with increased infiltration and

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proliferation of mucous cells. Proliferation of the mucous cell types and evidence of an intestinal phenotype with villin expression (intestinal metaplasia) is a major precursor lesion for gastric cancer. Overall, the specific goals of this project are to understand the impact of bacterial infection on gastric epithelial cell differentiation. The specific aims of the project are: 1) Study how H. pylori CagA modulates the pattern of gastric epithelial cell differentiation in vivo. 2) Study how cytokines modulate gastric epithelial cell differentiation in vivo. 3) Dissect the signaling pathways activated by CagA that regulate cell survival. 4) Study aberrant expression of villin in the stomach after bacterial colonization. The studies proposed will advance our understanding of how cell differentiation is regulated in vitro and in vivo by bacterial gene products and cytokines. Further, clues as to how modulating the pattern of gastric epithelial cell differentiation is linked to the development of pre-neoplastic lesions in the stomach will be examined. In this manner, we hope to gain significant insight into how common pathologic influences affect gastric cell identity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PEDIATRIC IBD--KEY TO EARLY PATHOGENIC EVENTS Principal Investigator & Institution: Fiocchi, Claudio; Professor; Medicine; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 15-SEP-2000; Project End 14-SEP-2005 Summary: The overall goal of the Program Project is to fill a major gap in current knowledge of IBD pathogenesis by studying children with Crohn's disease and ulcerative colitis, and the progression of early to late stages of disease in animal models of gastrointestinal inflammation. The proposal is the natural outcome of a vigorous and multi-disciplinary expertise in IBD pathophysiology, intestinal immunity, mucosal cytokines, animal model of colitis and gastritis, and immune-non immune cell interaction in intestinal inflammation. The Program Project will investigate will investigate mechanistic links of early to late events of gut inflammation by testing the specific hypotheses proposed in four Research Projects. Project 1: Early IBD in children results from loss of tolerance to antigens of the commensal flora, and its persistence contributes to the chronicity of IBD. Project 2: Inflammation in murine models of IBD is initiated by mucosal T-cell responses to enterobacterial antigens, and it is perpetuated during the late stage of disease by a pro-inflammatory response maintained by mucosal immune and non immune cells. Project 3: Chronic gastrointestinal inflammation results from an aberrant immune response against antigenic stimuli derived from the normal enteric flora, and this response is modulated by immunization and the presence or absence of Helicobacter organisms. Project 4: Specific changes in the composition of the extracellular matrix of mucosal basement membrane contributes crucially to early inflammation, while altered synthesis and modulation of interstitial extracellular matrix foster progression of inflammation from the early to the late stages of disease. These proje3cts will be performed using state-of-the-art methodological strategies including evaluation of tolerance to normal enteric antigens in pediatric and adult IBD patients, immunoregulatory studies in gene-deficient mice with early and late models of intestinal inflammation, colonization by commensal and infectious bacteria in these models, DNA microarray systems for differential gene expression in intestinal inflammation, extracellular matrix gene and protein expression in human and murine models of IBD, and induction of intestinal fibrosis in normal and proteoglycan-deficient mice. The four Projects will be supported by three Service Cores: a Patient Core (A), an Animal Core (B) and an Administrative Core (C). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PH III: CELLCEPT IMPAIRMENT ON NEORAL

IN

LIVER

TRANSPLANT

W/

RENAL

Principal Investigator & Institution: Clavien, Pierre A.; Duke University Durham, Nc 27706 Timing: Fiscal Year 2001 Summary: There is no consensus as to the optimal immunosuppressive regimen for preventing rejection and promoting graft survival after orthotopic liver transplant. Primary immunosuppression based on cyclosporine (CyA) contributes to progressive deterioration in renal function in some patients. Mycophenolate mofetil (MMF, Cellcept.) has been approved in the United States, Canada, and the European Union for the prophylaxis of organ rejection in renal allograft recipients. The major side effects of MMF are dose related gastritis, leukopenia, and anemia. Potential complications of treatment with MMF include opportunistic infections and rarely lymphoproliferative disorders. There is no nephrotoxicity related to MMF. Nephrotoxicity of oral CyA is generally dose related. Reducing the dose of CyA is the first stop in decreasing the nephrotoxicity and thus helping to improve renal function. It is likely that MMF, a potent immunosuppresive agent with no known nephrotoxicity, may provide adequate immunosuppression upon withdrawal of CyA and thus improve renal function or prevent further damage. However, the risk of allograft rejection may increase with the withdrawal or reduction of CyA. Purpose: The objective is the evaluate whether MMF can be used as a mainstay immunosuppressive therapy in post liver transplant patients with impaired renal function, thereby decreasing the exposure to other immunosuppressive agents which are potentially nephrotoxic. Safety and efficacy of each treatment regimen will be evaluated, including graft/patient survival, biopsyconfirmed or presumptive acute cellular rejection, and the incidence of adverse events, opportunistic infections and abnormal laboratory evaluations. Methods: This is a phase IIIB, open-label active controlled study to evaluate the use of Cellcept. (mycophenolate mofetil, MMF) in post-liver transplant patients with renal impairment who are currently on Neoral. (cyclosporine A). A study is currently underway to evaluate the use of MMF in combination with cyclosporine and corticosteroids compared to standard treatment with azathioprine, cyclosporine and corticosteroids in liver allograft recipients. Postliver transplant recipients > 18 years of age who meet all study entry requirements will be randomized (computer generated) with equal allocation to two groups. Both groups will have Imuran discontinued. Group A will be maintained on MMF 1.5 gm bid, prednisone, and CyA will be tapered to 50% at week 2 and discontinued at week 4. Group B will be maintained on MMF 1.5 gm bid, prednisone, and CyA will be tapered to 50% at week 2 and maintained throughout the study. Patients will be followed for 1 year post- enrollment. Glomerular filtration rate (GFR) using iohexol clearance will be measured on both groups of patients at enrollment, and at 1, 2, 4, 7, and 1 months following enrollment. In addition, routine labwork will be followed at months 3, 5, 6, 8, 9, and 10. A total of 35 ml of blood will be drawn for research purposes. A total of 30 patients will be enrolled at 3 centers. It is expected that 10 patients will be enrolled at Duke, 3 patients have been enrolled. The primary efficacy parameter will be measured by the change in GFR from baseline to week 28 post-randomization. Results: No results are available at this time. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: POTENTIAL PATHOGEN WITH TROPHISM FOR GASTRIC MUCIN Principal Investigator & Institution: Calhoun, David; City College of New York 138Th St and Convent Ave New York, Ny 10031

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Timing: Fiscal Year 2001 Summary: Description (Adapted from Application): A large proportion of a variety of gastric disorders occurring in the industrialized countries have been attributed to infections by Helicobacter pylori. However, some patients suffering these symptoms are culture negative and antibody negative for H. pylori, and these disorders are often attributed to other causes, such as the habitual use of certain drugs. There have been reports of uncharacterized coccoid organisms proposed as the causative agent for gastric inflammation in some patients, and coccoid forms have been detected in gastric biopsy samples. Experimental proof of a role of the coccoid forms in the transmission of infection has not been possible because the coccoid forms could not be cultivated in the laboratory. A coccoid organism was recently cultivated from biopsy material obtained from patients suffering gram gastritis. The prototype isolate, designated strain SL-100, infects the porcine gastric antrum and binds to porcine gastric mucin in vitro. These observations suggest that the coccoid organisms isolated from these gastric patients may be human pathogens. Major goals of the proposed research are to (1) further characterize strain SL-100 and related isolated, and (2) determine the incidence, in this country and abroad, of infection or disease due to this species. The PI will test serum samples from normal and infected individuals to test for antibodies specific for this organism. He currently has clinical collaborators in the New York area, and the initial goal will be to attempt to cultivate the organism from biopsy material and to determine if antibodies directed against specific microbial proteins are correlated with infection or disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF COLITIS BY CYCLOOXYGENASE-2 Principal Investigator & Institution: Wilson, Keith T.; Associate Professor of Medicine; Medicine; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-JAN-2003 Summary: (adapted from the application) Our investigations to date indicate that inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, enzymes which produce high output nitric oxide and prostanoids, respectively, are consistently upregulated in gastrointestinal mucosal inflammation. Further, expression of these genes can regulate inflammatory pathways. We have identified important protective effects of iNOS and COX-2 in specific in vivo and in vitro models. We have also found important differences in the effects of NOS and COX-2 on inflammatory events. We have used mice with targeted deletion of either iNOS or COX-2 to assess mucosal responses to a known and common pathogen, Helicobacter pylori. iNOS deletion had no effect on H. pylori infection or the severity of gastritis. In contrast, COX-2 deletion resulted in a marked exacerbation of both acute and chronic histologic gastritis, resulted in frequent duodenal ulcer formation, which was not present in controls, and increased colonization levels of H. pylori. In addition, the tissues from H. pylori-infected COX-2deficient [COX-2(-/-)] mice exhibited an exacerbation of the Th1-predominant, IL-12driven dysfunctional immune response which characterizes H. pylori gastritis. COX-2 deletion was also associated with increased epithelial injury due to apoptosis. We have also confirmed these alterations of the immune response and apoptosis in vitro. The importance of understanding the role of COX-2 in different forms of GI mucosal inflammation is highlighted by the recent FDA approval and rapid utilization of multiple COX-2 selective inhibitors for treatment of musculoskeletal diseases. Based on our preliminary data and my long-standing interest in inflammatory bowel disease, in the current proposal we will determine the role of COX-2 in several important mouse

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models of colitis. We will use hapten models in which the mucosal immune response has been described, as well as two pertinent colonic infections, namely Helicobacter hepaticus and Citrobacter rodentia. These infection models were selected because of our findings in H. pylori gastritis and the recognition that murine IBD models appear to depend on the presence of enteric bacteria. Our specific aims are to compare COX-2(-/-) vs. (+/+) mice and wild-type mice treated with COX-2 inhibitors vs. placebo and determine the regulatory role of COX-2 in: 1. models of Th1 (TNBS) and Th2 (oxazolone) mediated colitis and 2. Colonic inflammation and injury due to H. hepaticus and C. rodentia. In both aims we will assess the effect of COX-2 on A. gross and microscopic injury; B. I1-12, Th1, pro-inflammatory and Th2 cytokine levels; and C. epithelial apoptosis. These studies are designed to establish these models and the role of COX-2 in the associated diseases, and will serve as the basis for future investigations and funding applications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: RISK FACTORS AND GASTRIC DISEASE IN PEDIATRIC H PYLORI Principal Investigator & Institution: Gold, Benjamin D.; Professor; Pediatrics; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2001; Project Start 30-SEP-1997; Project End 30-SEP-2004 Summary: (taken from the application) Helicobacter pylori (Hp) is the major cause world-wide of chronic-active gastritis, primary duodenal ulcers, and is linked to gastric cancer. Most Hp infections are acquired in childhood; why some individuals develop symptomatic disease and others do not is unclear. Histopathological studies suggest that the degree and type of inflammatory infiltrate in gastroduodenal lesions are significantly different in Hp-infected children compared to adults. However, these differences remain unexplained. Studies of the host immune response following initial Hp infection in childhood and the relationship to Hp virulence factors (i.e., vacA) bolstered by the evaluation of host risk factors for infection are critical to understand the pathogenesis of Hp infection. Our preliminary studies of Hp infection in children developed accurate non-invasive methods for detection of infection and showed a unique gastric mucosal inflammatory response with increased numbers of macrophages. In vitro, we demonstrated the impotence of IL-8 and RANTES chemokines for leukocyte activation and recruitment. Furthermore, we demonstrated a difference in the T-cell responses of Hp-infected versus uninfected patients. Overall hypothesis: among Hp infected children, there are host factors (i.e., ethnicity) and environmental cofactors (i.e., water source) which result in symptomatic disease and children with symptoms will be infected by virulent Hp strains and have a more significant mucosal inflammatory response. Specific aims: 1) determine the host factors and environmental cofactors necessary for symptomatic Hp infection in children. Hpinfected symptomatic endoscopy cases at 4 centers will be compared to age, gender and region-matched Hp-infected asymptomatic controls. 2) characterize the bacterial properties (i.e., phenotype, genotype) associated with pediatric Hp infection. The phenotype and genotype prevalence of Hp isolates obtained from infected cases will be evaluated in comparison to gastroduodenal disease severity. 3) characterize the host inflammatory response of Hp-infected children. The histopathology in comparison to the chemokine and cellular response in the gastric mucosa of infected children will be determined. The proposed research provides a systematic examination of the association between Hp strains and host exposure characteristics and the severity of clinical disease in children. These studies are prerequisite for understanding the host-bacterial

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interaction in initial infection and evolution of gastroduodenal inflammation and overall pathogenesis of Hp. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: STUDY OF THE INTERFACE BETWEEN ALUMINUM HYDROXIDE AND SELECTED MOLECULES OF LIFE Principal Investigator & Institution: Phambu, Nsoki; Johnson C Smith University Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: The long-term goal of our work is to propose a new type of well-defined aluminum hydroxide as a new candidate for a stronger and safer antacid. It will be used to reduce absorption of phosphorus for people with kidney failure, and in the treatment of heartburn, gastritis, and peptic ulcer. The mechanisms of interactions between these well-defined aluminum hydroxides and enzymes, proteins, antibiotics, living cells, and dietary supplements will be investigated in order to recommend this chemical as an antacid. The first hypothesis being evaluated is that this new aluminum hydroxide will release fewer aluminum species into the body; will have a higher acid-neutralizing capability, neutralization velocity, acid consuming capacity, and chemical activity; will have less sodium content compared to the antacids in current use. The second hypothesis is that aluminum compounds may act via direct cytoprotective action or by binding to pathogens. Dissolution testers will be used to evaluate in-vitro release of the drug from solid form as a function of time. Autotitrators will be used to calculate kinetic and conditional stability constants. The ability of infrared and Raman spectroscopies to determine structural and environmental information concerning biomolecules at low concentration in solution make them very powerful bioanalytical and biophysical techniques. In particular, the attenuated total reflection will be used for in-situ and invivo studies. For the first time, an atomic absorption spectrometer will be an indispensable tool in determining the amount of aluminum species released into the body for people taking aluminum-containing antacids. Textural and superficial characterization of the aluminum hydroxide powder will be done by adsorption isotherms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SURVIVAL OF CD4+CD25+ REGULATORY T CELLS Principal Investigator & Institution: Yang, Xiao-Feng F.; Medicine; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Immunoregulatory T cells (Treg cells) have recently been identified as an active mechanism of immune suppression for maintaining T cell tolerance. Among several sets of Treg cells described, CD4+CD25+ Treg cells comprise 5-10% of peripheral CD4+ T cells. These cells, identified in mice and humans, exhibit potent immunoregulatory functions and are considered "professional regulatory T cells". In mouse models, transfer of CD4+CD25+ Treg cells can suppress autoimmune diseases. Treg cells have also been implicated in the regulation of anti-tumor immunity, graftversus-host disease (GVHD) associated with transplantation, and anti-microbial immunity. Thus, the survival or death of CD4+CD25+ Treg cells is likely to be important for immune homeostasis. The mechanisms that govern CD4+CD25+ Treg cell survival remains elusive, although the generation of CD4+CD25+ Treg cells is CD28-dependent. In preliminary studies, several Bcl-x isoforms were identified including a novel Bcl-x isoform, Bcl-x-gamma, which is characterized by a unique C-terminus and inhibits T cell

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apoptosis after TCR ligation. These results, as well as the reports of others, further showed that CD28 co-stimulatory signals can up-regulate the expression of the antiapoptotic proteins Bcl-xL and Bcl-x-gamma, suggesting that Bcl-xgamma and Bcl-xL promote T cell survival after CD3/CD28 co-ligation. This proposal will test the hypothesis that CD4+CD25+ Treg cells have a specific survival program in which Bcl-x genes play an important role through CD28. The corollary hypothesis is that a shift toward survival, rather than apoptosis, in CD4+CD25+ Treg cells may lead to reduced autoimmunity, decreased GVHD, and diminished, deleterious tissue damage associated with anti-microbial immunity. The primary goal of this proposal is to define the survival program of CD4+CD25+ Treg cells, and especially the roles of Bcl-x gene family members. This goal will be pursued through the following specific aims: (1) To determine the function of Bcl-x proteins in CD4+CD25+ Treg cells by analysis of the expression and pro-survival function of these genes in the Treg cells; (2) To determine whether Bcl-x up-regulation is responsible for the anergic state of CD4+CD25+ Treg cells; and (3) To determine the potential for CD4+CD25+ Treg cells, rescued from death by transfection with Bcl-x-gamma and Bcl-xL, to reduce the immunopathology in a mouse model of autoimmune gastritis. Molecular definition of the survival program of CD4+CD25+ Treg cells may lead to development of novel therapeutic strategies for autoimmune diseases, as well as viral and bacterial infections by specifically promoting Treg cell survival. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: TEN YEAR FOLLOW-UP OF DUAL DIAGNOSIS TREATMENT Principal Investigator & Institution: Drake, Robert E.; Director; Psychiatry; Dartmouth College 11 Rope Ferry Rd. #6210 Hanover, Nh 03755 Timing: Fiscal Year 2001; Project Start 01-DEC-1998; Project End 30-NOV-2002 Summary: Although several long-term studies of alcoholism and drug disorders in the general population exist, the long-term course of substance use disorder in patients with severe mental illness (i.e., dual diagnosis) is largely unknown. We have currently followed 223 adults with dual diagnosis in the New Hampshire Dual Diagnosis Study for 6-7 years with minimal attrition (85 percent with nearly complete data). By extending the study to 10 years of follow-up, the proposed project will yield unique data on the pattern, stability, prediction, timing, and correlates of remissions of substance use disorder in this population. We will also be able to examine treatment costs longitudinally. The 10- year data will allow us to chart the course of abstinence, asymptomatic use, remission, and recovery in dual-diagnosis patients. The study will increase our understanding of the relationships among substance disorder, clinical outcomes, and service costs. Longitudinal data will also allow us to examine several hypotheses from the literature regarding the effects of treatment and non-treatment experiences on the course of substance use disorder in this population. Specifically, we will examine response to new medications (such as olanzapine and naltrexone), prolonged intervals of close supervision (e.g., parole, conditional discharge, or living in a supervised setting), participation in peer support groups (such as dual-diagnosis groups or Alcoholics Anonymous), new sources of hope (like marriage, work, or religion), and medical illnesses related to substance disorder (e.g., gastritis). The results will be of interest to policy makers in many states that are replicating the model of integrated dual-diagnosis services that has been used in New Hampshire since 1988. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: THERAPY FOR GASTROINTESTINAL DISORDERS Principal Investigator & Institution: Dial, Elizabeth J.; Agennix, Inc. 8 Greenway Plz, Ste 910 Houston, Tx 77046 Timing: Fiscal Year 2001; Project Start 01-JUL-1999; Project End 30-JUN-2003 Summary: (Applicant's Abstract): The overall goal of this research proposal is to determine the effectiveness of recombinant human lactoferrin (rhLF) for treating gastrointestinal (GI) disorders. This Phase II proposal will focus on the ability of rhLF to treat the 01 side effects of non-steroidal anti-inflammatory drugs (NSAIDs), a class of drugs widely-used for reduction of pain, fever, and inflammation. The adverse GI side effects of ulceration and bleeding limit the usefulness of NSAIDs. Recombinant human lactoferrin, produced in high purity by advanced technological means, has a unique combination of antibiotic, anti-inflammatory. and mucosal healing properties that make it especially useful for the reduction of NSAID toxicity. The specific aims of this proposal are to use animal models to determine: 1) the efficacy of rhLF to prevent acute and chronic NSAID-induced GI side effects; 2) the ability of rhLF to heal GI lesions that are aggravated by NSAIDs; and 3) the mechanism for rhLF protection of the 0! tract in the presence of NSAIDs. Development of this therapeutic potential for rhLF will fulfill a crucial need for a way to safely administer NSAIDs. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TRANSGENIC MODELS OF AUTOIMMUNE GASTRITIS Principal Investigator & Institution: Lorenz, Robinna G.; Associate Professor; Pathology and Immunology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 30-JUN-2002 Summary: The ability to discriminate self from non-self (foreign) is one of the hallmarks of the immune response. Diseases such as autoimmune gastritis (AIG) have been attributed to a breakdown of the normal state of T-cell tolerance to tissue-specific self proteins. Experimental AIG can be initiated by T-cells reactive to the parietal cellspecific antigen-H+/K+-ATPase. This recognition of antigens localized to the gastric parietal cell can explain the damage to the parietal cells in AIG, but it does not provide any explanation for the loss of zymogenic cells or the gain of mucous cells and hyperproliferative cells which are a hallmark of both human and murine disease. We have now generated a novel experimental model of AIG to test our hypothesis that it is a secondary non-antigen specific phage of immune mediators which leads to the striking tissue-specific histopathologic changes that characterize AIG. This model utilizes transgenic mice which express human growth hormone (hGH) exclusively in a subset of the gastric parietal cell population of the stomach and are functionally tolerant to this hGH transgenic reporter. We now demonstrate that this tolerance can be ablated by immunization with hGH, resulting in antigen-specific T cell proliferation, antibody production, and altered epithelial architecture in the zymogenic glands of the stomach. This novel model of gastrointestinal autoimmune disease is ideally suited to investigate to what extent the contribution of T-cells is due to specific immune recognition events versus non antigen-specific events. In this grant application, we propose to: 1) establish a lymphocyte transfer model of AIG in a transgenic mouse by utilizing a T-cell mediated anti-self (transgene) immune response; and 2) define the cellular and molecular mechanisms critical in the direct or indirect effects of T-cells in tissue- specific gastric epithelial damage. These studies should result in a well- defined artificial model of autoimmune gastrointestinal disease, and will lead to a more detailed understanding of

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the cellular and molecular events underlying the tissue-specific pathogenesis of human gastric inflammatory disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: UREASE AND GENE EXPRESSION OF HELICOBACTER PYLORI Principal Investigator & Institution: Mobley, Harry L.; Professor; Microbiology and Immunology; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2001; Project Start 01-AUG-1989; Project End 31-AUG-2004 Summary: Helicobacter pylori, a gram-negative, microaerophilic spiral-shaped bacterium is the most frequently cited etiologic agent of human gastritis and peptic ulceration. This species, whose niche is highly restricted to the gastric mucosa of humans, has adopted a strategy of survival that includes synthesis of urease as its most abundant cellular protein. This enzyme hydrolyzes urea, releasing ammonia which allows colonization of this acid-sensitive organism at low gastric pH. In the previous funding period, we focused on factors that contribute to synthesis of a catalytically active urease. A rough topological model for the insertion of NixA, the high affinity nickel transport protein, into the cytoplasmic membrane has been established and we have identified 12 amino acid residues within the membrane domain that are critical for transport function. Three new urease-modulating factors including F1hA (flagellar biosynthesis/regulatory protein), Lpp (lipoprotein), and Hel (helicase) have been identified using a strategy similar to that used to isolate NixA. Glutamine synthetase which uses ammonia, the product of urea hydrolysis for production of glutamine from glutamate, has been characterized and demonstrated as essential for H. pylori survival. The role of Hpn, the histidine-rich protein, in bismuth sensitivity has also been elucidated. We postulate that NixA and other newly identified proteins are necessary for full activation of H. pylori urease. Since urea hydrolysis is 100 percent-dependent on nickel incorporation into urease, understanding this process could uncover targets for intervention. To address these research areas, we propose to use molecular genetic techniques, protein biochemistry, and bacterial physiology methodology: 1) To determine the mechanism by which urease activity is modulated. 2) To determine the fine structure of NixA, the mechanism of its gene regulation, and its contribution to virulence. 3) To determine the gene products that mediate transport of nickel ions across the inner and outer membranes of H. pylori. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: VALIDATION OF NON-INVASIVE DIAGNOSIS OF HP Principal Investigator & Institution: Snyder, John D.; Pediatrics; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2005 Summary: (provided by applicant): H. pylori causes gastritis, duodenal ulcers and is strongly linked to gastric cancer, but most infections are asymptomatic. No group of GI signs and symptoms have been shown to predict infection or associated disease. At present, no validated non-invasive tests exist to diagnose active H. pylori infection in children. Despite this, many clinicians test for H. pylori in children with gastrointestinal (GI) symptoms and will treat if the infection is "found". The urgent need for a rational approach to treatment of H. pylori in children is underscored by the fact that more than 11 million U.S. children are infected, using a conservative prevalence estimate of 15%. A randomized controlled trial of the effect of H. pylori eradication on GI symptoms in children is clearly needed. Before conducting such a trial, important preliminary

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validation studies are required. This study will test the overall hypothesis: that it is feasible to use non-invasive tests and a symptom assessment instrument (SAI) to determine the presence/absence of H. pylori infections in children with GI symptoms and can be used as diagnostic surrogates for the more invasive endoscopy and biopsy. Since commercial serology tests are not accurate in children, aim 1 will be to determine the feasibility of using the non-invasive 13C urea breath test and stool antigen test, preformed at the time of previously scheduled endoscopy and biopsy, to accurately detest active H. pylori infection in children and thus be considered as potential effective surrogate tests for diagnosis. Preliminary data on the sensitivity, specificity, positive and negative predictive value of these tests will also be compared using the standards for diagnosis established by the FDA. Aim 2 will be to determine the feasibility of using a pediatric gastrointestinal (GI) symptom assessment instrument (SAI), administered at the time of endoscopy, to evaluate GI symptoms of children with symptomatic H. pylori infection. Preliminary data will be obtained on the ability of the SAI to measure the severity of signs and symptoms based on endoscopic and histologic findings. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VASCULAR INFLAMMATION

ENDOTHELIAL

CADHERIN

FUNCTION

IN

Principal Investigator & Institution: Shaw, Sunil K.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 15-MAR-2000; Project End 31-DEC-2002 Summary: Candidate: The applicant has researched mucosal lymphocyte homing and recirculation for the past 8 years. Accomplishments include contributions at both molecular and cell biological levels to interaction of intra- epithelial lymphocytes with epithelial cells. Environment: Brigham and Women's hospital, affiliated with Harvard University, is recognized as a leader in medical research, and will provide a supportive and stimulating environment. The mentor's lab at the Vascular Research Division has access to specialized equipment and tissues necessary for this research. Research: Gastritis, ulceration, celiac sprue, Crohn disease and ulcerative colitis, glomerulonephritis, interstitial nephritis and pyelonephritis are all characterized by the activation of inflammatory cells leading to tissue injury. Leukocyte transmigration and accompanying increased vascular permeability are critical steps during the inflammatory response. Thus, integrity of the organ vasculature is necessary for normal system function, and the endothelial barrier must be breached to lead to tissue injury in these diseases. Although much is known about leukocyte-endothelial adhesion and inflammation, less information is available concerning the role played by endothelial cells in regulating permeability and leukocytes and macromolecules. Vascular endothelial cadherin is located at endothelial adherens and junctions and may regulate monolayer permeability to leukocytes and inflammatory factors. The objective of this proposal is to study the role of VE-cadherin in barrier function and cell growth in vascular endothelial cells by disruption via a dominant negative mechanism. A high efficiency if transfection will be achieved using an adenoviral expression system. This approach will allow specific disruption of one component of the adherens junction, and allow subsequent analysis of endothelial specific functions. These techniques will be used to probe the function of adherens junctions in endothelium from various vascular beds and their contribution to inflammation. The proposed studies are anticipated to allow a better understanding of the role of endothelial adherens junctions in normal and disease conditions, and may lead to novel therapeutic approaches and targets for intervention.

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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 “gastritis” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for gastritis in the PubMed Central database: •

Antrum- and Corpus Mucosa-Infiltrating CD4 + Lymphocytes in Helicobacter pylori Gastritis Display a Th1 Phenotype. by Sommer F, Faller G, Konturek P, Kirchner T, Hahn EG, Zeus J, Rollinghoff M, Lohoff M.; 1998 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108696

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CagA Antibodies in Japanese Children with Nodular Gastritis or Peptic Ulcer Disease. by Kato S, Sugiyama T, Kudo M, Ohnuma K, Ozawa K, Iinuma K, Asaka M, Blaser MJ.; 2000 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=86021

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Characterization of feline Helicobacter pylori strains and associated gastritis in a colony of domestic cats. by Handt LK, Fox JG, Stalis IH, Rufo R, Lee G, Linn J, Li X, Kleanthous H.; 1995 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=228395

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Chronic Atrophic Gastritis in SCID Mice Experimentally Infected with Campylobacter fetus. by Young VB, Dangler CA, Fox JG, Schauer DB.; 2000 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97392

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Clearance of Helicobacter pylori Infection and Resolution of Postimmunization Gastritis in a Kinetic Study of Prophylactically Immunized Mice. by Garhart CA, Redline RW, Nedrud JG, Czinn SJ.; 2002 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128038

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Comparison of CXC Chemokines ENA-78 and Interleukin-8 Expression in Helicobacter pylori-Associated Gastritis. by Rieder G, Einsiedl W, Hatz RA, Stolte M, Enders GA, Walz A.; 2001 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97858

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Composition and Gene Expression of the cag Pathogenicity Island in Helicobacter pylori Strains Isolated from Gastric Carcinoma and Gastritis Patients in Costa Rica. by Occhialini A, Marais A, Urdaci M, Sierra R, Munoz N, Covacci A, Megraud F.; 2001 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98100

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.

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Cure of Helicobacter pylori Infection and Resolution of Gastritis by Adoptive Transfer of Splenocytes in Mice. by Eaton KA, Mefford ME.; 2001 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97983

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Detection of serum antibodies to CagA and VacA and of serum neutralizing activity for vacuolating cytotoxin in patients with Helicobacter pylori-induced gastritis. by Donati M, Moreno S, Storni E, Tucci A, Poli L, Mazzoni C, Varoli O, Sambri V, Farencena A, Cevenini R.; 1997 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=170554

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Differential Induction of Colitis and Gastritis in HLA-B27 Transgenic Rats Selectively Colonized with Bacteroides vulgatus or Escherichia coli. by Rath HC, Wilson KH, Sartor RB.; 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96608

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Direct Evidence by DNA Fingerprinting that Endoscopic Cross-Infection of Helicobacter pylori Is a Cause of Postendoscopic Acute Gastritis. by Sugiyama T, Naka H, Yachi A, Asaka M.; 2000 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=86812

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Discrimination between Cases of Duodenal Ulcer and Gastritis on the Basis of Putative Virulence Factors of Helicobacter pylori. by Yamaoka Y, Souchek J, Odenbreit S, Haas R, Arnqvist A, Boren T, Kodama T, Osato MS, Gutierrez O, Kim JG, Graham DY.; 2002 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130665

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Distribution of Open Reading Frames of Plasticity Region of Strain J99 in Helicobacter pylori Strains Isolated from Gastric Carcinoma and Gastritis Patients in Costa Rica. by Occhialini A, Marais A, Alm R, Garcia F, Sierra R, Megraud F.; 2000 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97705

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Effect of oral immunization with recombinant urease on murine Helicobacter felis gastritis. by Pappo J, Thomas WD Jr, Kabok Z, Taylor NS, Murphy JC, Fox JG.; 1995 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173142

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Effects of Oral Vaccination and Immunomodulation by Cholera Toxin on Experimental Helicobacter pylori Infection, Reinfection, and Gastritis. by Raghavan S, Svennerholm AM, Holmgren J.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128197

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Equally high prevalences of infection with cagA-positive Helicobacter pylori in Chinese patients with peptic ulcer disease and those with chronic gastritis-associated dyspepsia. by Pan ZJ, van der Hulst RW, Feller M, Xiao SD, Tytgat GN, Dankert J, van der Ende A.; 1997 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=229746

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Experimental Helicobacter pylori Infection Induces Antral Gastritis and Gastric Mucosa-Associated Lymphoid Tissue in Guinea Pigs. by Shomer NH, Dangler CA, Whary MT, Fox JG.; 1998 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108246

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Gastritis and Hypergastrinemia Due to Acinetobacter lwoffii in Mice. by Zavros Y, Rieder G, Ferguson A, Merchant JL.; 2002 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=127939

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Healthy Cats Are Commonly Colonized with "Helicobacter heilmannii" That Is Associated with Minimal Gastritis. by Norris CR, Marks SL, Eaton KA, Torabian SZ, Munn RJ, Solnick JV.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=84203

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Helicobacter felis Infection Is Associated with Lymphoid Follicular Hyperplasia and Mild Gastritis but Normal Gastric Secretory Function in Cats. by Simpson KW, Strauss-Ayali D, Scanziani E, Straubinger RK, McDonough PL, Straubinger AF, Chang YF, Domeneghini C, Arebi N, Calam J.; 2000 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97205

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Helicobacter pylori-Associated Gastritis in Mice is Host and Strain Specific. by van Doorn NE, Namavar F, Sparrius M, Stoof J, van Rees EP, van Doorn LJ, VandenbrouckeGrauls CM.; 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96618

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Helicobacter pylori-induced gastritis in the domestic cat. by Fox JG, Batchelder M, Marini R, Yan L, Handt L, Li X, Shames B, Hayward A, Campbell J, Murphy JC.; 1995 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173358

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Helicobacter-associated gastritis in SCID mice. by Blanchard TG, Czinn SJ, Nedrud JG, Redline RW.; 1995 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173118

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Heterogeneity in susceptibility to metronidazole among Helicobacter pylori isolates from patients with gastritis or peptic ulcer disease. by Weel JF, van der Hulst RW, Gerrits Y, Tytgat GN, van der Ende A, Dankert J.; 1996 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=229209

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Importance in diagnosis of gastritis of detection by PCR of the cagA gene in Helicobacter pylori strains isolated from children. by Husson MO, Gottrand F, Vachee A, Dhaenens L, de la Salle EM, Turck D, Houcke M, Leclerc H.; 1995 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=228692

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Induction of Follicular Gastritis following Postthymectomy Autoimmune Gastritis in Helicobacter pylori-Infected BALB/c Mice. by Oshima C, Okazaki K, Matsushima Y, Sawada M, Chiba T, Takahashi K, Hiai H, Katakai T, Kasakura S, Masuda T.; 2000 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97107

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Local Secretory Immunoglobulin A and Postimmunization Gastritis Correlate with Protection against Helicobacter pylori Infection after Oral Vaccination of Mice. by Goto T, Nishizono A, Fujioka T, Ikewaki J, Mifune K, Nasu M.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=116000

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Murine Splenocytes Induce Severe Gastritis and Delayed-Type Hypersensitivity and Suppress Bacterial Colonization in Helicobacter pylori-Infected SCID Mice. by Eaton KA, Ringler SR, Danon SJ.; 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96783

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Positive Result by Serology Indicates Active Helicobacter pylori Infection in Patients with Atrophic Gastritis. by Kokkola A, Rautelin H, Puolakkainen P, Sipponen P, Farkkila M, Haapiainen R, Kosunen TU.; 1998 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=104930

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Prevalence of CagA and VacA Antibodies in Children with Helicobacter pyloriAssociated Peptic Ulcer Compared to Prevalence in Pediatric Patients with Active or Nonactive Chronic Gastritis. by Alarcon T, Martinez MJ, Urruzuno P, Cilleruelo ML, Madruga D, Sebastian M, Domingo D, Sanz JC, Lopez-Brea M.; 2000 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=95968

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Relationship of Anti-Lewis x and Anti-Lewis y Antibodies in Serum Samples from Gastric Cancer and Chronic Gastritis Patients to Helicobacter pylori-Mediated Autoimmunity. by Heneghan MA, McCarthy CF, Janulaityte D, Moran AP.; 2001 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98564

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Role of Activated Protein C in Helicobacter pylori-Associated Gastritis. by Oka S, Gabazza EC, Taguchi Y, Yamaguchi M, Nakashima S, Suzuki K, Adachi Y, Imoto I.; 2000 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97498

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Role of adherence in interleukin-8 induction in Helicobacter pylori-associated gastritis. by Rieder G, Hatz RA, Moran AP, Walz A, Stolte M, Enders G.; 1997 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=175515

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Role of Corpus Gastritis and cagA-Positive Helicobacter pylori Infection in Reflux Esophagitis. by Queiroz DM, Rocha GA, Oliveira CA, Rocha AM, Santos A, Cabral MM, Nogueira AM.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=120632

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Role of Helicobacter pylori cag Region Genes in Colonization and Gastritis in Two Animal Models. by Eaton KA, Kersulyte D, Mefford M, Danon SJ, Krakowka S, Berg DE.; 2001 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98241

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Role of the host in pathogenesis of Helicobacter-associated gastritis: H. felis infection of inbred and congenic mouse strains. by Mohammadi M, Redline R, Nedrud J, Czinn S.; 1996 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173751

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Role of Tumor Necrosis Factor Alpha in Helicobacter pylori Gastritis in Tumor Necrosis Factor Receptor 1-Deficient Mice. by Thalmaier U, Lehn N, Pfeffer K, Stolte M, Vieth M, Schneider-Brachert W.; 2002 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=127975

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Role of vacuolating cytotoxin in gastritis due to Helicobacter pylori in gnotobiotic piglets. by Eaton KA, Cover TL, Tummuru MK, Blaser MJ, Krakowka S.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=175490

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The 60- to 90-kDa Parietal Cell Autoantigen Associated with Autoimmune Gastritis is a [beta] Subunit of the Gastric H+/K+-ATPase (Proton Pump). by Toh B, Gleeson PA, Simpson RJ, Moritz RL, Callaghan JM, Goldkorn I, Jones CM, Martinelli TM, Mu F, Humphris DC, Pettitt JM, Mori Y, Masuda T, Sobieszczuk P, Weinstock J, Mantamadiotis T, Baldwin GS.; 1990 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=54545

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The endotoxin of Helicobacter pylori is a modulator of host-dependent gastritis. by Sakagami T, Vella J, Dixon MF, O'Rourke J, Radcliff F, Sutton P, Shimoyama T, Beagley K, Lee A.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=175469

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Use of serum-specific immunoglobulins A and G for detection of Helicobacter pylori infection in patients with chronic gastritis by immunoblot analysis. by Karvar S, Karch H, Frosch M, Burghardt W, Gross U.; 1997 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230122

The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with gastritis, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “gastritis” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for gastritis (hyperlinks lead to article summaries): •

A case of phlegmonous gastritis diagnosed by echography. Author(s): Staroverov VV, Kisel AT, Sumarokov UA, Kachanova TN. Source: European Journal of Ultrasound : Official Journal of the European Federation of Societies for Ultrasound in Medicine and Biology. 2001 July; 13(3): 197-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11516630&dopt=Abstract

6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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A coordinated cytotoxic effect of IFN-gamma and cross-reactive antibodies in the pathogenesis of Helicobacter pylori gastritis. Author(s): Itoh T, Yoshida M, Chiba T, Kita T, Wakatsuki Y. Source: Helicobacter. 2003 August; 8(4): 268-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950599&dopt=Abstract

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A genetic basis for atrophy: dominant nonresponsiveness and Helicobacter-induced gastritis in F1 hybrid mice. Author(s): Bebb JR, Logan RP. Source: Helicobacter. 2000 December; 5(4): 250-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179992&dopt=Abstract

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A novel method for assessing gastritis in the murine model demonstrates genetically determined variation in response to Helicobacter felis infection. Author(s): Walker MM, Worku M, Coggle S, Thursz MR. Source: Helicobacter. 2002 August; 7(4): 265-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12165035&dopt=Abstract

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A patient with autoimmune hepatitis type I, Addison's disease, atrophic thyroiditis, atrophic gastritis, exocrine pancreatic insufficiency, and heterozygous alpha1antitrypsin deficiency. Author(s): Bergwitz C, Brabant G, Trautwein C, Manns MP. Source: The American Journal of Gastroenterology. 2002 April; 97(4): 1050-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12003388&dopt=Abstract

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A proinflammatory genetic profile increases the risk for chronic atrophic gastritis and gastric carcinoma. Author(s): Machado JC, Figueiredo C, Canedo P, Pharoah P, Carvalho R, Nabais S, Castro Alves C, Campos ML, Van Doorn LJ, Caldas C, Seruca R, Carneiro F, SobrinhoSimoes M. Source: Gastroenterology. 2003 August; 125(2): 364-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891537&dopt=Abstract

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A short-term eradication therapy for Helicobacter pylori acute gastritis. Author(s): Nomura H, Miyake K, Kashiwagi S, Sugiyama T, Asaka M. Source: Journal of Gastroenterology and Hepatology. 2000 December; 15(12): 1377-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11197046&dopt=Abstract

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A study of the concordance between endoscopic gastritis and histological gastritis in an area with a low background prevalence of Helicobacter pylori infection. Author(s): Kaur G, Raj SM. Source: Singapore Med J. 2002 February; 43(2): 090-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11993896&dopt=Abstract

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A unique early gastric tubular adenocarcinoma arising from a pre-existent carcinoid tumor in a patient with a more than 20-year history of type A gastritis: an immunohistochemical and ultrastructural study. Author(s): Kikuyama S, Orikasa H, Oyama R, Yamazaki K. Source: J Submicrosc Cytol Pathol. 2002 April; 34(2): 109-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12117270&dopt=Abstract

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Aberrant CpG island hypermethylation of chronic gastritis, in relation to aging, gender, intestinal metaplasia, and chronic inflammation. Author(s): Kang GH, Lee HJ, Hwang KS, Lee S, Kim JH, Kim JS. Source: American Journal of Pathology. 2003 October; 163(4): 1551-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507661&dopt=Abstract

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Accumulation of mast cells and macrophages in focal active gastritis of patients with Crohn's disease. Author(s): Furusu H, Murase K, Nishida Y, Isomoto H, Takeshima F, Mizuta Y, Hewlett BR, Riddell RH, Kohno S. Source: Hepatogastroenterology. 2002 May-June; 49(45): 639-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063959&dopt=Abstract

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Acid secretion in H pylori associated enlarged fold gastritis. Author(s): Beales IL. Source: Gut. 2000 August; 47(2): 313-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10960279&dopt=Abstract

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Acinetobacter lwoffii infection and gastritis. Author(s): Rathinavelu S, Zavros Y, Merchant JL. Source: Microbes and Infection / Institut Pasteur. 2003 June; 5(7): 651-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12787741&dopt=Abstract

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Acute Aspergillosis gastritis in a case of fatal aplastic anemia. Author(s): Konstantopoulos K, Agapitos E, Komninaka V, Kritsova V, Meletis J, Delaveris E, Loukopoulos D. Source: Scandinavian Journal of Infectious Diseases. 2002; 34(2): 148-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11928854&dopt=Abstract

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Acute diffuse phlegmonous esophagogastritis: radiologic diagnosis. Author(s): Jung C, Choi YW, Jeon SC, Chung WS. Source: Ajr. American Journal of Roentgenology. 2003 March; 180(3): 862-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12591713&dopt=Abstract

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Acute gastritis with hypochlorhydria: report of 35 cases with long term follow up. Author(s): Harford WV, Barnett C, Lee E, Perez-Perez G, Blaser MJ, Peterson WL. Source: Gut. 2000 October; 47(4): 467-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10986205&dopt=Abstract

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Acute ischaemic gastritis--an unrecognized hypoxic phenomenon at extreme altitude? Author(s): Jutley RS, Johnston R, Watt SJ, Phull PS. Source: Wilderness Environ Med. 2002 Fall; 13(3): 234-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12353603&dopt=Abstract

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Adenosine deaminase activity in the gastric mucosa of duodenal ulcer patients in relation to the severity of chronic gastritis and gastric acid secretion. Author(s): Namiot Z, Namiot A, Kemona A, Stasiewicz J, Gorski J. Source: Rocz Akad Med Bialymst. 2001; 46: 309-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11780574&dopt=Abstract

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Alteration of histological gastritis after cure of Helicobacter pylori infection. Author(s): Hojo M, Miwa H, Ohkusa T, Ohkura R, Kurosawa A, Sato N. Source: Alimentary Pharmacology & Therapeutics. 2002 November; 16(11): 1923-32. Review. Erratum In: Aliment Pharmacol Ther. 2003 May 15; 17(10): 1331-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390101&dopt=Abstract

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Altered expression and allelic association of the hypervariable membrane mucin MUC1 in Helicobacter pylori gastritis. Author(s): Vinall LE, King M, Novelli M, Green CA, Daniels G, Hilkens J, Sarner M, Swallow DM. Source: Gastroenterology. 2002 July; 123(1): 41-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12105832&dopt=Abstract

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Analysis of cell damage in Helicobacter pylori-associated gastritis. Author(s): Noguchi K, Kato K, Moriya T, Suzuki T, Saito M, Kikuchi T, Yang J, Imatani A, Sekine H, Ohara S, Toyota T, Shimosegawa T, Sasano H. Source: Pathology International. 2002 February; 52(2): 110-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11940215&dopt=Abstract

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Anti-inflammatory and tissue-protectant drug effects: results from a randomized placebo-controlled trial of gastritis patients at high risk for gastric cancer. Author(s): Fischbach LA, Correa P, Ramirez H, Realpe JL, Collazos T, Ruiz B, Bravo LE, Bravo JC, Casabon AL, Schmidt BA. Source: Alimentary Pharmacology & Therapeutics. 2001 June; 15(6): 831-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11380321&dopt=Abstract

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Antioxidant vitamin supplements do not reduce reactive oxygen species activity in Helicobacter pylori gastritis in the short term. Author(s): Everett SM, Drake IM, White KL, Mapstone NP, Chalmers DM, Schorah CJ, Axon AT. Source: The British Journal of Nutrition. 2002 January; 87(1): 3-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11898768&dopt=Abstract

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Apoptosis in different compartments of antrum and corpus mucosa in chronic Helicobacter pylori gastritis. An 18-year follow-up study. Author(s): Vorobjova T, Maaroos HI, Sipponen P, Villako K, Uibo R. Source: Scandinavian Journal of Gastroenterology. 2001 February; 36(2): 136-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11252404&dopt=Abstract

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Are lymphocytic monoclonality and immunoglobulin heavy chain (IgH) rearrangement premalignant conditions in chronic gastritis? Author(s): Wundisch T, Thiede C, Alpen B, Stolte M, Neubauer A. Source: Microscopy Research and Technique. 2001 June 15; 53(6): 414-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11525259&dopt=Abstract

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Association between gastroesophageal flap valve, reflux esophagitis, Barrett's epithelium, and atrophic gastritis assessed by endoscopy in Japanese patients. Author(s): Fujiwara Y, Higuchi K, Shiba M, Watanabe T, Tominaga K, Oshitani N, Matsumoto T, Arakawa T. Source: Journal of Gastroenterology. 2003; 38(6): 533-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12825128&dopt=Abstract

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Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia. Author(s): Ohkuma K, Okada M, Murayama H, Seo M, Maeda K, Kanda M, Okabe N. Source: Journal of Gastroenterology and Hepatology. 2000 October; 15(10): 1105-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11106088&dopt=Abstract

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Association of the myeloperoxidase -463G-->A polymorphism with development of atrophy in Helicobacter pylori-infected gastritis. Author(s): Roe I, Nam S, Kim J, Shin J, Bang W, Yang M. Source: The American Journal of Gastroenterology. 2002 July; 97(7): 1629-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12135010&dopt=Abstract

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Associations of food-cobalamin malabsorption with ethnic origin, age, Helicobacter pylori infection, and serum markers of gastritis. Author(s): Carmel R, Aurangzeb I, Qian D. Source: The American Journal of Gastroenterology. 2001 January; 96(1): 63-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11197289&dopt=Abstract

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Atrophic body gastritis patients with enterochromaffin-like cell dysplasia are at increased risk for the development of type I gastric carcinoid. Author(s): Annibale B, Azzoni C, Corleto VD, di Giulio E, Caruana P, D'Ambra G, Bordi C, Delle Fave G. Source: European Journal of Gastroenterology & Hepatology. 2001 December; 13(12): 1449-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11742193&dopt=Abstract

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Atrophic corpus gastritis and Helicobacter pylori infection in primary biliary cirrhosis. Author(s): Dohmen K, Shigematsu H, Miyamoto Y, Yamasaki F, Irie K, Ishibashi H. Source: Digestive Diseases and Sciences. 2002 January; 47(1): 162-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11837719&dopt=Abstract

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Atrophic gastritis and intestinal metaplasia in Japan: results of a large multicenter study. Author(s): Asaka M, Sugiyama T, Nobuta A, Kato M, Takeda H, Graham DY. Source: Helicobacter. 2001 December; 6(4): 294-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11843961&dopt=Abstract

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Atrophic gastritis: pathology and endoscopy in the reversibility assessment. Author(s): Rugge M, Cassaro M, Pennelli G, Leandro G, Di Mario F, Farinati F. Source: Gut. 2003 September; 52(9): 1387-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912881&dopt=Abstract

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Autoimmune gastritis: distinct histological and immunohistochemical findings before complete loss of oxyntic glands. Author(s): Torbenson M, Abraham SC, Boitnott J, Yardley JH, Wu TT. Source: Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc. 2002 February; 15(2): 102-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11850538&dopt=Abstract

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B-cell monoclonality in Helicobacter pylori-associated chronic atrophic gastritis. Author(s): Hiyama T, Haruma K, Kitadai Y, Miyamoto M, Tanaka S, Yoshihara M, Sumii K, Shimamoto F, Kajiyama G. Source: Virchows Archiv : an International Journal of Pathology. 2001 March; 438(3): 232-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11315619&dopt=Abstract

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B-cell monoclonality is associated with lymphoid follicles in gastritis. Author(s): Wundisch T, Neubauer A, Stolte M, Ritter M, Thiede C. Source: The American Journal of Surgical Pathology. 2003 July; 27(7): 882-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826879&dopt=Abstract

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Bile reflux gastritis and Barrett's oesophagus: further evidence of a role for duodenogastro-oesophageal reflux? Author(s): Dixon MF, Neville PM, Mapstone NP, Moayyedi P, Axon AT. Source: Gut. 2001 September; 49(3): 359-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11511557&dopt=Abstract

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Bile reflux gastritis and intestinal metaplasia at the cardia. Author(s): Dixon MF, Mapstone NP, Neville PM, Moayyedi P, Axon AT. Source: Gut. 2002 September; 51(3): 351-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12171955&dopt=Abstract

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Carditis is associated with Helicobacter pylori-induced gastritis and not reflux esophagitis. Author(s): Jang TJ, Kim NI, Yang CH. Source: Journal of Clinical Gastroenterology. 2003 January; 36(1): 26-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488703&dopt=Abstract

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Cell proliferation in type C gastritis affecting the intact stomach. Author(s): Dowall JE, Willis P, Prescott R, Lamonby S, Lynch DA. Source: Journal of Clinical Pathology. 2000 October; 53(10): 784-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11064674&dopt=Abstract

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Changing patterns of Helicobacter pylori gastritis in long-standing acid suppression. Author(s): Moayyedi P, Wason C, Peacock R, Walan A, Bardhan K, Axon AT, Dixon MF. Source: Helicobacter. 2000 December; 5(4): 206-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179985&dopt=Abstract

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Characterisation of proton pump antibodies and stomach pathology in gastritis induced by neonatal immunisation without adjuvant. Author(s): Greenwood DL, Sentry JW, Toh BH. Source: Autoimmunity. 2001; 34(2): 81-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11905846&dopt=Abstract

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Characterization of H+,K+-ATPase T cell epitopes in human autoimmune gastritis. Author(s): Bergman MP, Amedei A, D'Elios MM, Azzurri A, Benagiano M, Tamburini C, van der Zee R, Vandenbroucke-Grauls CM, Appelmelk BJ, Del Prete G. Source: European Journal of Immunology. 2003 February; 33(2): 539-45. Erratum In: Eur J Immunol. 2003 April; 33(4): 1139. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645953&dopt=Abstract

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Chronic gastritis and Helicobacter pylori. Author(s): Cave DR. Source: Semin Gastrointest Dis. 2001 July; 12(3): 196-202. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11478752&dopt=Abstract

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Chronic inactive gastritis and coccoid Helicobacter pylori in patients treated for gastroesophageal reflux disease or with H pylori eradication therapy. Author(s): Goldstein NS. Source: American Journal of Clinical Pathology. 2002 November; 118(5): 719-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12428792&dopt=Abstract

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Cigarette smoking promotes atrophic gastritis in Helicobacter pylori-positive subjects. Author(s): Nakamura M, Haruma K, Kamada T, Mihara M, Yoshihara M, Sumioka M, Fukuhara T, Chayama K. Source: Digestive Diseases and Sciences. 2002 March; 47(3): 675-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11911358&dopt=Abstract

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Clinical and endoscopic improvement of lymphocytic gastritis with eradication of Helicobacter pylori. Author(s): Shimoyama Y, Mukai M, Asato Y, Ochiai A. Source: Gastrointestinal Endoscopy. 2001 August; 54(2): 251-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11474405&dopt=Abstract

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Close correlation of intestinal metaplasia and corpus gastritis in patients infected with Helicobacter pylori. Author(s): Meining A, Stolte M. Source: Zeitschrift Fur Gastroenterologie. 2002 August; 40(8): 557-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12297978&dopt=Abstract

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Cobalamin, folate, methylmalonic acid, homocysteine, and gastritis markers in dementia. Author(s): Nagga K, Rajani R, Mardh E, Borch K, Mardh S, Marcusson J. Source: Dementia and Geriatric Cognitive Disorders. 2003; 16(4): 269-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512723&dopt=Abstract

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Coexistence of eosinophilic gastroenteritis and Helicobacter pylori gastritis: causality versus coincidence. Author(s): Muller MJ, Sewell GS. Source: Digestive Diseases and Sciences. 2001 August; 46(8): 1784-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11508683&dopt=Abstract

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Collagenous gastritis associated with lymphocytic gastritis and celiac disease. Author(s): Stancu M, De Petris G, Palumbo TP, Lev R. Source: Archives of Pathology & Laboratory Medicine. 2001 December; 125(12): 1579-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11735694&dopt=Abstract

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Collagenous gastritis: a long-term follow-up with the development of endocrine cell hyperplasia, intestinal metaplasia, and epithelial changes indeterminate for dysplasia. Author(s): Winslow JL, Trainer TD, Colletti RB. Source: American Journal of Clinical Pathology. 2001 November; 116(5): 753-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11710694&dopt=Abstract

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Collagenous gastritis: a report of six cases. Author(s): Lagorce-Pages C, Fabiani B, Bouvier R, Scoazec JY, Durand L, Flejou JF. Source: The American Journal of Surgical Pathology. 2001 September; 25(9): 1174-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11688577&dopt=Abstract

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Combined adenocarcinoma and carcinoid tumor in atrophic gastritis. Author(s): Adhikari D, Conte C, Eskreis D, Urmacher C, Ellen K. Source: Ann Clin Lab Sci. 2002 Fall; 32(4): 422-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458898&dopt=Abstract

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Community acquired acute Helicobacter pylori gastritis. Author(s): Graham DY. Source: Journal of Gastroenterology and Hepatology. 2000 December; 15(12): 1353-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11197042&dopt=Abstract

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Comparison of CXC chemokines ENA-78 and interleukin-8 expression in Helicobacter pylori-associated gastritis. Author(s): Rieder G, Einsiedl W, Hatz RA, Stolte M, Enders GA, Walz A. Source: Infection and Immunity. 2001 January; 69(1): 81-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11119492&dopt=Abstract

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Comparison of precancerous conditions: atrophy and intestinal metaplasia in Helicobacter pylori gastritis among Chinese and Dutch patients. Author(s): Chen XY, van Der Hulst RW, Shi Y, Xiao SD, Tytgat GN, Ten Kate FJ. Source: Journal of Clinical Pathology. 2001 May; 54(5): 367-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11328835&dopt=Abstract

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Compartment analysis of T cell receptor gamma--and immunoglobulin V(H) rearrangements by microdissection in patients with malt lymphoma and chronic gastritis with lymphatic hyperplasia. Author(s): Kraft M, Tiemann M, Riedel S, Gockel H, Kucharzik T, Parwaresch R, Domschike W, Lugering N. Source: Cell Mol Biol (Noisy-Le-Grand). 2002 May; 48(3): 253-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12030429&dopt=Abstract

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Composition and gene expression of the cag pathogenicity island in Helicobacter pylori strains isolated from gastric carcinoma and gastritis patients in Costa Rica. Author(s): Occhialini A, Marais A, Urdaci M, Sierra R, Munoz N, Covacci A, Megraud F. Source: Infection and Immunity. 2001 March; 69(3): 1902-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179371&dopt=Abstract

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Concomitant alterations in intragastric pH and ascorbic acid concentration in patients with Helicobacter pylori gastritis and associated iron deficiency anaemia. Author(s): Annibale B, Capurso G, Lahner E, Passi S, Ricci R, Maggio F, Delle Fave G. Source: Gut. 2003 April; 52(4): 496-501. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12631657&dopt=Abstract

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Corpus gastritis in patients with endoscopic diagnosis of reflux oesophagitis and Barrett's oesophagus. Author(s): Laheij RJ, Van Rossum LG, De Boer WA, Jansen JB. Source: Alimentary Pharmacology & Therapeutics. 2002 May; 16(5): 887-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11966496&dopt=Abstract

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Correlation between Helicobacter pylori infection and food allergy in chronic gastritis. Author(s): Bartuzi Z, Korenkiewicz J, Romanski B. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2000 May-June; 6(3): 530-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11208366&dopt=Abstract

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Correlation of H. pylori density with grading of chronic gastritis. Author(s): Choudhary CK, Bhanot UK, Agarwal A, Garbyal RS. Source: Indian J Pathol Microbiol. 2001 July; 44(3): 325-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12024923&dopt=Abstract

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CT features of acute phlegmonous gastritis. Author(s): Sood BP, Kalra N, Suri S. Source: Clinical Imaging. 2000 September-October; 24(5): 287-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11331158&dopt=Abstract

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Cure of Helicobacter pylori infection and resolution of gastritis by adoptive transfer of splenocytes in mice. Author(s): Eaton KA, Mefford ME. Source: Infection and Immunity. 2001 February; 69(2): 1025-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11159999&dopt=Abstract

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CXC chemokines Gro(alpha)/IL-8 and IP-10/MIG in Helicobacter pylori gastritis. Author(s): Eck M, Schmausser B, Scheller K, Toksoy A, Kraus M, Menzel T, MullerHermelink HK, Gillitzer R. Source: Clinical and Experimental Immunology. 2000 November; 122(2): 192-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11091274&dopt=Abstract

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Cytomegalovirus hemorrhagic gastritis. Author(s): Ruiz AR Jr, Borum ML. Source: Aids Patient Care and Stds. 2001 January; 15(1): 1-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11177582&dopt=Abstract

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Cytoskeletal and kinetic epithelial differences between NSAID gastropathy and Helicobacter pylori gastritis: an immunohistochemical determination. Author(s): Lauwers GY, Furman J, Michael LE, Balis UJ, Kubilis PS. Source: Histopathology. 2001 August; 39(2): 133-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11493329&dopt=Abstract

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Defensin pattern in chronic gastritis: HBD-2 is differentially expressed with respect to Helicobacter pylori status. Author(s): Wehkamp J, Schmidt K, Herrlinger KR, Baxmann S, Behling S, Wohlschlager C, Feller AC, Stange EF, Fellermann K. Source: Journal of Clinical Pathology. 2003 May; 56(5): 352-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12719455&dopt=Abstract

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Detection and analysis of Helicobacter pylori in oral cavity and stomach from chronic gastritis patients. Author(s): Hu W, Cao C, Meng H, Zhang J, Ma D, Zhang L. Source: Zhonghua Yi Xue Za Zhi. 2002 August 10; 82(15): 1037-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12194794&dopt=Abstract

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Detection of Helicobacter pylori colonization in dental plaques and tongue scrapings of patients with chronic gastritis. Author(s): Ozdemir A, Mas MR, Sahin S, Saglamkaya U, Ateskan U. Source: Quintessence Int. 2001 February; 32(2): 131-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12066673&dopt=Abstract

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Diagnosis of atrophic gastritis from a serum sample. Author(s): Sipponen P, Harkonen M, Alanko A, Suovaniemi O. Source: Clin Lab. 2002; 48(9-10): 505-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12389711&dopt=Abstract

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Diagnosis of chronic atrophic gastritis by morphometric image analysis. A new method to overcome the confounding effect of the inflammatory infiltrate. Author(s): Staibano S, Rocco A, Mezza E, De Rosa G, Budillon G, Nardone G. Source: The Journal of Pathology. 2002 September; 198(1): 47-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12210062&dopt=Abstract

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Diagnosis of gastritis by means of a combination of serological analyses. Author(s): Mardh E, Mardh S, Mardh B, Borch K. Source: Clinica Chimica Acta; International Journal of Clinical Chemistry. 2002 June; 320(1-2): 17-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11983196&dopt=Abstract

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Differential expression of laminin isoform (alpha2), integrins (alpha3beta1 and alpha6beta4) and cytokeratin 20 in H. pylori gastritis. Author(s): Sales MG, Nasciutti LE, Lorena DE, Muzzi M, Porto LC. Source: Histology and Histopathology. 2001 October; 16(4): 1021-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11642721&dopt=Abstract

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Discrimination between cases of duodenal ulcer and gastritis on the basis of putative virulence factors of Helicobacter pylori. Author(s): Yamaoka Y, Souchek J, Odenbreit S, Haas R, Arnqvist A, Boren T, Kodama T, Osato MS, Gutierrez O, Kim JG, Graham DY. Source: Journal of Clinical Microbiology. 2002 June; 40(6): 2244-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12037098&dopt=Abstract

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Distribution of open reading frames of plasticity region of strain J99 in Helicobacter pylori strains isolated from gastric carcinoma and gastritis patients in Costa Rica. Author(s): Occhialini A, Marais A, Alm R, Garcia F, Sierra R, Megraud F. Source: Infection and Immunity. 2000 November; 68(11): 6240-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11035731&dopt=Abstract

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Distribution of vacA genotypes in Helicobacter pylori strains isolated from Brazilian adult patients with gastritis, duodenal ulcer or gastric carcinoma. Author(s): Ashour AA, Magalhaes PP, Mendes EN, Collares GB, de Gusmao VR, Queiroz DM, Nogueira AM, Rocha GA, de Oliveira CA. Source: Fems Immunology and Medical Microbiology. 2002 July 12; 33(3): 173-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12110479&dopt=Abstract

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Does eradication of Helicobacter pylori reverse atrophic gastritis or intestinal metaplasia? Data from Japan. Author(s): Satoh K. Source: Gastroenterology Clinics of North America. 2000 December; 29(4): 829-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11190067&dopt=Abstract

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Does Helicobacter pylori gastritis affect motor function of proximal stomach in dyspeptic patients? Author(s): van der Schaar PJ, Straathof JW, Veenendaal RA, Lamers CB, Masclee AA. Source: Digestive Diseases and Sciences. 2001 September; 46(9): 1833-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11575433&dopt=Abstract

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Double gastric infection with Helicobacter pylori and non-Helicobacter pylori bacteria during acid-suppressive therapy: increase of pro-inflammatory cytokines and development of atrophic gastritis. Author(s): Sanduleanu S, Jonkers D, De Bruine A, Hameeteman W, Stockbrugger RW. Source: Alimentary Pharmacology & Therapeutics. 2001 August; 15(8): 1163-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11472319&dopt=Abstract

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Duodenogastric reflux is associated with antral metaplastic gastritis. Author(s): Nakamura M, Haruma K, Kamada T, Mihara M, Yoshihara M, Imagawa M, Kajiyama G. Source: Gastrointestinal Endoscopy. 2001 January; 53(1): 53-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11154489&dopt=Abstract

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Early events in proton pump inhibitor-associated exacerbation of corpus gastritis. Author(s): Graham DY, Opekun AR, Yamaoka Y, Osato MS, el-Zimaity HM. Source: Alimentary Pharmacology & Therapeutics. 2003 January; 17(2): 193-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534403&dopt=Abstract

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Effect of cyclooxygenase-2 inhibition on human Helicobacter pylori gastritis: mechanisms underlying gastrointestinal safety and implications for cancer chemoprevention. Author(s): Scheiman JM, Greenson JK, Lee J, Cryer B. Source: Alimentary Pharmacology & Therapeutics. 2003 June 15; 17(12): 1535-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823157&dopt=Abstract

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Effect of Helicobacter pylori eradication on extent of duodenal gastric metaplasia and grade of gastritis. Author(s): Bago J, Strinic D, Halle ZB, Jandric D, Tomic M, Bilic A, Bago P. Source: Coll Antropol. 2002 December; 26(2): 557-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528281&dopt=Abstract

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Effect of lactoferrin on Helicobacter felis induced gastritis. Author(s): Dial EJ, Lichtenberger LM. Source: Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire. 2002; 80(1): 113-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11908634&dopt=Abstract

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Effects of polyunsaturated fatty acids on atrophic gastritis in a Japanese population. Author(s): Ito Y, Suzuki K, Imai H, Sakamoto H, Nakano H. Source: Cancer Letters. 2001 February 26; 163(2): 171-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11165751&dopt=Abstract

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Electron microscopic evaluation of adhesion of Helicobacter pylori to the gastric epithelial cells in chronic gastritis. Author(s): Chun HJ, Park DK, Park CH, Park JH, Jeen YT, Um SH, Lee SW, Choi JH, Kim CD, Ryu HS, Hyun JH, Chae YS, Uhm CS. Source: Korean J Intern Med. 2002 March; 17(1): 45-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12014212&dopt=Abstract

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Emphysematous gastritis and severe aplastic anemia. Author(s): Gutierrez O, Cantalapiedra A, Tabuyo MI, Del Villar R, Penarrubia MJ, Sales R, Garcia-Frade LJ. Source: The Hematology Journal : the Official Journal of the European Haematology Association / Eha. 2003; 4(1): 82-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692527&dopt=Abstract

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Emphysematous gastritis associated with gastric infarction in a patient with adult polycystic renal disease: CT diagnosis. Author(s): Wong YY, Chu WC. Source: Ajr. American Journal of Roentgenology. 2002 May; 178(5): 1291. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11959754&dopt=Abstract

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Emphysematous gastritis in a hemodialysis patient. Author(s): Yalamanchili M, Cady W. Source: Southern Medical Journal. 2003 January; 96(1): 84-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12602725&dopt=Abstract

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Emphysematous gastritis: case report and literature review. Author(s): Shipman PJ, Drury P. Source: Australasian Radiology. 2001 February; 45(1): 64-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11259977&dopt=Abstract

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Endoscopic nodular gastritis: an endoscopic indicator of high-grade bacterial colonization and severe gastritis in children with Helicobacter pylori. Author(s): Bahu Mda G, da Silveira TR, Maguilnick I, Ulbrich-Kulczynski J. Source: Journal of Pediatric Gastroenterology and Nutrition. 2003 February; 36(2): 21722. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548057&dopt=Abstract

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Endoscopic treatment of gastritis cystica polyposa found in an unoperated stomach. Author(s): Park JS, Myung SJ, Jung HY, Yang SK, Hong WS, Kim JH, Kang GH, Ha HK, Min YI. Source: Gastrointestinal Endoscopy. 2001 July; 54(1): 101-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11427856&dopt=Abstract

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Enterococcus gastritis. Author(s): El-Zimaity HM, Ramchatesingh J, Clarridge JE, Abudayyeh S, Osato MS, Graham DY. Source: Human Pathology. 2003 September; 34(9): 944-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14562292&dopt=Abstract

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Eosinophilic antral gastritis presenting as pyloric obstruction. Author(s): Kulkarni SH, Kshirsagar AY, Wader JV. Source: J Assoc Physicians India. 1998 August; 46(8): 744. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11229292&dopt=Abstract

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Eosinophilic gastritis--an unusual cause of gastric outlet obstruction. Author(s): Chaudhary R, Shrivastava RK, Mukhopadhyay HG, Diwan RN, Das AK. Source: Indian J Gastroenterol. 2001 May-June; 20(3): 110. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11400803&dopt=Abstract

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Epidermal growth factor and its receptor in chronic active gastritis and gastroduodenal ulcer before and after Helicobacter pylori eradication. Author(s): Wong BC, Wang WP, So WH, Shin VY, Wong WM, Fung FM, Liu ES, Hiu WM, Lam SK, Cho CH. Source: Alimentary Pharmacology & Therapeutics. 2001 September; 15(9): 1459-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11552919&dopt=Abstract

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Ethanol-derived microbial production of carcinogenic acetaldehyde in achlorhydric atrophic gastritis. Author(s): Vakevainen S, Mentula S, Nuutinen H, Salmela KS, Jousimies-Somer H, Farkkila M, Salaspuro M. Source: Scandinavian Journal of Gastroenterology. 2002 June; 37(6): 648-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12126241&dopt=Abstract

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Evaluating the profile of selected cytokines in patients with food allergy and chronic gastritis. Author(s): Bartuzi Z, Zbikowska-Gotz M, Romanski B, Sinkiewicz W. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2000 November-December; 6(6): 1128-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11208468&dopt=Abstract

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Expression and cellular localization of COX-1 and -2 in Helicobacter pylori gastritis. Author(s): Chan FK, To KF, Ng YP, Lee TL, Cheng AS, Leung WK, Sung JJ. Source: Alimentary Pharmacology & Therapeutics. 2001 February; 15(2): 187-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11148436&dopt=Abstract

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Expression of cell-cycle related proteins in Helicobacter pylori gastritis and association with gastric carcinoma. Author(s): Polat A, Cinel L, Dusmez D, Aydin O, Egilmez R. Source: Neoplasma. 2002; 49(2): 95-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12088113&dopt=Abstract

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Expression of human beta-defensin 2 (hBD-2) in Helicobacter pylori induced gastritis: antibacterial effect of hBD-2 against Helicobacter pylori. Author(s): Hamanaka Y, Nakashima M, Wada A, Ito M, Kurazono H, Hojo H, Nakahara Y, Kohno S, Hirayama T, Sekine I. Source: Gut. 2001 October; 49(4): 481-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11559643&dopt=Abstract

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Extensive hemorrhagic erosive gastritis associated with acute pancreatitis successfully treated with a somatostatin analog. Author(s): Yabuki K, Maekawa T, Satoh K, Tamasaki Y, Maekawa H, Kudoh K, Aoki E. Source: Journal of Gastroenterology. 2002; 37(9): 737-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12375148&dopt=Abstract

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Extreme hypergastrinemia caused by atrophic gastritis and Helicobacter pylori infection--a case report. Author(s): Huang SM, Lin HH, Wen TY, Hsu YH. Source: Hepatogastroenterology. 2001 July-August; 48(40): 1215-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11490838&dopt=Abstract

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Favourable effect of an acidified milk (LC-1) on Helicobacter pylori gastritis in man. Author(s): Felley CP, Corthesy-Theulaz I, Rivero JL, Sipponen P, Kaufmann M, Bauerfeind P, Wiesel PH, Brassart D, Pfeifer A, Blum AL, Michetti P. Source: European Journal of Gastroenterology & Hepatology. 2001 January; 13(1): 25-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11204805&dopt=Abstract

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Features of gastritis predisposing to gastric adenoma and early gastric cancer. Author(s): Meining A, Riedl B, Stolte M. Source: Journal of Clinical Pathology. 2002 October; 55(10): 770-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12354805&dopt=Abstract

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First endoscopic-histologic follow-up in patients with body-predominant atrophic gastritis: when should it be done? Author(s): Lahner E, Caruana P, D'Ambra G, Ferraro G, Di Giulio E, Delle Fave G, Bordi C, Annibale B. Source: Gastrointestinal Endoscopy. 2001 April; 53(4): 443-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11275884&dopt=Abstract

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Five cases of nodular gastritis and gastric cancer: a possible association between nodular gastritis and gastric cancer. Author(s): Miyamoto M, Haruma K, Yoshihara M, Sumioka M, Nishisaka T, Tanaka S, Inoue K, Chayama K. Source: Dig Liver Dis. 2002 November; 34(11): 819-20. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546520&dopt=Abstract

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Focally enhanced gastritis in children with Crohn's disease and ulcerative colitis. Author(s): Sharif F, McDermott M, Dillon M, Drumm B, Rowland M, Imrie C, Kelleher S, Harty S, Bourke B. Source: The American Journal of Gastroenterology. 2002 June; 97(6): 1415-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12094859&dopt=Abstract

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Follicular gastritis associated with Helicobacter pylori. Author(s): Ma ZQ, Tanizawa T, Nihei Z, Sugihara K, Nakamura K. Source: J Med Dent Sci. 2000 March; 47(1): 39-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12162525&dopt=Abstract

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Fundal gastritis as a potential cause of reflux oesophagitis. Author(s): Newton M, Kamm MA, Talbot IC, Bryan R, Burnham WR. Source: Diseases of the Esophagus : Official Journal of the International Society for Diseases of the Esophagus / I.S.D.E. 2000; 13(1): 56-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11005333&dopt=Abstract

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Gas within the wall of the stomach due to emphysematous gastritis: case report and review. Author(s): van Mook WN, van der Geest S, Goessens ML, Schoon EJ, Ramsay G. Source: European Journal of Gastroenterology & Hepatology. 2002 October; 14(10): 115560. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12362108&dopt=Abstract

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Gastric adenocarcinoma associated with granulomatous gastritis. Case report and review of the literature. Author(s): Bigotti G, Coli A, Magistrelli P, De Ninno M, Antonacci V, Crucitti A, Federico F, Antinori A, Massi G. Source: Tumori. 2002 March-April; 88(2): 163-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12088259&dopt=Abstract

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Gastric carcinoid in a young woman with systemic lupus erythematosus and atrophic autoimmune gastritis. Author(s): Papadimitraki E, de Bree E, Tzardi M, Skordilis P, Kofteridis D, Tsiftsis DD. Source: Scandinavian Journal of Gastroenterology. 2003 May; 38(5): 477-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12795456&dopt=Abstract

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Gastric carcinoid tumors without autoimmune gastritis in Japan: a relationship with Helicobacter pylori infection. Author(s): Sato Y, Iwafuchi M, Ueki J, Yoshimura A, Mochizuki T, Motoyama H, Sugimura K, Honma T, Narisawa R, Ichida T, Asakura H, Van Thiel DH. Source: Digestive Diseases and Sciences. 2002 March; 47(3): 579-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11911346&dopt=Abstract

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Gastric epithelium proliferation in early Hp+ and Hp- gastritis: a flow cytometry study. Author(s): Melato M, Sidari L, Rizzardi C, Kovac D, Stimac D, Baxa P, Jonjic N. Source: Anticancer Res. 2001 March-April; 21(2B): 1347-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11396211&dopt=Abstract

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Gastric inverted hyperplastic polyp. Report of four cases and relation to gastritis cystica profunda. Author(s): Yamashita M, Hirokawa M, Nakasono M, Kiyoku H, Sano N, Fujii M, Koyama T, Yoshida S, Sano T. Source: Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica. 2002 October; 110(10): 717-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12583438&dopt=Abstract

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Gastric juice nitrite and vitamin C in patients with gastric cancer and atrophic gastritis: is low acidity solely responsible for cancer risk? Author(s): Kodama K, Sumii K, Kawano M, Kido T, Nojima K, Sumii M, Haruma K, Yoshihara M, Chayama K. Source: European Journal of Gastroenterology & Hepatology. 2003 September; 15(9): 987-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12923371&dopt=Abstract

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Gastric mucosal cytokine responses in Helicobacter pylori-infected patients with gastritis and peptic ulcers. Association with inflammatory parameters and bacteria load. Author(s): Holck S, Norgaard A, Bennedsen M, Permin H, Norn S, Andersen LP. Source: Fems Immunology and Medical Microbiology. 2003 May 25; 36(3): 175-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738388&dopt=Abstract

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Gastric-juice ammonia assay for diagnosis of Helicobacter pylori infection and the relationship of ammonia concentration to gastritis severity. Author(s): Kearney DJ, Ritchie K, Peacock JS. Source: The American Journal of Gastroenterology. 2000 December; 95(12): 3399-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11151868&dopt=Abstract

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Gastritis and carditis. Author(s): Owen DA. Source: Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc. 2003 April; 16(4): 325-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12692198&dopt=Abstract

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Gastritis and gastric cancer. Asia. Author(s): Kimura K. Source: Gastroenterology Clinics of North America. 2000 September; 29(3): 609-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11030076&dopt=Abstract

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Gastritis and gastric cancer. Western countries. Author(s): Sipponen P, Marshall BJ. Source: Gastroenterology Clinics of North America. 2000 September; 29(3): 579-92, V-Vi. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11030074&dopt=Abstract

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Gastritis. Author(s): Glickman JN, Antonioli DA. Source: Gastrointest Endosc Clin N Am. 2001 October; 11(4): 717-40, Vii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11689363&dopt=Abstract

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Gastritis: classification, pathology, and radiology. Author(s): Chen MY, Ott DJ, Clark HP, Gelfand DW. Source: Southern Medical Journal. 2001 February; 94(2): 184-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11235032&dopt=Abstract

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Gastronomy and gastritis: less-than-fun food. Author(s): Stephenson J. Source: Jama : the Journal of the American Medical Association. 2002 January 2; 287(1): 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11754688&dopt=Abstract

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Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori gastritis. Author(s): Manifold DK, Anggiansah A, Rowe I, Sanderson JD, Chinyama CN, Owen WJ. Source: European Journal of Gastroenterology & Hepatology. 2001 May; 13(5): 535-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11396533&dopt=Abstract

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Georg Ernst Konjetzny, German surgeon of the 20th century: a great pioneer who suggested the bacterial genesis of gastritis and its relationship to peptic ulcer and gastric cancer. Author(s): Massarrat S. Source: The American Journal of Gastroenterology. 2003 August; 98(8): 1899-900. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907359&dopt=Abstract

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Grading of gastritis: an impossible dream? Author(s): Sugano K. Source: Gastric Cancer : Official Journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association. 2002; 5(2): 58-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12132513&dopt=Abstract

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Green tea consumption and chronic atrophic gastritis: a cross-sectional study in a green tea production village. Author(s): Shibata K, Moriyama M, Fukushima T, Kaetsu A, Miyazaki M, Une H. Source: J Epidemiol. 2000 September; 10(5): 310-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11059513&dopt=Abstract

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H(+),K(+)-atpase (proton pump) is the target autoantigen of Th1-type cytotoxic T cells in autoimmune gastritis. Author(s): D'Elios MM, Bergman MP, Azzurri A, Amedei A, Benagiano M, De Pont JJ, Cianchi F, Vandenbroucke-Grauls CM, Romagnani S, Appelmelk BJ, Del Prete G. Source: Gastroenterology. 2001 February; 120(2): 377-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11159878&dopt=Abstract

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Healing of active, non-atrophic autoimmune gastritis by H. pylori eradication. Author(s): Muller H, Rappel S, Wundisch T, Bayerdorffer E, Stolte M. Source: Digestion. 2001; 64(1): 30-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11549834&dopt=Abstract

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Healing of lymphocytic gastritis by eradication of Helicobacter pylori. Author(s): Muller H, Volkholz H, Stolte M. Source: Digestion. 2001; 63(1): 14-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11173895&dopt=Abstract

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Helicobacter heilmannii as causative agent of chronic active gastritis. Author(s): Kaklikkaya N, Ozgur O, Aydin F, Cobanoglu U. Source: Scandinavian Journal of Infectious Diseases. 2002; 34(10): 768-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12477332&dopt=Abstract

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Helicobacter heilmannii gastritis caused by cat to child transmission. Author(s): van Loon S, Bart A, den Hertog EJ, Nikkels PG, Houwen RH, De Schryver JE, Oudshoorn JH. Source: Journal of Pediatric Gastroenterology and Nutrition. 2003 March; 36(3): 407-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604984&dopt=Abstract

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Helicobacter heilmannii gastritis: a histological and immunohistochemical trait. Author(s): Ierardi E, Monno RA, Gentile A, Francavilla R, Burattini O, Marangi S, Pollice L, Francavilla A. Source: Journal of Clinical Pathology. 2001 October; 54(10): 774-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11577125&dopt=Abstract

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Helicobacter pylori and different topographic types of gastritis: treatment response after successful eradication therapy in functional dyspepsia. Author(s): Koskenpato J, Farkkila M, Sipponen P. Source: Scandinavian Journal of Gastroenterology. 2002 July; 37(7): 778-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12190090&dopt=Abstract

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Helicobacter pylori antigens in stool specimens of gastritis children before and after treatment. Author(s): Gosciniak G, Przondo-Mordarska A, Iwanczak B, Blitek A. Source: Journal of Pediatric Gastroenterology and Nutrition. 2003 March; 36(3): 376-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604978&dopt=Abstract

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Helicobacter pylori antigen-specific T-cell responses at gastric level in chronic gastritis, peptic ulcer, gastric cancer and low-grade mucosa-associated lymphoid tissue (MALT) lymphoma. Author(s): D'Elios MM, Amedei A, Del Prete G. Source: Microbes and Infection / Institut Pasteur. 2003 July; 5(8): 723-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814773&dopt=Abstract

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Helicobacter pylori CagA status, mucosal oxidative damage and gastritis phenotype: a potential pathway to cancer? Author(s): Farinati F, Cardin R, Russo VM, Busatto G, Franco M, Rugge M. Source: Helicobacter. 2003 June; 8(3): 227-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752735&dopt=Abstract

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Helicobacter pylori eradication therapy improves atrophic gastritis and intestinal metaplasia: a 5-year prospective study of patients with atrophic gastritis. Author(s): Ito M, Haruma K, Kamada T, Mihara M, Kim S, Kitadai Y, Sumii M, Tanaka S, Yoshihara M, Chayama K. Source: Alimentary Pharmacology & Therapeutics. 2002 August; 16(8): 1449-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12182744&dopt=Abstract

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Helicobacter pylori eradication versus one-year maintenance therapy: effect on relapse and gastritis outcome. Author(s): Mones J, Rodrigo L, Sancho F, Martin L, Boixeda D, Artes MT, Garcia-Cases C; Club Espanol para el Estudio del Helicobacter Pylori. Source: Rev Esp Enferm Dig. 2001 June; 93(6): 372-89. English, Spanish. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11482041&dopt=Abstract

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Helicobacter pylori gastritis in children: endoscopical and histological aspects. Author(s): Serban R, Grigorescu-Sido P, Gheban D, Kiss E. Source: Rom J Gastroenterol. 2002 December; 11(4): 297-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532200&dopt=Abstract

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Helicobacter pylori genotypes and expression of gastritis in erosive gastrooesophageal reflux disease. Author(s): Leodolter A, Wolle K, Peitz U, Ebert M, Gunther T, Kahl S, Malfertheiner P. Source: Scandinavian Journal of Gastroenterology. 2003 May; 38(5): 498-502. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12795459&dopt=Abstract

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Helicobacter pylori infection and erosive gastritis. Author(s): Kate V, Ananthakrishnan N, Badrinath S, Amarnath SK, Balamurugan M, Ratnakar C. Source: J Assoc Physicians India. 1998 May; 46(5): 436-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11273284&dopt=Abstract

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Helicobacter pylori infection and gastric function in patients with fundic atrophic gastritis. Author(s): Tucci A, Poli L, Biasco G, Paparo GF, Tosetti C, Fusaroli P, Sambri V, Donati M, Grigioni W, Labate AM, Stanghellini V, Caletti G. Source: Digestive Diseases and Sciences. 2001 July; 46(7): 1573-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11478512&dopt=Abstract

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Helicobacter pylori status and cell proliferation activity in chronic antral gastritis. Author(s): Gurbuz Y, Muezzinoglu B, Senturk O. Source: Indian J Gastroenterol. 2001 March-April; 20(2): 50-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11305489&dopt=Abstract

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Helicobacter pylori strain and the pattern of gastritis among first-degree relatives of patients with gastric carcinoma. Author(s): Li L, Genta RM, Go MF, Gutierrez O, Kim JG, Graham DY. Source: Helicobacter. 2002 December; 7(6): 349-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12485121&dopt=Abstract

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Helicobacter pylori vacA, iceA, and cagA status and pattern of gastritis in patients with malignant and benign gastroduodenal disease. Author(s): Miehlke S, Yu J, Schuppler M, Frings C, Kirsch C, Negraszus N, Morgner A, Stolte M, Ehninger G, Bayerdorffer E. Source: The American Journal of Gastroenterology. 2001 April; 96(4): 1008-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11316139&dopt=Abstract

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Helicobacter pylori-associated gastritis and the ascorbic acid concentration in gastric juice. Author(s): Rood JC, Ruiz B, Fontham ET, Malcom GT, Hunter FM, Sobhan M, Johnson WD, Correa P. Source: Nutrition and Cancer. 1994; 22(1): 65-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11304911&dopt=Abstract

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Helicobacter pylori-induced gastritis in experimentally infected conventional piglets. Author(s): Poutahidis T, Tsangaris T, Kanakoudis G, Vlemmas I, Iliadis N, Sofianou D. Source: Veterinary Pathology. 2001 November; 38(6): 667-78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11732801&dopt=Abstract

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Hemorrhagic gastritis from topical isopropanol exposure. Author(s): Dyer S, Mycyk MB, Ahrens WR, Zell-Kanter M. Source: The Annals of Pharmacotherapy. 2002 November; 36(11): 1733-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12398569&dopt=Abstract

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High amoxycillin resistance in Helicobacter pylori isolated from gastritis and peptic ulcer patients in western Nigeria. Author(s): Smith SI, Oyedeji KS, Arigbabu AO, Atimomo C, Coker AO. Source: Journal of Gastroenterology. 2001; 36(1): 67-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11211216&dopt=Abstract

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High incidence of B-cell monoclonality in follicular gastritis: a possible association between follicular gastritis and MALT lymphoma. Author(s): Miyamoto M, Haruma K, Hiyama T, Kamada T, Masuda H, Shimamoto F, Inoue K, Chayama K. Source: Virchows Archiv : an International Journal of Pathology. 2002 April; 440(4): 37680. Epub 2002 January 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11956817&dopt=Abstract

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Histological analysis of gastritis and Helicobacter pylori infection in patients with early gastric cancer: a case-control study. Author(s): Fukuda S, Tanaka M, Soma Y, Shimoyama T, Mikami T, Crabtree JE, Saito H, Munakata A, Yoshida Y. Source: Journal of Gastroenterology and Hepatology. 2000 December; 15(12): 1370-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11197045&dopt=Abstract

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Histological patterns of gastritis in H. pylori-infected individuals with a family history of gastric cancer. Author(s): Sepulveda A, Peterson LE, Shelton J, Gutierrez O, Graham DY. Source: The American Journal of Gastroenterology. 2002 June; 97(6): 1365-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12094851&dopt=Abstract

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Histology of gastritis and Helicobacter pylori infection in Thailand: a nationwide study of 3776 cases. Author(s): Atisook K, Kachinthorn U, Luengrojanakul P, Tanwandee T, Pakdirat P, Puapairoj A. Source: Helicobacter. 2003 April; 8(2): 132-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12662381&dopt=Abstract

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Histopathology of gastritis in Helicobacter pylori-infected children from populations at high and low gastric cancer risk. Author(s): Bedoya A, Garay J, Sanzon F, Bravo LE, Bravo JC, Correa H, Craver R, Fontham E, Du JX, Correa P. Source: Human Pathology. 2003 March; 34(3): 206-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673553&dopt=Abstract

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Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy. Author(s): Stolte M. Source: The American Journal of Surgical Pathology. 2001 October; 25(10): 1342-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11688474&dopt=Abstract

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Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy. Author(s): Abraham SC, Singh VK, Yardley JH, Wu TT. Source: The American Journal of Surgical Pathology. 2001 April; 25(4): 500-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11257625&dopt=Abstract

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Immunohistochemical expression of Fhit protein in Helicobacter pylori related chronic gastritis, gastric precancerous lesions and gastric carcinoma: correlation with conventional clinicopathologic parameters. Author(s): Skopelitou AS, Mitselou A, Katsanos KH, Alexopoulou V, Tsianos EV. Source: European Journal of Gastroenterology & Hepatology. 2003 May; 15(5): 515-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702909&dopt=Abstract

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Immunopathogenesis, loss of T cell tolerance and genetics of autoimmune gastritis. Author(s): van Driel IR, Baxter AG, Laurie KL, Zwar TD, La Gruta NL, Judd LM, Scarff KL, Silveira PA, Gleeson PA. Source: Autoimmunity Reviews. 2002 October; 1(5): 290-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848983&dopt=Abstract

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Immunopathology of autoimmune gastritis: lessons from mouse models. Author(s): Alderuccio F, Toh BH. Source: Histology and Histopathology. 2000 July; 15(3): 869-79. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10963131&dopt=Abstract

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Implication of NF-kappaB in Helicobacter pylori-associated gastritis. Author(s): Isomoto H, Mizuta Y, Miyazaki M, Takeshima F, Omagari K, Murase K, Nishiyama T, Inoue K, Murata I, Kohno S. Source: The American Journal of Gastroenterology. 2000 October; 95(10): 2768-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11051346&dopt=Abstract

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Implications of serum pepsinogen I in early endoscopic diagnosis of gastric cancer and dysplasia. Helsinki Gastritis Study Group. Author(s): Varis K, Sipponen P, Laxen F, Samloff IM, Huttunen JK, Taylor PR, Heinonen OP, Albanes D, Sande N, Virtamo J, Harkonen M. Source: Scandinavian Journal of Gastroenterology. 2000 September; 35(9): 950-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11063155&dopt=Abstract

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Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated. Author(s): Ohkusa T, Fujiki K, Takashimizu I, Kumagai J, Tanizawa T, Eishi Y, Yokoyama T, Watanabe M. Source: Annals of Internal Medicine. 2001 March 6; 134(5): 380-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11242498&dopt=Abstract

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In chronic gastritis with atrophy, biopsy sampling underestimates Helicobacter pylori infection. Author(s): Testoni PA, Bonassi U, Bagnolo F, Colombo E, Lella F, Scelsi R. Source: Dig Liver Dis. 2001 November; 33(8): 733-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11785723&dopt=Abstract

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In diffuse atrophic gastritis, routine histology underestimates Helicobacter pylori infection. Author(s): Testoni PA, Bonassi U, Bagnolo F, Colombo E, Scelsi R. Source: Journal of Clinical Gastroenterology. 2002 September; 35(3): 234-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12192199&dopt=Abstract

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In situ correlation of cytokine secretion and apoptosis in Helicobacter pyloriassociated gastritis. Author(s): Lehmann FS, Terracciano L, Carena I, Baeriswyl C, Drewe J, Tornillo L, De Libero G, Beglinger C. Source: American Journal of Physiology. Gastrointestinal and Liver Physiology. 2002 August; 283(2): G481-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121897&dopt=Abstract

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In through the out door: serology for atrophic gastritis. Author(s): Kuipers EJ. Source: European Journal of Gastroenterology & Hepatology. 2003 August; 15(8): 877-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12867797&dopt=Abstract

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Increased cell proliferation in chronic Helicobacter pylori positive gastritis and gastric carcinoma--correlation between immuno-histochemistry and Tv image cytometry. Author(s): Szaleczky E, Pronai L, Molnar B, Berczi L, Feher J, Tulassay Z. Source: Analytical Cellular Pathology : the Journal of the European Society for Analytical Cellular Pathology. 2000; 20(2-3): 131-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11153608&dopt=Abstract

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Increased risk of developing atrophic gastritis in patients infected with CagA+ Helicobacter pylori. Author(s): Sande N, Nikulin M, Nilsson I, Wadstrom T, Laxen F, Harkonen M, Suovaniemi O, Sipponen P. Source: Scandinavian Journal of Gastroenterology. 2001 September; 36(9): 928-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11521982&dopt=Abstract

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Inducible nitric oxide synthase expression before and after eradication of Helicobacter pylori in different forms of gastritis. Author(s): Antos D, Enders G, Rieder G, Stolte M, Bayerdorffer E, Hatz RA. Source: Fems Immunology and Medical Microbiology. 2001 March; 30(2): 127-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11267845&dopt=Abstract

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Infectious emphysematous gastritis in multiple sclerosis. Author(s): Buyl L, Smeets P, Verstraete K. Source: Jbr-Btr. 2003 May-June; 86(3): 148-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12880158&dopt=Abstract

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Interleukin 10 in Helicobacter pylori associated gastritis: immunohistochemical localisation and in vitro effects on cytokine secretion. Author(s): Bodger K, Bromelow K, Wyatt JI, Heatley RV. Source: Journal of Clinical Pathology. 2001 April; 54(4): 285-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11304845&dopt=Abstract

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Interleukin 1beta polymorphisms increase risk of hypochlorhydria and atrophic gastritis and reduce risk of duodenal ulcer recurrence in Japan. Author(s): Furuta T, El-Omar EM, Xiao F, Shirai N, Takashima M, Sugimura H, Sugimurra H. Source: Gastroenterology. 2002 July; 123(1): 92-105. Erratum In: Gastroenterology 2002 September; 123(3): 957. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12105837&dopt=Abstract

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Intragastric ascorbic but not uric acid is depleted in relation with the increased pH in patients with atrophic body gastritis and H. pylori gastritis. Author(s): Capurso G, Ricci R, Panzuto F, Baccini F, Passi S, Di Giulio E, Delle Fave G, Annibale B. Source: Helicobacter. 2003 August; 8(4): 300-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950602&dopt=Abstract

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Intramucosal Helicobacter pylori in the human and murine stomach: its relationship to the inflammatory reaction in human Helicobacter pylori gastritis. Author(s): Min K, Hong SM, Kim KR, Ro JY, Park MJ, Kim JS, Kim JM, Jung HC, Yu E. Source: Pathology, Research and Practice. 2003; 199(1): 1-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12650511&dopt=Abstract

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Is there any relationship between functional dyspepsia and chronic gastritis associated with Helicobacter pylori infection? Author(s): Kyzekove J, Arlt J, Arltova M. Source: Hepatogastroenterology. 2001 March-April; 48(38): 594-602. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11379362&dopt=Abstract

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Jejunal interposition helps prevent reflux gastritis. Author(s): Nakane Y, Michiura T, Inoue K, Habara K, Nakai K, Sato M, Okumura S, Yamamichi K. Source: Hepatogastroenterology. 2002 September-October; 49(47): 1461-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12239967&dopt=Abstract

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Key molecules in metaplastic gastritis: sequential analysis of CDX1/2 homeobox gene expression. Author(s): Chiba T, Seno H. Source: Journal of Gastroenterology. 2002; 37(2): 147-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11871768&dopt=Abstract

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K-ras mutation in helicobacter pylori-associated chronic gastritis in patients with and without gastric cancer. Author(s): Hiyama T, Haruma K, Kitadai Y, Masuda H, Miyamoto M, Tanaka S, Yoshihara M, Shimamoto F, Chayama K. Source: International Journal of Cancer. Journal International Du Cancer. 2002 February 10; 97(5): 562-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11807778&dopt=Abstract

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Level of serum cytokines in biliary gastritis and erosive gastritis with Helicobacter pylori coinfection. Author(s): Cichoz-Lach H, Slomka M, Celinski K, Baczek A. Source: Ann Univ Mariae Curie Sklodowska [med]. 2001; 56: 271-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11977324&dopt=Abstract

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Lewis antigen expression and other pathogenic factors in the presence of atrophic chronic gastritis in a European population. Author(s): Broutet N, Moran A, Hynes S, Sakarovitch C, Megraud F; Eurohepygast Study Group. Source: The Journal of Infectious Diseases. 2002 February 15; 185(4): 503-12. Epub 2002 January 31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11865403&dopt=Abstract

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Light and electron microscopic immunohistochemical investigation on G and D cells in antral mucosa in Helicobacter pylori-related gastritis. Author(s): Tzaneva M. Source: Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Fur Toxikologische Pathologie. 2001 February; 52(6): 523-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11256754&dopt=Abstract

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Long-term Helicobacter pylori infection and the development of atrophic gastritis and gastric cancer in Japan. Author(s): Takahashi S. Source: Journal of Gastroenterology. 2002; 37 Suppl 13: 24-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12109661&dopt=Abstract

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Long-term rebamipide therapy improves Helicobacter pylori-associated chronic gastritis. Author(s): Haruma K, Ito M, Kido S, Manabe N, Kitadai Y, Sumii M, Tanaka S, Yoshihara M, Chayama K. Source: Digestive Diseases and Sciences. 2002 April; 47(4): 862-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11991622&dopt=Abstract

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Low prevalence of latently Epstein-Barr virus-infected cells in chronic gastritis. Author(s): Hungermann D, Muller S, Spieker T, Lisner R, Niedobitek G, Herbst H. Source: Microscopy Research and Technique. 2001 June 15; 53(6): 409-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11525258&dopt=Abstract

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Low serum vitamin B12 is common in coeliac disease and is not due to autoimmune gastritis. Author(s): Dickey W. Source: European Journal of Gastroenterology & Hepatology. 2002 April; 14(4): 425-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11943958&dopt=Abstract

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Lymphocytic gastritis and Helicobacter pylori: reluctant mucosal partners? Author(s): Sundaram KK, Mendall MA. Source: Helicobacter. 2000 December; 5(4): 248-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179991&dopt=Abstract

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Lymphocytic gastritis and protein-losing gastropathy. Author(s): Perardi S, Todros L, Musso A, David E, Repici A, Rizzetto M. Source: Dig Liver Dis. 2000 June-July; 32(5): 422-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11030189&dopt=Abstract

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Macroscopic picture of gastric mucosa in endoscopic examination of patients with chronic gastritis and food allergy. Author(s): Bartuzi Z, Gawronska-Ukleja E, Romanski B. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2000 November-December; 6(6): 1203-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11208480&dopt=Abstract

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Malgun (clear) cell change in Helicobacter pylori gastritis reflects epithelial genomic damage and repair. Author(s): Jang J, Lee S, Jung Y, Song K, Fukumoto M, Gould VE, Lee I. Source: American Journal of Pathology. 2003 April; 162(4): 1203-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12651612&dopt=Abstract

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Metaplasia, intraepithelial neoplasia and early cancer of the stomach are related to dedifferentiated epithelial cells defined by cytokeratin-7 expression in gastritis. Author(s): Kirchner T, Muller S, Hattori T, Mukaisyo K, Papadopoulos T, Brabletz T, Jung A. Source: Virchows Archiv : an International Journal of Pathology. 2001 October; 439(4): 512-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11710638&dopt=Abstract

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Modulation of host antimicrobial peptide (beta-defensins 1 and 2) expression during gastritis. Author(s): Bajaj-Elliott M, Fedeli P, Smith GV, Domizio P, Maher L, Ali RS, Quinn AG, Farthing MJ. Source: Gut. 2002 September; 51(3): 356-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12171956&dopt=Abstract

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Molecular testing of Helicobacter pylori-associated chronic gastritis and premalignant gastric lesions: clinical implications. Author(s): Sepulveda AR. Source: Journal of Clinical Gastroenterology. 2001 May-June; 32(5): 377-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11319306&dopt=Abstract

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mRNA expression of EGF receptor ligands in atrophic gastritis before and after Helicobacter pylori eradication. Author(s): Schiemann U, Konturek J, Assert R, Rembiasz K, Domschke W, Konturek S, Pfeiffer A. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 February; 8(2): Cr53-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11859273&dopt=Abstract

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Mucosal adenosine deaminase activity and gastritis histology: a comparative study of partially resected and intact stomachs. Author(s): Namiot A, Namiot Z, Stasiewicz J, Kemona A, Gorski J. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2003 January; 9(1): Cr24-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552246&dopt=Abstract

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Mucosal production of antigastric autoantibodies in Helicobacter pylori gastritis. Author(s): Faller G, Ruff S, Reiche N, Hochberger J, Hahn EG, Kirchner T. Source: Helicobacter. 2000 September; 5(3): 129-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10971676&dopt=Abstract

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Multifocal atrophic gastritis and gastric carcinoma. Author(s): Faraji EI, Frank BB. Source: Gastroenterology Clinics of North America. 2002 June; 31(2): 499-516. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12134615&dopt=Abstract

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Multiple carcinoids in the stomach with hypergastrinemia and type A gastritis: a case report. Author(s): Aoyagi K, Koufuji K, Yano S, Murakami N, Terasaki Y, Yamasaki Y, Takeda J, Shirouzu K. Source: Kurume Med J. 2000; 47(4): 329-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11197155&dopt=Abstract

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Multiple gastric carcinoid tumors with type A gastritis concomitant with gastric cancer: a case report. Author(s): Kitago M, Inada T, Igarashi S, Mizutani S, Ogata Y, Kubota T. Source: Oncol Rep. 2001 March-April; 8(2): 343-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11182053&dopt=Abstract

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Multiple minute carcinoids in type A gastritis: attempt at 3-D reconstruction. Author(s): Nojiri T, Ikegami M. Source: Pathology International. 2001 July; 51(7): 504-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11472562&dopt=Abstract

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Mutant p53 expression and apoptotic activity of Helicobacter pylori positive and negative gastritis in correlation with the presence of intestinal metaplasia. Author(s): Unger Z, Molnar B, Pronai L, Szaleczky E, Zagoni T, Tulassay Z. Source: European Journal of Gastroenterology & Hepatology. 2003 April; 15(4): 389-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655259&dopt=Abstract

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Nature and extent of gastric lesions in symptomatic Chilean children with Helicobacter pylori-associated gastritis. Author(s): Guiraldes E, Pena A, Duarte I, Trivino X, Schultz M, Larrain F, Espinosa MN, Harris P. Source: Acta Paediatrica (Oslo, Norway : 1992). 2002; 91(1): 39-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11883816&dopt=Abstract

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Neonatal acute haemorrhagic gastritis and antenatal exposure to indomethacin for tocolysis. Author(s): Bolisetty S, Patole S, Koh G, Stalewski H, Whitehall J. Source: Anz Journal of Surgery. 2001 February; 71(2): 122-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11413591&dopt=Abstract

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Nodular gastritis in adults is caused by Helicobacter pylori infection. Author(s): Miyamoto M, Haruma K, Yoshihara M, Hiyama T, Sumioka M, Nishisaka T, Tanaka S, Chayama K. Source: Digestive Diseases and Sciences. 2003 May; 48(5): 968-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12772798&dopt=Abstract

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Non-endoscopic diagnosis of atrophic gastritis with a blood test. Correlation between gastric histology and serum levels of gastrin-17 and pepsinogen I: a multicentre study. Author(s): Vaananen H, Vauhkonen M, Helske T, Kaariainen I, Rasmussen M, TunturiHihnala H, Koskenpato J, Sotka M, Turunen M, Sandstrom R, Ristikankare M, Jussila A, Sipponen P. Source: European Journal of Gastroenterology & Hepatology. 2003 August; 15(8): 885-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12867799&dopt=Abstract

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Non-invasive approach for diagnosing atrophic gastritis using the 13C-bicarbonate breath test. Author(s): Kubo Y, Matsui H, Ninomiya T, Mizukami Y, Onji M. Source: International Journal of Molecular Medicine. 2001 April; 7(4): 381-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11254877&dopt=Abstract

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Non-urease producing Helicobacter pylori in chronic gastritis. Author(s): Ren Z, Pang G, Batey R, Routley D, Russell A, Musicka M, Dunkley M, Beagley K, Clancy R. Source: Aust N Z J Med. 2000 October; 30(5): 578-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11108068&dopt=Abstract

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Omeprazole combined with amoxicillin and clarithromycin in the eradication of Helicobacter pylori in children with gastritis: A prospective randomized doubleblind trial. Author(s): Gottrand F, Kalach N, Spyckerelle C, Guimber D, Mougenot JF, Tounian P, Lenaerts C, Roquelaure B, Lachaux A, Morali A, Dupont C, Maurage C, Husson MO, Barthelemy P. Source: The Journal of Pediatrics. 2001 November; 139(5): 664-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11713443&dopt=Abstract

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Oxyntic mucosa pseudopolyps: a presentation of atrophic autoimmune gastritis. Author(s): Krasinskas AM, Abraham SC, Metz DC, Furth EE. Source: The American Journal of Surgical Pathology. 2003 February; 27(2): 236-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12548171&dopt=Abstract

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p16Ink4a is overexpressed in H. pylori-associated gastritis and is correlated with increased epithelial apoptosis. Author(s): Shirin H, Hibshoosh H, Kawabata Y, Weinstein IB, Moss SF. Source: Helicobacter. 2003 February; 8(1): 66-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12603618&dopt=Abstract

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p53 Codon 72 polymorphism in gastric cancer susceptibility in patients with Helicobacter pylori-associated chronic gastritis. Author(s): Hiyama T, Tanaka S, Kitadai Y, Ito M, Sumii M, Yoshihara M, Shimamoto F, Haruma K, Chayama K. Source: International Journal of Cancer. Journal International Du Cancer. 2002 July 20; 100(3): 304-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12115545&dopt=Abstract

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Pancreatic acinar cell metaplasia in autoimmune gastritis. Author(s): Jhala NC, Montemor M, Jhala D, Lu L, Talley L, Haber MM, Lechago J. Source: Archives of Pathology & Laboratory Medicine. 2003 July; 127(7): 854-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823041&dopt=Abstract

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Patients with endoscopic gastritis and/or duodenitis improve markedly following eradication of Helicobacter pylori, although less so than patients with ulcers. Author(s): Olafsson S, Hatlebakk JG, Berstad A. Source: Scandinavian Journal of Gastroenterology. 2002 December; 37(12): 1386-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12523587&dopt=Abstract

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Peptic ulcer occurrence in follow-up of chronic gastritis in patients with treated and not eradicated CagA-positive Helicobacter pylori infection. Author(s): Carratu R, Iuliano D, Iovene MR, Ferraraccio F, Esposito P, Russo MI, Montella F, Abbate G, Tufano MA. Source: Digestive Diseases and Sciences. 2001 March; 46(3): 581-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11318536&dopt=Abstract

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Phlegmonous gastritis: successful treatment with antibiotics and resolution documented by EUS. Author(s): Hu DC, McGrath KM, Jowell PS, Killenberg PG. Source: Gastrointestinal Endoscopy. 2000 December; 52(6): 793-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11115924&dopt=Abstract

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Phosphorylation of Helicobacter pylori CagA in patients with gastric ulcer and gastritis. Author(s): Cheng KS, Lu MC, Tang HL, Chou FT. Source: Adv Ther. 2002 March-April; 19(2): 85-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12069371&dopt=Abstract

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Possible association of active gastritis, featuring accelerated cell turnover and p53 overexpression, with cancer development at anastomoses after gastrojejunostomy. Comparison with gastroduodenostomy. Author(s): Tanigawa H, Uesugi H, Mitomi H, Saigenji K, Okayasu I. Source: American Journal of Clinical Pathology. 2000 September; 114(3): 354-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10989635&dopt=Abstract

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Post-cholecystectomy alkaline reactive gastritis: a randomized trial comparing sucralfate versus rabeprazole or no treatment. Author(s): Santarelli L, Gabrielli M, Candelli M, Cremonini F, Nista EC, Cammarota G, Gasbarrini G, Gasbarrini A. Source: European Journal of Gastroenterology & Hepatology. 2003 September; 15(9): 975-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12923369&dopt=Abstract

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Prevalence of CagA and VacA antibodies in children with Helicobacter pyloriassociated peptic ulcer compared to prevalence in pediatric patients with active or nonactive chronic gastritis. Author(s): Alarcon T, Martinez MJ, Urruzuno P, Cilleruelo ML, Madruga D, Sebastian M, Domingo D, Sanz JC, Lopez-Brea M. Source: Clinical and Diagnostic Laboratory Immunology. 2000 September; 7(5): 842-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10973467&dopt=Abstract

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Prevalence of subtypes of intestinal metaplasia in the general population and in patients with autoimmune chronic atrophic gastritis. Author(s): Petersson F, Borch K, Franzen LE. Source: Scandinavian Journal of Gastroenterology. 2002 March; 37(3): 262-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11916187&dopt=Abstract

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Primary bile reflux gastritis: diagnosis and surgical treatment. Author(s): Madura JA. Source: American Journal of Surgery. 2003 September; 186(3): 269-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12946831&dopt=Abstract

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Profiling of bacterial flora in gastric biopsies from patients with Helicobacter pyloriassociated gastritis and histologically normal control individuals by temperature gradient gel electrophoresis and 16S rDNA sequence analysis. Author(s): Monstein HJ, Tiveljung A, Kraft CH, Borch K, Jonasson J. Source: Journal of Medical Microbiology. 2000 September; 49(9): 817-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10966230&dopt=Abstract

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Progression of gastric enterochromaffin-like cells growth in Zollinger-Ellison syndrome and atrophic body gastritis patients. Author(s): Delle Fave G, Marignani M, Corleto VD, Angeletti S, D'Ambra G, Ferraro G, D'Adda T, Azzoni C, Jensen RT, Annibale B, Bordi C. Source: Dig Liver Dis. 2002 April; 34(4): 270-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12038811&dopt=Abstract

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Proinflammatory cytokine expression in gastric tissue from children with Helicobacter pylori-associated gastritis. Author(s): Guiraldes E, Duarte I, Pena A, Godoy A, Espinosa MN, Bravo R, Larrain F, Schultz M, Harris P. Source: Journal of Pediatric Gastroenterology and Nutrition. 2001 August; 33(2): 127-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11568511&dopt=Abstract

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Prolonged use of proton pump inhibitors, CagA status, and the outcome of Helicobacter pylori gastritis. Author(s): Gudlaugsdottir S, van Dekken H, Stijnen T, Wilson JH. Source: Journal of Clinical Gastroenterology. 2002 May-June; 34(5): 536-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11960065&dopt=Abstract

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Protective effect of green tea on the risks of chronic gastritis and stomach cancer. Author(s): Setiawan VW, Zhang ZF, Yu GP, Lu QY, Li YL, Lu ML, Wang MR, Guo CH, Yu SZ, Kurtz RC, Hsieh CC. Source: International Journal of Cancer. Journal International Du Cancer. 2001 May 15; 92(4): 600-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11304697&dopt=Abstract

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Protein-losing cytomegalovirus gastritis in a patient with Stevens-Johnson syndrome. Author(s): Yoshioka M, Ishiguro N, Ma X, Kikuta H, Kodaira J, Itoh T, Kobayashi K. Source: Digestion. 2002; 65(4): 234-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12239465&dopt=Abstract

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Pseudomembranous gastritis: a complication from aspergillus infection. Author(s): Sanders DL, Pfeiffer RB, Hashimoto LA, Subramony C, Chen F. Source: The American Surgeon. 2003 June; 69(6): 536-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852516&dopt=Abstract

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Quantitative correlation of Helicobacter pylori stool antigen (HpSA) test with 13Curea breath test (13C-UBT) by the updated Sydney grading system of gastritis. Author(s): Chang MC, Chang YT, Sun CT, Wu MS, Wang HP, Lin JT. Source: Hepatogastroenterology. 2002 March-April; 49(44): 576-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11995501&dopt=Abstract

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Radiographically diagnosed antral gastritis: findings in patients with and without Helicobacter pylori infection. Author(s): Dheer S, Levine MS, Redfern RO, Metz DC, Rubesin SE, Laufer I. Source: The British Journal of Radiology. 2002 October; 75(898): 805-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12381689&dopt=Abstract

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Ratio between serum IL-8 and pepsinogen A/C: a marker for atrophic body gastritis. Author(s): Sanduleanu S, Bruine AD, Biemond I, Stridsberg M, Jonkers D, Lundqvist G, Hameeteman W, Stockbrugger RW. Source: European Journal of Clinical Investigation. 2003 February; 33(2): 147-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12588289&dopt=Abstract

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Reactive oxygen species analysis in gastritis patients and p53 methylation analysis in gastric tumor cell line AGS infected by Helicobacter pylori. Author(s): Rudi J, Bruchhausen B, Kuck D, Stremmel W, von Herbay A, Bauer H, Berger M, Owen RW. Source: Advances in Experimental Medicine and Biology. 2001; 500: 199-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11764935&dopt=Abstract

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Refractory iron-deficiency anaemia due to silent Helicobacter pylori gastritis in children. Author(s): Kostaki M, Fessatou S, Karpathios T. Source: European Journal of Pediatrics. 2003 March; 162(3): 177-9. Epub 2003 January 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655422&dopt=Abstract

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Relation of Helicobacter pylori infection and lifestyle to the risk of chronic atrophic gastritis: a cross-sectional study in Japan. Author(s): Shibata K, Moriyama M, Fukushima T, Une H, Miyazaki M, Yamaguchi N. Source: J Epidemiol. 2002 March; 12(2): 105-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12033520&dopt=Abstract

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Relationship between mast cells/parietal cells and maximal/basal acid output ratio in chronic gastritis. Author(s): Biernacka D, Muszynski J, Tomaszewska A, Moskalewski S. Source: Research in Experimental Medicine. Zeitschrift Fur Die Gesamte Experimentelle Medizin Einschliesslich Experimenteller Chirurgie. 2000 December; 200(1): 35-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11197920&dopt=Abstract

98

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Relationship of anti-Lewis x and anti-Lewis y antibodies in serum samples from gastric cancer and chronic gastritis patients to Helicobacter pylori-mediated autoimmunity. Author(s): Heneghan MA, McCarthy CF, Janulaityte D, Moran AP. Source: Infection and Immunity. 2001 August; 69(8): 4774-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11447150&dopt=Abstract

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Relationship of TT virus and Helicobacter pylori infections in gastric tissues of patients with gastritis. Author(s): Maggi F, Marchi S, Fornai C, Tempestini E, Andreoli E, Lanini L, Vatteroni ML, Bellini M, De Bortoli N, Costa F, Pistello M, Specter S, Bendinelli M. Source: Journal of Medical Virology. 2003 September; 71(1): 160-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12858422&dopt=Abstract

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Residents' corner. Answer to case of the month #86. Emphysematous gastritis. Author(s): Ho DC, Moore LA, Downey DB. Source: Canadian Association of Radiologists Journal = Journal L'association Canadienne Des Radiologistes. 2002 December; 53(5): 309-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12500386&dopt=Abstract

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Review article: after gastritis--an imaginary journey into a Helicobacter-free world. Author(s): Genta RM. Source: Alimentary Pharmacology & Therapeutics. 2002 July; 16 Suppl 4: 89-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12047267&dopt=Abstract

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Risk factors for atrophic chronic gastritis in a European population: results of the Eurohepygast study. Author(s): Eurohepygast Study Group. Source: Gut. 2002 June; 50(6): 779-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12010878&dopt=Abstract

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Risk factors for cancer development in Helicobacter pylori gastritis. Author(s): Nardone G. Source: Dig Liver Dis. 2000 December; 32 Suppl 3: S190-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11245292&dopt=Abstract

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Risk of gastric carcinoma in patients with atrophic gastritis and intestinal metaplasia. Author(s): Kang JY, Finlayson C, Maxwell JD, Neild P. Source: Gut. 2002 December; 51(6): 899. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12427804&dopt=Abstract

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Role of anti-parietal cell antibody in Helicobacter pylori-associated atrophic gastritis: evaluation in a country of high prevalence of atrophic gastritis. Author(s): Ito M, Haruma K, Kaya S, Kamada T, Kim S, Sasaki A, Sumii M, Tanaka S, Yoshihara M, Chayama K. Source: Scandinavian Journal of Gastroenterology. 2002 March; 37(3): 287-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11916190&dopt=Abstract

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Role of corpus gastritis and cagA-positive Helicobacter pylori infection in reflux esophagitis. Author(s): Queiroz DM, Rocha GA, Oliveira CA, Rocha AM, Santos A, Cabral MM, Nogueira AM. Source: Journal of Clinical Microbiology. 2002 August; 40(8): 2849-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12149341&dopt=Abstract

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Role of Helicobacter pylori cag region genes in colonization and gastritis in two animal models. Author(s): Eaton KA, Kersulyte D, Mefford M, Danon SJ, Krakowka S, Berg DE. Source: Infection and Immunity. 2001 May; 69(5): 2902-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11292705&dopt=Abstract

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Role of Helicobacter pylori serology in atrophic body gastritis after eradication treatment. Author(s): Lahner E, Bordi C, Di Giulio E, Caruana P, D'Ambra G, Milione M, Grossi C, Delle Fave G, Annibale B. Source: Alimentary Pharmacology & Therapeutics. 2002 March; 16(3): 507-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11876704&dopt=Abstract

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Role of tumor necrosis factor alpha in Helicobacter pylori gastritis in tumor necrosis factor receptor 1-deficient mice. Author(s): Thalmaier U, Lehn N, Pfeffer K, Stolte M, Vieth M, Schneider-Brachert W. Source: Infection and Immunity. 2002 June; 70(6): 3149-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011009&dopt=Abstract

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Screening markers for chronic atrophic gastritis in Chiapas, Mexico. Author(s): Ley C, Mohar A, Guarner J, Herrera-Goepfert R, Figueroa LS, Halperin D, Parsonnet J. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2001 February; 10(2): 107-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11219766&dopt=Abstract

100 Gastritis

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Seropositivity to Helicobacter pylori heat shock protein 60 is strongly associated with intensity of chronic inflammation, particularly in antrum mucosa: an extension of an 18-year follow-up study of chronic gastritis in Saaremaa, Estonia. Author(s): Vorobjova T, Ananieva O, Maaroos H, Sipponen P, Villako K, Utt M, Nilsson I, Wadstrom T, Uibo R. Source: Fems Immunology and Medical Microbiology. 2001 March; 30(2): 143-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11267848&dopt=Abstract

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Seroprevalence of Helicobacter pylori infection in patients with gastritis and peptic ulcer in western Nigeria. Author(s): Smith SI, Oyedeji KS, Arigbabu AO, Chibututu CC, Anomneze EE, Agbakwuru AE, Ndububa DA, Coker AO. Source: British Journal of Biomedical Science. 2001; 58(2): 97-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11440214&dopt=Abstract

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Serum and plasma concentration of oxidant and antioxidants in patients of Helicobacter pylori gastritis and its correlation with gastric cancer. Author(s): Khanzode SS, Khanzode SD, Dakhale GN. Source: Cancer Letters. 2003 May 30; 195(1): 27-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767508&dopt=Abstract

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Serum anti-Lewis X antibody is associated with VacA seropositivity but not atrophic gastritis in patients with Helicobacter pylori infection. Author(s): Shimoyama T, Fukuda S, Tanaka M, Sugawara N, Kurimoto F, Munakata A. Source: European Journal of Gastroenterology & Hepatology. 2001 March; 13(3): 227-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11293440&dopt=Abstract

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Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study. Author(s): Sipponen P, Ranta P, Helske T, Kaariainen I, Maki T, Linnala A, Suovaniemi O, Alanko A, Harkonen M. Source: Scandinavian Journal of Gastroenterology. 2002 July; 37(7): 785-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12190091&dopt=Abstract

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Severe acute gastritis associated with Helicobacter pylori infection. Author(s): Caletti G, Fusaroli P, Tucci A, Fedrigo M, Bettini G, Roda E. Source: Dig Liver Dis. 2000 January-February; 32(1): 34-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10975753&dopt=Abstract

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Severe gastritis secondary to Epstein-Barr viral infection. Unusual presentation of infectious mononucleosis and associated diffuse lymphoid hyperplasia in gastric mucosa. Author(s): Zhang Y, Molot R. Source: Archives of Pathology & Laboratory Medicine. 2003 April; 127(4): 478-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12683879&dopt=Abstract

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Severity of chronic atrophic gastritis and subsequent gastric cancer occurrence: a 10year prospective cohort study in Japan. Author(s): Inoue M, Tajima K, Matsuura A, Suzuki T, Nakamura T, Ohashi K, Nakamura S, Tominaga S. Source: Cancer Letters. 2000 December 8; 161(1): 105-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11078919&dopt=Abstract

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Short-term changes in Helicobacter pylori gastritis and bulbitis during and after 2 weeks of treatment with omeprazole and amoxicillin in duodenal ulcer patients. Author(s): Plein K, Madisch A, Stolte M, Hotz J. Source: Zeitschrift Fur Gastroenterologie. 2001 July; 39(7): 503-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11505330&dopt=Abstract

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SIALYL-Tn antigen distribution in Helicobacter pylori chronic gastritis in children: an immunohistochemical study. Author(s): Cohen M, Drut R, Cueto Rua E. Source: Pediatric Pathology & Molecular Medicine. 2003 March-April; 22(2): 117-29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12556292&dopt=Abstract

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Significant increase in antigastric autoantibodies in a long-term follow-up study of H. pylori gastritis. Author(s): Vorobjova T, Faller G, Maaroos HI, Sipponen P, Villako K, Uibo R, Kirchner T. Source: Virchows Archiv : an International Journal of Pathology. 2000 July; 437(1): 37-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10963378&dopt=Abstract

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Somatic mutation of mitochondrial DNA in Helicobacter pylori-associated chronic gastritis in patients with and without gastric cancer. Author(s): Hiyama T, Tanaka S, Shima H, Kose K, Kitadai Y, Ito M, Sumii M, Yoshihara M, Shimamoto F, Haruma K, Chayama K. Source: International Journal of Molecular Medicine. 2003 August; 12(2): 169-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851712&dopt=Abstract

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Somatostatin and D cells in patients with gastritis in the course of Helicobacter pylori eradication: a six-month, follow-up study. Author(s): Milutinovic AS, Todorovic V, Milosavljevic T, Micev M, Spuran M, Drndarevic N. Source: European Journal of Gastroenterology & Hepatology. 2003 July; 15(7): 755-66. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811306&dopt=Abstract

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Spontaneous disappearance of Helicobacter pylori antibodies in patients with advanced atrophic corpus gastritis. Author(s): Kokkola A, Kosunen TU, Puolakkainen P, Sipponen P, Harkonen M, Laxen F, Virtamo J, Haapiainen R, Rautelin H. Source: Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica. 2003 June; 111(6): 619-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12969017&dopt=Abstract

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Stem cell factor expressed in human gastric mucosa in relation to mast cell increase in Helicobacter pylori-infected gastritis. Author(s): Bamba N, Nakajima S, Andoh A, Bamba M, Sugihara H, Bamba T, Hattori T. Source: Digestive Diseases and Sciences. 2002 February; 47(2): 274-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11855541&dopt=Abstract

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Study of p53 immunostaining in the gastric epithelium of cagA-positive and cagAnegative Helicobacter pylori gastritis. Author(s): Teh M, Tan KB, Seet BL, Yeoh KG. Source: Cancer. 2002 August 1; 95(3): 499-505. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12209741&dopt=Abstract

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Study on the classification of chronic gastritis at molecular biological level. Author(s): Yin GY, Zhang WN, He XF, Chen Y, Shen XJ. Source: World Journal of Gastroenterology : Wjg. 2003 April; 9(4): 836-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679944&dopt=Abstract

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Symptom score does not correlate with gastritis grade and Helicobacter pylori infection in non ulcer dyspepsia. Author(s): Joshi A, Gupta SD, Ahuja V, Sharma MP. Source: Trop Gastroenterol. 2001 October-December; 22(4): 194-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11963323&dopt=Abstract

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Synergistic interaction between Helicobacter pylori gastritis and diet in gastric cancer. Author(s): Yamaguchi N, Kakizoe T. Source: The Lancet Oncology. 2001 February; 2(2): 88-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11905800&dopt=Abstract

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Ten-year prospective follow-up study on the relationship between Helicobacter pylori infection and progression of atrophic gastritis, particularly assessed by endoscopic findings. Author(s): Sakaki N, Kozawa H, Egawa N, Tu Y, Sanaka M. Source: Alimentary Pharmacology & Therapeutics. 2002 April; 16 Suppl 2: 198-203. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11966542&dopt=Abstract

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The clinical and histological spectrum of esophagitis in pediatrics. Some keys to its links to gastritis. Author(s): Cohen MC, Rua R, Balcarce N, Drut R. Source: Acta Gastroenterol Latinoam. 2001; 31(3): 143-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11577566&dopt=Abstract

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The dynamics of gastritis. Author(s): Kuipers EJ, Grool TA. Source: Current Gastroenterology Reports. 2001 December; 3(6): 509-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11696289&dopt=Abstract

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The effect of Helicobacter pylori eradication on the natural course of atrophic gastritis with dysplasia. Author(s): Kokkola A, Sipponen P, Rautelin H, Harkonen M, Kosunen TU, Haapiainen R, Puolakkainen P. Source: Alimentary Pharmacology & Therapeutics. 2002 March; 16(3): 515-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11876705&dopt=Abstract

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The gastritis connection: prevention and early detection of gastric neoplasms. Author(s): Genta RM. Source: Journal of Clinical Gastroenterology. 2003 May-June; 36(5 Suppl): S44-9; Discussion S61-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702965&dopt=Abstract

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The immunoexpression of Tn, sialyl-Tn and T antigens in chronic active gastritis in relation to Helicobacter pylori infection. Author(s): Barresi G, Giuffre G, Vitarelli E, Grosso M, Tuccari G. Source: Pathology. 2001 August; 33(3): 298-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11523928&dopt=Abstract

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The immuno-inflammatory mechanism for tissue injury in inflammatory bowel disease and Helicobacter pylori-infected chronic active gastritis. Roles of the mucosal immune system. Author(s): Nagura H, Ohtani H, Sasano H, Matsumoto T. Source: Digestion. 2001; 63 Suppl 1: 12-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11173904&dopt=Abstract

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The interaction between vitamin K nutriture and warfarin administration in patients with bacterial overgrowth due to atrophic gastritis. Author(s): Camilo ME, Paiva SA, O'Brien ME, Booth SL, Davidson KW, Sokoll LJ, Sadowski JA, Russell RM. Source: J Nutr Health Aging. 1998; 2(2): 73-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10993569&dopt=Abstract

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The long-term effect of Helicobacter pylori eradication therapy on symptoms in dyspeptic patients with fundic atrophic gastritis. Author(s): Kamada T, Haruma K, Hata J, Kusunoki H, Sasaki A, Ito M, Tanaka S, Yoshihara M. Source: Alimentary Pharmacology & Therapeutics. 2003 July 15; 18(2): 245-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869086&dopt=Abstract

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The long-term effects of cure of Helicobacter pylori infection on patients with atrophic body gastritis. Author(s): Annibale B, Di Giulio E, Caruana P, Lahner E, Capurso G, Bordi C, Delle Fave G. Source: Alimentary Pharmacology & Therapeutics. 2002 October; 16(10): 1723-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12269964&dopt=Abstract

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The prevalence of Helicobacter pylori infection and the pattern of gastritis in Barrett's esophagus. Author(s): Peitz U, Hackelsberger A, Gunther T, Clara L, Malfertheiner P. Source: Digestive Diseases (Basel, Switzerland). 2001; 19(2): 164-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11549827&dopt=Abstract

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The systemic cellular immune response in the Helicobacter pylori-associated duodenal ulcer and chronic antral gastritis. Author(s): Yuceyar H, Saruc M, Kokuludag A, Terzioglu E, Goksel G, Isisag A. Source: Hepatogastroenterology. 2002 July-August; 49(46): 1177-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12143230&dopt=Abstract

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The updated Sydney system: classification and grading of gastritis as the basis of diagnosis and treatment. Author(s): Stolte M, Meining A. Source: Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie. 2001 September; 15(9): 591-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11573102&dopt=Abstract

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Topographic mapping of collagenous gastritis. Author(s): Freeman HJ. Source: Canadian Journal of Gastroenterology = Journal Canadien De Gastroenterologie. 2001 July; 15(7): 475-8. Review. English, French. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11493952&dopt=Abstract

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Treatment of Helicobacter pylori gastritis improves dyspeptic symptoms in children. Author(s): Uc A, Chong SK. Source: Journal of Pediatric Gastroenterology and Nutrition. 2002 March; 34(3): 281-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11964952&dopt=Abstract

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Treatment of Helicobacter pylori gastritis improves dyspeptic symptoms in Turkish children. Author(s): Ozgenc F, Akman SA, Arikan C, Alkanat MB, Aydogdu S, Yagci RV. Source: Journal of Pediatric Gastroenterology and Nutrition. 2003 April; 36(4): 507. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12658048&dopt=Abstract

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Treatment of Helicobacter pylori in patients with lymphocytic gastritis. Author(s): Niemela S, Karttunen TJ, Kerola T. Source: Hepatogastroenterology. 2001 July-August; 48(40): 1176-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11490827&dopt=Abstract

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Treatment with a proton pump inhibitor promotes corpus gastritis in patients with Helicobacter pylori-infected antrum-predominant gastritis. Author(s): Suzuki M, Suzuki H, Kitahora T, Miyazawa M, Nagahashi S, Suzuki K, Ishii H. Source: Alimentary Pharmacology & Therapeutics. 2002 January; 16(1): 159-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11856091&dopt=Abstract

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Trend toward a reduced prevalence of Helicobacter pylori infection, chronic gastritis, and gastric cancer in Japan. Author(s): Haruma K. Source: Gastroenterology Clinics of North America. 2000 September; 29(3): 623-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11030077&dopt=Abstract

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Two cases of cancer in the remnant stomach derived from gastritis cystica polyposa. Author(s): Aoyagi K, Koufuji K, Yano S, Murakami N, Terasaki Y, Yamasaki Y, Takeda J, Tanaka M, Shirouzu K. Source: Kurume Med J. 2000; 47(3): 243-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11059228&dopt=Abstract

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Two-thirds of atrophic body gastritis patients have evidence of Helicobacter pylori infection. Author(s): Annibale B, Negrini R, Caruana P, Lahner E, Grossi C, Bordi C, Delle Fave G. Source: Helicobacter. 2001 September; 6(3): 225-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11683925&dopt=Abstract

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Ulcer and gastritis. Author(s): Wu JC, Sung JJ. Source: Endoscopy. 2002 February; 34(2): 104-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11822005&dopt=Abstract

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Ulcer and gastritis. Author(s): Leung WK, Graham DY. Source: Endoscopy. 2001 January; 33(1): 8-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11204993&dopt=Abstract

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Ulcers and gastritis. Author(s): Kashiwagi H. Source: Endoscopy. 2003 January; 35(1): 9-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12510220&dopt=Abstract

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Ultrastructure and molecular biological changes of chronic gastritis, gastric cancer and gastric precancerous lesions: a comparative study. Author(s): Yin GY, Zhang WN, Shen XJ, Chen Y, He XF. Source: World Journal of Gastroenterology : Wjg. 2003 April; 9(4): 851-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12679947&dopt=Abstract

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Update on the pathologic approach to the diagnosis of gastritis, gastric atrophy, and Helicobacter pylori and its sequelae. Author(s): Sipponen P. Source: Journal of Clinical Gastroenterology. 2001 March; 32(3): 196-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11246343&dopt=Abstract

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Use of direct Gram stain of stomach biopsy as a rapid screening method for detection of Helicobacter pylori from peptic ulcer and gastritis patients. Author(s): Oyedeji KS, Smith SI, Arigbabu AO, Coker AO, Ndububa DA, Agbakwuru EA, Atoyebi OA. Source: Journal of Basic Microbiology. 2002; 42(2): 121-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11981876&dopt=Abstract

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Variation in serum pepsinogens with severity and topography of Helicobacter pyloriassociated chronic gastritis in dyspeptic patients referred for endoscopy. Author(s): Bodger K, Wyatt JI, Heatley RV. Source: Helicobacter. 2001 September; 6(3): 216-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11683924&dopt=Abstract

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Varicella zoster gastritis 3 years after bone marrow transplantation for treatment of acute leukemia. Author(s): Rivera-Vaquerizo PA, Gomez-Garrido J, Vicente-Gutierrez M, BlascoColmenarejo M, Mayor-Lopez J, Perez-Flores R. Source: Gastrointestinal Endoscopy. 2001 June; 53(7): 809-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11375599&dopt=Abstract

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CHAPTER 2. NUTRITION AND GASTRITIS Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and gastritis.

Finding Nutrition Studies on Gastritis 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 “gastritis” (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 “gastritis” (or a synonym): •

47 cases of chronic atrophic gastritis treated with the modality of depressing the upward adverse flow of qi. Source: Xie, Q S J-Tradit-Chin-Med. 1989 December; 9(4): 285-6 0254-6272

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A placebo controlled trial of bismuth salicylate in Helicobacter pylori associated gastritis. Author(s): Department of Pathology, Pakistan Medical Research Council, Karachi. Source: Kazi, J I Jafarey, N A Alam, S M Zuberi, S J Kazi, A M Qureshi, H Ahmed, W JPak-Med-Assoc. 1990 July; 40(7): 154-6 0030-9982

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A prospective study of atrophic gastritis and stomach cancer risk. Author(s): Division of Epidemiology, Aichi Cancer Center Hospital, Nagoya. Source: Kato, I Tominaga, S Ito, Y Kobayashi, S Yoshii, Y Matsuura, A Kameya, A Kano, T Ikari, A Jpn-J-Cancer-Res. 1992 November; 83(11): 1137-42 0910-5050

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Atrophic gastritis and vitamin C status in two towns with different stomach cancer death-rates. Author(s): MRC Epidemiology Unit, Cardiff, UK. Source: Burr, M L Samloff, I M Bates, C J Holliday, R M Br-J-Cancer. 1987 August; 56(2): 163-7 0007-0920

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Campylobacter pylori-associated gastritis: attempts to eradicate the bacteria by various antibiotics and anti-ulcer regimens. Source: Glupczynski, Y Burette, A Nyst, J F De Prez, C De Koster, E Deltenre, M ActaGastroenterol-Belg. 1988 Jul-October; 51(4-5): 329-37 0001-5644

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Classification of gastritis--yesterday, today and tomorrow. Author(s): Department of Cellular Pathology, Northwick Park & St. Mark's Hospitals, Middlesex, U.K. Source: Price, A B Verh-Dtsch-Ges-Pathol. 1999; 8352-5 0070-4113

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Clinical and experimental studies of chronic gastritis in patients with qi-deficiency of spleen. Source: Jin, J S Zhao, Z H Wei, B H Hu, Y F Chen, L H Li, W S He, J R Liang, D Y Zheng, M Z Li, J D et al. J-Tradit-Chin-Med. 1989 December; 9(4): 297-8 0254-6272

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Collagenous gastritis associated with lymphocytic gastritis and celiac disease. Author(s): Department of Pathology and Laboratory Medicine, Roger Williams Medical Center, Boston University, Providence, RI 02908, USA. Source: Stancu, M De Petris, G Palumbo, T P Lev, R Arch-Pathol-Lab-Med. 2001 December; 125(12): 1579-84 0003-9985

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Dementia patients with low serum cobalamin concentration: relationship to atrophic gastritis. Author(s): Department of Psychiatry and Neurochemistry, St. Jorgen Hospital, Goteborg, Sweden. Source: Regland, B Gottfries, C G Lindstedt, G Aging-(Milano). 1992 March; 4(1): 35-41 0394-9532

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Duodenogastric reflux is associated with antral metaplastic gastritis. Author(s): Department of Internal Medicine, Hiroshima Prefectural Hiroshima Hospital, Hiroshima, Japan. Source: Nakamura, M Haruma, K Kamada, T Mihara, M Yoshihara, M Imagawa, M Kajiyama, G Gastrointest-Endosc. 2001 January; 53(1): 53-9 0016-5107

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Eosinophilic gastritis due to Anisakis: a case report. Author(s): Department of Allergology and Clinical Immunology, University Clinic of Navarra, Pamplona, Navarra, 31080, Espana. Source: Esteve, C Resano, A Diaz Tejeiro, P Fernandez Benitez, M AllergolImmunopathol-(Madr). 2000 Jan-February; 28(1): 21-3 0301-0546

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Gastrin content in the blood serum on an empty stomach and after food intake in patients suffering from peptic ulcers and chronic gastritis with secretory failure. Source: Valenkevich, L.N. Zaichik, A.Sh. Vopr-Pitan. Moskva : “Meditsina”. Nov/December 1982. (6) page 34-36. 0042-8833

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Green tea consumption and chronic atrophic gastritis: a cross-sectional study in a green tea production village. Author(s): Department of Public Health, School of Medicine, Fukuoka University, Japan. Source: Shibata, K Moriyama, M Fukushima, T Kaetsu, A Miyazaki, M Une, H JEpidemiol. 2000 September; 10(5): 310-6 0917-5040

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Helicobacter pylori infection on the risk of stomach cancer and chronic atrophic gastritis. Author(s): Department of Epidemiology, School of Public Health, University of California, Los Angeles 90095-1772, USA. [email protected] Source: Zhang, Z F Kurtz, R C Klimstra, D S Yu, G P Sun, M Harlap, S Marshall, J R Cancer-Detect-Prevolume 1999; 23(5): 357-67 0361-090X

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Helicobacter pylori, gastritis, and ulcers in pediatrics. Author(s): University of Wisconsin Hospitals, Madison. Source: Judd, R H Adv-Pediatr. 1992; 39283-306 0065-3101

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Marked enhancement by fish meal of Helicobacter pylori-induced gastritis in Mongolian gerbils. Author(s): Cancer Prevention Division, National Cancer Center Research Institute, Chuo-ku, Tokyo 104-0045, Japan. Source: Tanigawa, T Kawamori, T Iimuro, M Ohta, T Higuchi, K Arakawa, T Sugimura, T Wakabayashi, K Jpn-J-Cancer-Res. 2000 August; 91(8): 769-73 0910-5050

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Neonatal acute haemorrhagic gastritis and antenatal exposure to indomethacin for tocolysis. Author(s): Neonatal Intensive Care Unit, Kirwan Hospital for Women, Townsville, Queensland, Australia. [email protected] Source: Bolisetty, S Patole, S Koh, G Stalewski, H Whitehall, J ANZ-J-Surg. 2001 February; 71(2): 122-3 1445-1433

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Primary biliary cirrhosis associated with type A gastritis and chronic thyroiditis. Author(s): Department of Gastroenterology, Saiseikai Kanazawa Hospital, Kanazawa, Japan. Source: Wakabayashi, T Ohno, H Hayakawa, Y Kawashima, A Sawabu, N JGastroenterol. 1999 June; 34(3): 415-9 0944-1174

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Short- and long-term treatment with rosaprostol of patients with gastritis. Author(s): Department of Medical Pathology, I School of Medicine and Surgery, University of Naples, Italy. Source: Di Simone, A Riegler, G Esposito, P Ciani, D Int-J-Clin-Pharmacol-Res. 1988; 8(3): 217-21 0251-1649

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Synergistic interaction between Helicobacter pylori gastritis and diet in gastric cancer. Author(s): Cancer Information and Epidemiology Division, National Cancer Center Research Institute, Tokyo, Japan. [email protected] Source: Yamaguchi, N Kakizoe, T Lancet-Oncol. 2001 February; 2(2): 88-94 1470-2045

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TCM differential treatment of 57 cases of chronic gastritis complicated by ulcerative colitis. Author(s): Second Affiliated Hospital, Guangxi TCM College, Nanning. Source: Meng, M J-Tradit-Chin-Med. 1999 March; 19(1): 10-5 0254-6272

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The interaction between vitamin K nutriture and warfarin administration in patients with bacterial overgrowth due to atrophic gastritis. Author(s): Jean Mayer, United States Department of Agriculture, Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA. Source: Camilo, M E Paiva, S A O'Brien, M E Booth, S L Davidson, K W Sokoll, L J Sadowski, J A Russell, R M J-Nutr-Health-Aging. 1998; 2(2): 73-8 1279-7707

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Traditional Chinese treatment of chronic gastritis with gastric dysplasia--a clinical analysis of 70 cases. Source: Zhang, W Y Shen, L H Xu, H Wang, X L Xu, Y R J-Tradit-Chin-Med. 1989 June; 9(2): 79-83 0254-6272

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Treatment of 910 cases of atrophic gastritis with wei you decoction. Author(s): Qindao Navy Sanatorium, PLA. Source: Ma, S Liang, F Wang, S Dong, S Yin, S Xue, C Lin, Z J-Tradit-Chin-Med. 1990 September; 10(3): 168-71 0254-6272

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Treatment of Campylobacter pylori gastritis: a pilot study using pirenzepine dihydrochloride (Gastrozepin) and three formulations of colloidal bismuth subcitrate (De-Nol). Author(s): Department of Microbiology, Middlemore Hospital, Otahuhu, Auckland. Source: Morris, A Brown, P Ali, M R Lane, M Palmer, R N-Z-Med-J. 1988 October 26; 101(856 Pt 1): 651-4 0028-8446

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

Vitamins Vitamin A Source: Healthnotes, Inc.; www.healthnotes.com Vitamin B12 Source: Healthnotes, Inc.; www.healthnotes.com Vitamin B12 Source: Prima Communications, Inc.www.personalhealthzone.com Vitamin B3 Source: Healthnotes, Inc.; www.healthnotes.com Vitamin C Source: Healthnotes, Inc.; www.healthnotes.com

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Minerals Betaine Hydrochloride Source: Healthnotes, Inc.; www.healthnotes.com Zinc Source: Healthnotes, Inc.; www.healthnotes.com

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Food and Diet Chocolate Source: Healthnotes, Inc.; www.healthnotes.com Coffee Source: Healthnotes, Inc.; www.healthnotes.com Low-salt Diet Source: Healthnotes, Inc.; www.healthnotes.com Tea Source: Healthnotes, Inc.; www.healthnotes.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND GASTRITIS Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to gastritis. 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 gastritis 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 “gastritis” (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 gastritis: •

47 cases of chronic atrophic gastritis treated with the modality of depressing the upward adverse flow of qi. Author(s): Xie QS. Source: J Tradit Chin Med. 1989 December; 9(4): 285-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2630819&dopt=Abstract

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A double-blind study of effectiveness of hericium erinaceus pers therapy on chronic atrophic gastritis. A preliminary report. Author(s): Xu CP, Liu WW, Liu FX, Chen SS, Liao FQ, Xu Z, Jiang LG, Wang CA, Lu XH. Source: Chinese Medical Journal. 1985 June; 98(6): 455-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3932005&dopt=Abstract

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A study of Helicobacterium pylori and prevention and treatment of chronic atrophic gastritis. Author(s): Zhang L, Yang L, Zheng X. Source: J Tradit Chin Med. 1997 March; 17(1): 3-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10437235&dopt=Abstract

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Ascorbic acid and total vitamin C concentrations in plasma, gastric juice, and gastrointestinal mucosa: effects of gastritis and oral supplementation. Author(s): Waring AJ, Drake IM, Schorah CJ, White KL, Lynch DA, Axon AT, Dixon MF. Source: Gut. 1996 February; 38(2): 171-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8801192&dopt=Abstract

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Clinical and experimental studies of chronic gastritis in patients with qi-deficiency of spleen. Author(s): Jin JS, Zhao ZH, Wei BH, Hu YF, Chen LH, Li WS, He JR, Liang DY, Zheng MZ, Li JD, et al. Source: J Tradit Chin Med. 1989 December; 9(4): 297-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2630823&dopt=Abstract

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Clinical observation on the method of supplementing qi, clearing away heat and promoting blood circulation for treating 53 cases of gastritis related to pyrolic Helicobacterium. Author(s): Wang Y. Source: J Tradit Chin Med. 2003 June; 23(2): 83-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12875059&dopt=Abstract

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Comparative observations on the types of atrophic gastritis and biopsy pathology of gastric mucosa. Author(s): Ren H, Liu W, Niu L, Lu G, Lu Y. Source: J Tradit Chin Med. 1994 December; 14(4): 303-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7877344&dopt=Abstract

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Effect of beta-carotene supplementation on the activity of ornithine decarboxylase (ODC) in stomach mucosa of patients with chronic atrophic gastritis. Author(s): Bukin YV, Zaridze DG, Draudin-Krylenko VA, Orlov EN, Sigacheva NA, Dawei F, Kurtzman MYa, Schlenskaya IN, Gorbacheva ON, Nechipai AM, et al. Source: European Journal of Cancer Prevention : the Official Journal of the European Cancer Prevention Organisation (Ecp). 1993 January; 2(1): 61-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8428179&dopt=Abstract

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Effect of liu-junzi-tang on the symptom of bitter taste in patients with chronic gastritis. Author(s): Motoo Y, Watanabe H, Okai T, Sawabu N.

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Source: The American Journal of Chinese Medicine. 1995; 23(2): 153-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7572776&dopt=Abstract •

Effect of N alpha-methyl-histamine on acid secretion in isolated cultured rabbit parietal cells: implications for Helicobacter pylori associated gastritis and gastric physiology. Author(s): Beales IL, Calam J. Source: Gut. 1997 January; 40(1): 14-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9155569&dopt=Abstract

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Effects of pH on mineral-phytate, protein-mineral-phytate, and mineral-fiber interactions. Possible consequences of atrophic gastritis on mineral bioavailability from high-fiber foods. Author(s): Champagne ET. Source: Journal of the American College of Nutrition. 1988 December; 7(6): 499-508. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2852683&dopt=Abstract

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Effects of polyunsaturated fatty acids on atrophic gastritis in a Japanese population. Author(s): Ito Y, Suzuki K, Imai H, Sakamoto H, Nakano H. Source: Cancer Letters. 2001 February 26; 163(2): 171-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11165751&dopt=Abstract

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Effects of the clearing-heat and nourishing-stomach method in the treatment of chronic gastritis with positive Campylobacter pylori. Author(s): Wu D, Sun B, Sun L, Chai K, Ye C. Source: J Tradit Chin Med. 1995 March; 15(1): 28-30. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7783456&dopt=Abstract

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Gastric cancer and premalignant lesions in atrophic gastritis: a controlled trial on the effect of supplementation with alpha-tocopherol and beta-carotene. The Helsinki Gastritis Study Group. Author(s): Varis K, Taylor PR, Sipponen P, Samloff IM, Heinonen OP, Albanes D, Harkonen M, Huttunen JK, Laxen F, Virtamo J. Source: Scandinavian Journal of Gastroenterology. 1998 March; 33(3): 294-300. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9548624&dopt=Abstract

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Gastritis varioliformis. Chronic erosive gastritis with protein-losing gastropathy. Author(s): Clarke AC, Lee SP, Nicholson GI. Source: The American Journal of Gastroenterology. 1977 December; 68(6): 599-602. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=612216&dopt=Abstract

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Granulomatous gastroenteritis. Case report with comparison to idiopathic isolated granulomatous gastritis. Author(s): Zuckerman MJ, al-Samman M, Boman DA. Source: Digestive Diseases and Sciences. 1994 August; 39(8): 1649-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8050313&dopt=Abstract

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Green tea consumption and chronic atrophic gastritis: a cross-sectional study in a green tea production village. Author(s): Shibata K, Moriyama M, Fukushima T, Kaetsu A, Miyazaki M, Une H. Source: J Epidemiol. 2000 September; 10(5): 310-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11059513&dopt=Abstract

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Hemorrhagic gastritis from topical isopropanol exposure. Author(s): Dyer S, Mycyk MB, Ahrens WR, Zell-Kanter M. Source: The Annals of Pharmacotherapy. 2002 November; 36(11): 1733-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12398569&dopt=Abstract

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High prevalence of Helicobacter heilmannii-associated gastritis in a small, predominantly rural area: further evidence in support of a zoonosis? Author(s): Svec A, Kordas P, Pavlis Z, Novotny J. Source: Scandinavian Journal of Gastroenterology. 2000 September; 35(9): 925-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11063150&dopt=Abstract

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Observation on 110 cases of chronic atrophic gastritis treated with Gastric Ease capsules. Author(s): Yang XZ, Hu CH, Zhuang KY, Zhu HL. Source: J Tradit Chin Med. 1983 March; 3(1): 55-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6553133&dopt=Abstract

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Production of metalloproteinase in gastric tissue with acetic acid-induced ulcer or taurocholic acid-induced gastritis. Author(s): Nakanishi J, Murakami S, Ishikura Y, Tsuchiya S, Mori Y. Source: J Pharmacobiodyn. 1987 February; 10(2): 92-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3298612&dopt=Abstract

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Protective effect of green tea on the risks of chronic gastritis and stomach cancer. Author(s): Setiawan VW, Zhang ZF, Yu GP, Lu QY, Li YL, Lu ML, Wang MR, Guo CH, Yu SZ, Kurtz RC, Hsieh CC. Source: International Journal of Cancer. Journal International Du Cancer. 2001 May 15; 92(4): 600-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11304697&dopt=Abstract

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Reflux bile gastritis. Author(s): Thorfinnson PC, Brow JR. Source: J Can Assoc Radiol. 1974 December; 25(4): 263-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4443360&dopt=Abstract

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Relationship between serologically diagnosed chronic atrophic gastritis, Helicobacter pylori, and environmental factors in Japanese men. Author(s): Kuwahara Y, Kono S, Eguchi H, Hamada H, Shinchi K, Imanishi K. Source: Scandinavian Journal of Gastroenterology. 2000 May; 35(5): 476-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10868449&dopt=Abstract

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Suppression of Helicobacter pylori-induced gastritis by green tea extract in Mongolian gerbils. Author(s): Matsubara S, Shibata H, Ishikawa F, Yokokura T, Takahashi M, Sugimura T, Wakabayashi K. Source: Biochemical and Biophysical Research Communications. 2003 October 24; 310(3): 715-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14550260&dopt=Abstract

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Suppressive effects of garlic extract on Helicobacter pylori-induced gastritis in Mongolian gerbils. Author(s): Iimuro M, Shibata H, Kawamori T, Matsumoto T, Arakawa T, Sugimura T, Wakabayashi K. Source: Cancer Letters. 2002 December 10; 187(1-2): 61-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359352&dopt=Abstract

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TCM differential treatment of 57 cases of chronic gastritis complicated by ulcerative colitis. Author(s): Meng M. Source: J Tradit Chin Med. 1999 March; 19(1): 10-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10453577&dopt=Abstract

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Traditional Chinese treatment of chronic gastritis with gastric dysplasia--a clinical analysis of 70 cases. Author(s): Zhang WY, Shen LH, Xu H, Wang XL, Xu YR. Source: J Tradit Chin Med. 1989 June; 9(2): 79-83. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2779280&dopt=Abstract

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Treatment of 910 cases of atrophic gastritis with wei you decoction. Author(s): Ma S, Liang F, Wang S, Dong S, Yin S, Xue C, Lin Z. Source: J Tradit Chin Med. 1990 September; 10(3): 168-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2277511&dopt=Abstract

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Treatment of bile reflux gastritis with traditional Chinese medicine. An analysis of 21 cases. Author(s): Jiang YQ. Source: J Tradit Chin Med. 1984 September; 4(3): 233-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6570156&dopt=Abstract

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Treatment of chronic gastritis with acupuncture. Author(s): Chen Z. Source: J Tradit Chin Med. 1994 September; 14(3): 233-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7799660&dopt=Abstract

Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •

Alternative Medicine Foundation, Inc.: http://www.herbmed.org/

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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats

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

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

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

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

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

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

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

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

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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 gastritis; 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 Chronic Obstructive Pulmonary Disease Source: Integrative Medicine Communications; www.drkoop.com

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Dermatitis Herpetiformis Source: Healthnotes, Inc.; www.healthnotes.com Diabetes Source: Healthnotes, Inc.; www.healthnotes.com Emphysema Source: Integrative Medicine Communications; www.drkoop.com Food Poisoning Source: Integrative Medicine Communications; www.drkoop.com Gastritis Source: Healthnotes, Inc.; www.healthnotes.com Gastritis Source: Integrative Medicine Communications; www.drkoop.com High Cholesterol Source: Healthnotes, Inc.; www.healthnotes.com Peptic Ulcer Source: Healthnotes, Inc.; www.healthnotes.com Pyloric Stenosis Source: Integrative Medicine Communications; www.drkoop.com Stomach Inflammation Source: Integrative Medicine Communications; www.drkoop.com Vitamin B12 Deficiency Source: Healthnotes, Inc.; www.healthnotes.com •

Alternative Therapy Homeopathy Source: Integrative Medicine Communications; www.drkoop.com

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Chinese Medicine Anwei Pian Alternative names: (An Wei Pian) Source: Pharmacopoeia Commission of the Ministry of Health, People's Republic of China

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Herbs and Supplements Achillea Alternative names: Yarrow; Achillea millefolium L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org

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Aluminum Hydroxide Source: Healthnotes, Inc.; www.healthnotes.com Arginine Source: Healthnotes, Inc.; www.healthnotes.com Aspirin Source: Healthnotes, Inc.; www.healthnotes.com Barberry Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Beta-carotene Source: Healthnotes, Inc.; www.healthnotes.com Calendula Alternative names: Calendula officinalis L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Cayenne Alternative names: Capsicum annuum, Capsicum frutescens Source: Healthnotes, Inc.; www.healthnotes.com Chamomile Alternative names: Matricaria recutita Source: Healthnotes, Inc.; www.healthnotes.com Dandelion Alternative names: Taraxacum officinale Source: Healthnotes, Inc.; www.healthnotes.com Devil’s Claw Alternative names: Harpagophytum procumbens Source: Healthnotes, Inc.; www.healthnotes.com Flaxseed Alternative names: Linum usitatissimum, Linseed Source: Integrative Medicine Communications; www.drkoop.com Gamma Oryzanol Source: Healthnotes, Inc.; www.healthnotes.com Gamma-oryzanol Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10028,00.html Gentian Alternative names: Gentiana lutea Source: Healthnotes, Inc.; www.healthnotes.com

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Glutamine Source: Healthnotes, Inc.; www.healthnotes.com Glycyrrhiza Glabra Source: Integrative Medicine Communications; www.drkoop.com Glycyrrhiza1 Alternative names: Licorice; Glycyrrhiza glabra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Goldenseal Alternative names: Hydrastis canadensis Source: Healthnotes, Inc.; www.healthnotes.com Horehound Alternative names: Marrubium vulgare Source: Healthnotes, Inc.; www.healthnotes.com Horseradish Alternative names: Cochlearia armoracia Source: Healthnotes, Inc.; www.healthnotes.com Lansoprazole Source: Healthnotes, Inc.; www.healthnotes.com Licorice Alternative names: Glycyrrhiza glabra, Glycyrrhiza uralensis Source: Healthnotes, Inc.; www.healthnotes.com Licorice Alternative names: Glycyrrhiza glabra, Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com Linseed Source: Integrative Medicine Communications; www.drkoop.com Linum Usitatissimum Source: Integrative Medicine Communications; www.drkoop.com Liquorice Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Marshmallow Alternative names: Althea officinalis Source: Healthnotes, Inc.; www.healthnotes.com Marshmallow Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca

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Matricaria Alternative names: Chamomile; Matricaria chamomilla Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Meadowsweet Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca N-acetyl Cysteine Source: Healthnotes, Inc.; www.healthnotes.com Omeprazole Source: Healthnotes, Inc.; www.healthnotes.com Proton Pump Inhibitors Source: Prima Communications, Inc.www.personalhealthzone.com Proton Pump Inhibitors (gastric Acid Secretion Inhibitors) Source: Integrative Medicine Communications; www.drkoop.com Slippery Elm Alternative names: Ulmus rubra, Ulmus fulva Source: Healthnotes, Inc.; www.healthnotes.com Slippery Elm Source: Prima Communications, Inc.www.personalhealthzone.com Slippery Elm Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10056,00.html Spanish Licorice Source: Integrative Medicine Communications; www.drkoop.com Willow Alternative names: Salix alba Source: Healthnotes, Inc.; www.healthnotes.com Willow Bark Alternative names: There are several species of willow includingSalix alba, Salix nigra, Salix fragilis, Salix purpurea, Salix babylonica, White Willow, European Willow, Black Willow, Pussy Willow, Crack Willow, Purple Willow, Weeping Willow, Liu-zhi Source: Integrative Medicine Communications; www.drkoop.com

General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the

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MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.

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CHAPTER 4. DISSERTATIONS ON GASTRITIS Overview In this chapter, we will give you a bibliography on recent dissertations relating to gastritis. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “gastritis” (or a synonym) in their titles.

Dissertations on Gastritis ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to gastritis. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •

Chemokine Expression and Regulation in Human Gastric Epithelial Cells: Association with Gastritis and Helicobacter Pylori by Abdullah, Norina Binti; PhD from University of Bath (United Kingdom), 2002, 2 pages http://wwwlib.umi.com/dissertations/fullcit/f830785

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Helicobacter Pylori-induced Gastritis in Guinea Pigs: Model Development, Diagnostic Methods and Comparison with Mouse Protocols by Sjunnesson, Hakan; PhD from Lunds Universitet (Sweden), 2002, 136 pages http://wwwlib.umi.com/dissertations/fullcit/f807345

Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.

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CHAPTER 5. PATENTS ON GASTRITIS 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 “gastritis” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on gastritis, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Gastritis By performing a patent search focusing on gastritis, 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

8Adapted

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

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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on gastritis: •

4-[aryl(8-azabicyclo[3.2.1]octan-3-yl)]aminobenzoic acid derivatives Inventor(s): Boyd; Robert E. (Horsham, PA), Carson; John R. (Norristown, PA), Neilson; Lou Anne (Sellersville, PA) Assignee(s): Ortho-McNeil Pharmaceutical, Inc. (Raritan, NJ) Patent Number: 6,306,876 Date filed: December 4, 2000 Abstract: 4-[aryl(8-azabicyclo[3.2.1]octan-3yl)]aminobenzoic acid derivatives are deltaopioid receptor modulators. As delta-opioid receptor agonists, such compounds are useful as analgesics. Depending on their antagonist effect, such compounds may also be useful immunosuppressants, antiinflammatory agents, agents for the treatment of neurological and psychiatric conditions, medicaments for drug and alcohol abuse, agents for treating gastritis and diarrhea, cardiovascular agents and agents for the treatment of respiratory diseases. Excerpt(s): The present invention is directed to delta-opioid receptor modulators. More particularly, the present invention is directed to 4-[aryl(8-azabicyclo[3.2.1]octan-3yl)]aminobenzoic acid derivatives which are delta-opioid receptor modulators useful as effective analgesics. The foregoing reference compounds have been described as either delta- or mu-opioid receptor agonists or antagonists. It is an object of the present invention to provide delta-opioid receptor modulators. It is another object of the present invention to provide delta-opioid receptor selective agonists as analgesics having reduced side-effects. It is also another object of the present invention to provide deltaopioid receptor antagonists as immunosuppressants, antiinflammatory agents, agents for the treatment of neurological and psychiatric conditions, medicaments for drug and alcohol abuse, agents for treating gastritis and diarrhea, cardiovascular agents and agents for the treatment of respiratory diseases, having reduced side-effects. It is a further object of the present invention to provide a method for treating a disorder modulated by the delta-opioid receptor. Web site: http://www.delphion.com/details?pn=US06306876__

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4-[aryl(piperidin-4-yl)]aminobenzamides Inventor(s): Carmosin; Richard J. (late of Quakertown, PA), Carson; John R. (Norristown, PA), Fitzpatrick; Louis J. (Souderton, PA), Jetter; Michele C. (Norristown, PA), Reitz; Allen B. (Lansdale, PA) Assignee(s): Ortho-McNeil Pharmaceutical, Inc. (Raritan, NJ) Patent Number: 6,436,959 Date filed: December 23, 1998 Abstract: 4-[aryl(piperidin-4-yl)]aminobenzamides are delta-opioid receptor agonists/antagonists. As delta-opioid receptor agonists, such compounds are useful as analgesics. Depending on their agonist/antagonist effect, such compounds may also be useful immunosuppressants, antiinflammatory agents, agents for the treatment of mental illness, medicaments for drug and alcohol abuse, agents for treating gastritis and diarrhea, cardiovascular agents, and agents for the treatment of respiratory diseases.

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Excerpt(s): The present invention relates to delta-opioid receptor agonists/antagonists. More particularly, the present invention relates to 4-[aryl(piperidin-4yl)]aminobenzamides which are delta-opioid receptor agonists useful as analgesics. which are mu-opioid antagonists. which are delta-opioid agonists/antagonists. Web site: http://www.delphion.com/details?pn=US06436959__ •

Antisense oligonucleotides for inhibiting helicobacter pylori activity Inventor(s): Colote; Soudhir (Les Ulis, FR), Pirotzky; Eduardo (Paris, FR) Assignee(s): Societe de Conseils de Recherches et d'Applications Scientifiques (FR) Patent Number: 5,977,340 Date filed: October 1, 1997 Abstract: Antisense oligonucleotides that selectively hybridise with one or more genes necessary for Helicobacter pylori (H. pylori) activity, and particularly with the CagA cytotoxicity-associated immunodominant antigen, flagellin (flaA and flaB) or vacuolating cytotoxin (vacA), are disclosed. Pharmaceutical compositions containing said antisense oligonucleotides, and the use thereof for treating atrophic gastritis, peptic and duodenal ulcers, gastric atrophy or stomach cancer, are also disclosed. Excerpt(s): The present invention concerns antisense oligonucleotides which selectively hybridize with one or more genes necessary for the action of Helicobacter pylori (H. pylori), pharmaceutical compounds comprising them and their use as Helicobacter pylori inhibitors. Helicobacter pylori (H. pylori) is a microaerophilic bacterium, gram negative, colonizing the intercellular interstices and junctions of the human gastric mucous membrane and establishing a chronic infection with numerous different clinical manifestations such as atrophic gastritis, peptic and duodenal ulcer, gastric atrophy, and gastric carcinoma. The numerous clinical isolated substances have permitted classification of H. pylori into two groups based on the presence or the absence of vacuolizing cytotoxin. In vitro experiments have shown that the virulent nature of the bacterium may be connected to its mobility and to the presence of vacuolizing cytotoxin. Likewise, there is a direct relationship between the expression of cytotoxin and the presence of an immuno-dominant CagA antigen exposed on the surface. Thus, inhibition of the mobility of the bacterium and/or expression of the cytotoxic factor may prevent the manifestation of clinical symptoms. One of the ways to inhibit these factors comprises using antisense oligonucleotides to block the expression of the coding of the genes for the immuno-dominant antigen associated with the CagA cytotoxicity and/or flagellin (flaA and flaB) and/or the vacuolizing cytotoxin (vacA). The antisense strategy is a therapeutic approach whose purpose is the selective modulation of the expression of the genes by a highly selective association of a chain of nucleotides (oligonucleotides) with its supplementary sequence on RNA or DNA and consequently the inhibition of the synthesis of the corresponding protein. Web site: http://www.delphion.com/details?pn=US05977340__

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Blood group antigen binding protein and corresponding agents Inventor(s): Arnqvist; Anna (Ume.ang., SE), Boren; Thomas (Torelv.ang.gen 68, S-906 28 Ume.ang., SE), Ilver; Dag (Ume.ang., SE), Normark; Staffan (Stockholm, SE) Assignee(s): Boren; Thomas (Umea, SE) Patent Number: 6,410,719 Date filed: February 10, 1998 Abstract: A novel bacterial blood group antigen binding (BAB) adhesin protein was isolated and purified, whereby said protein or fractions thereof bind specifically to Helicobacter pylori fucosylated blood group antibodies. The protein sequence of said adhesin is disclosed in this application. Simultaneously the DNA sequences for two genes, babA and babB, producing highly similar proteins, are disclosed. Said adhesin and/or DNA is useful for diagnose and therapy and/or profylax directed against H. pylori induced infections, e.g. gastritis and acid peptic disease. Excerpt(s): The present invention relates to materials and methods for prevention, treatment and diagnosing of infections caused by Helicobacter pylori. More specifically the present invention relates to polypeptides and antibodies useful in vaccines for the treatment and prevention of pathologic infections caused by Helicobacter pylori strains. The present invention specifically relates to a bacterial blood group antigen binding adhesin (BAB-adhesin). The present invention further relates to polynucleotides useful for the recombinant production of said polypeptides and for use in immunization therapies. In addition, it relates to polypeptides, antibodies, and polynucleotides used for the detection of said bacteria. Helicobacter pylori is a causative agent for acid peptic disease and the presence of this organism is highly correlated to the development of gastric adenocarcinoma. Bacterial adherence to the human gastric epithelial lining was recently shown to be mediated by fucosylated blood group antigens. The foregoing makes the prevention, diagnosing and treatment of H. pylori infections an urgent task. Further, the fact that developing countries frequently lack the resources for conventional treatment of gastric ulcers further underlines the importance of finding new ways of diagnosing, treatment and prevention of H. pylori induced infections. It is obvious, for many reasons, that disease prevention with vaccines is a preferable mode. A vaccine would provide an easily administered and economical prophylactic regimen against H. pylori infections. An effective vaccine against H. pylori is nevertheless presently lacking. Web site: http://www.delphion.com/details?pn=US06410719__

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Composition and method for treating and preventing helicobactor-pylori-associated stomach gastritis, ulcers and cancer Inventor(s): Segelman; Alvin Burton (Orem, UT) Assignee(s): Nature's Sunshine Products, Inc. (Provo, UT) Patent Number: 6,187,313 Date filed: February 17, 1998 Abstract: The present invention is an orally-administrable composition for preventing and treating Helicobacter pylori-associated stomach gastritis and ulcers, and for preventing Helicobacter pylori-associated stomach cancer. The invention is a herb or herb extract containing an anti-H. pylori activity. The invention further includes methods for making and methods for using the invention.

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Excerpt(s): This invention relates to the field of compositions and methods for treating and preventing Helicobactor pylori-associated stomach gastritis, ulcers and cancer. More specifically, this invention relates to the field of compositions of herbs, herb parts or herb extracts which can be used to treat or prevent Helicobactor pylori-associated stomach gastritis, ulcers and cancer, and methods for making and using such compositions. Twelve years ago it was first reported and subsequently verified by many scientific studies that a particular bacterium known as Helicobacter pylori ("H. pylori") commonly infects the human stomach. Many people so infected subsequently acquire what is known as chronic superficial gastritis ("stomach inflammation") which may continue on for many decades. It is now known that left untreated, this condition may lead to stomach ulcers and even stomach cancer disease. (Marshall, B. J. and Warren, J. B. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet, No.8390: 1311-1315 (1984); Nomura, A., Stemmermann, G. N., Chyou, P.-H., et al., Helicobacter pylori infection and gastric carcinoma among Japanese Americans in Hawaii. New Engl. J. Med., 325: 1132-1136 (1991); Blaser, M. J. and Parsonnet, J., Parasitism by the "slow" bacterium Helicobacter leads to altered gastric homeostasis and neoplasia. J. Clin, Invest., 94: 4-8 (1994).) Extensive laboratory as well as clinical studies have been reported which clearly show that people suffering from chronic gastritis and/or stomach ulcer disease caused by H. pylori infection can be cured when administered certain antibiotics which eradicate H. pylori [Rubinstein, G., Dunkin, K. and Howard, A. J., The susceptibility of Helicobacter pylori to 12 antimicrobial agents, omeprazole and bismuth salts. J. Antimicrob. Chemother., 34: 409413 (1994); Rosioru, C. Glassman, M. S., Berezin, S. H., et al., Treatment of Helicobacter pylori--associated gastroduodenal disease in children. Dig. Dis. Sci., 38: 123-128 (1993); Blaser, M. J., The bacteria behind the ulcers. Sci. Amer., February 1996, 104-107]. On the other hand, the use of antibiotics has some drawbacks, including the rapid resistance of H. pylori to antimicrobial agents (Rubinstein, G. et al., op. cit.) as well as the well known fact that many people are allergic to antibiotics and some develop severe diarrhea and/or secondary infections which complicate antibiotic therapy. Furthermore, the antibiotics used to treat (i.e., kill H. pylori) ulcers also kill a wide variety of nonpathogenic bacteria in the body, a most undesirable feature of antibiotic therapy (i.e., "non-selectivity"). The present invention is based on the unexpected discovery that several herbs and an insect product are capable of being orally administered to humans, either singly or in combination, to destroy or inhibit the growth of H. pylori so that gastritis and ulcer disease can be prevented or cured. In this manner stomach cancer can also be prevented. The composition may also be combined with certain other beneficial and healing substances (i.e., licorice root (Glycyrrhiza glabra)). Web site: http://www.delphion.com/details?pn=US06187313__ •

Compositions and methods relating to drug discovery and detection and treatment of gastrointestinal diseases Inventor(s): Corthesy-Theulaz; Irene (Epalinges, CH) Assignee(s): Kieta Holding SA (St-Prex, CH) Patent Number: 6,060,241 Date filed: April 3, 1997 Abstract: A poly-3-hydroxybutyrate metabolic pathway essential for Helicobacter pylori survival in a host is provided. A novel Helicobacter pylori Coenzyme A transferase (Hp CoA-t), thiolase and PHB synthase as well as methods for their preparation and use are

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provided. Hp CoA-t and thiolase polynucleotides and proteins are provided as well as detection and preparative methods using such molecules. Methods for the determination of a propensity to develop gastritis, peptic ulcer disease, or gastric cancer is provided for by detection methods. Methods are also provided for the use of Hp CoAt, thiolase or PHB synthase proteins and fragments retaining enzymatic activity in the identification of potential drug candidates for the treatment of some types of gastric disease. Pharmaceutical compositions containing Hp CoA-t protein fragments, antisense nucleic acids or other inhibitors of Hp CoA-t, thiolase and PHB synthase as well as methods for their use in the treatment of some types of gastric disease are also provided. Excerpt(s): This invention provides for compositions and methods relating to enzymes in the poly-3-hydroxybutyrate metabolic pathway in bacteria that can propagate at low pH, such as Helicobacter pylori. Safe, efficacious and cost effective methods for the treatment and diagnosis of peptic ulcers and gastritis continue to elude physicians. Traditionally ulcerogenesis was blamed on a myriad of factors, such as nervous tension, hot spicy foods, and hormonal imbalance. Bed rest and a bland diet were commonly prescribed along with drugs to neutralize the gastric acid and enzymes. The advent of H.sub.2 antagonists and acid pump blockers decreased acid secretion in the stomach, but was not necessarily curative or cost effective. More recently workers have investigated Helicobacter pylori (Hp), a spiral Gram-negative, microaerophilic bacterium, as a cause of ulcers due to Hp chronic infections of the human stomach. Hp has been identified as the causal agent of type B gastritis, peptic ulcers and gastric cancer (Cover et al., ASM News Vol. 61 No. 1 pp. 21-26 (1995)). At least sixteen other species of Helicobacter have been isolated from the stomachs or intestines of mammals and additional Helicobacter species are likely to be identified in the future. It is estimated that 40% of the population in developed countries and 80% of the population in underdeveloped countries have or have had Hp infections. If left untreated, the Helicobacter pylori infection can result in chronic gastritis and can persist for life. Web site: http://www.delphion.com/details?pn=US06060241__ •

Compositions comprising isolated Helicobacter pylori CagI polynucleotides and method of preparation thereof Inventor(s): Covacci; Antonello (Siena, IT) Assignee(s): Chiron S.p.A. (IT) Patent Number: 5,928,865 Date filed: June 7, 1995 Abstract: Helicobacter pylori is known to cause or be a cofactor in type B gastritis, peptic ulcers, and gastric tumors. In both developed and developing countries, a high percentage of people are infected with this bacterium. The present invention relates generally to a certain H. pylori region located 5' to the CagA gene locus, to proteins encoded thereby, and to the use of these genes and proteins for diagnostic and vaccine applications. Excerpt(s): The present invention relates generally to certain Helicobacter pylori genetic regions, to the proteins expressed by these regions, and to the use of these genes and proteins for diagnostic and vaccine applications. Helicobacter pylori is a curved, microaerophilic, gram negative bacterium that has been isolated for the first time in 1982 from stomach biopsies of patients with chronic gastritis, Warren et al., Lancet i: 1273-75 (1983). Originally named Campylobacter pylori, it has been recognized to be part of a

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separate genus named Helicobacter, Goodwin et al., Int. J. Syst. Bacteriol. 39: 397-405 (1989). The bacterium colonizes the human gastric mucosa, and infection can persist for decades. During the last few years, the presence of the bacterium has been associated with chronic gastritis type B, a condition that may remain asymptomatic in most infected persons but increases considerably the risk of peptic ulcer and gastric adenocarcinoma. The most recent studies strongly suggest that H. pylori infection may be either a cause or a cofactor of type B gastritis, peptic ulcers, and gastric tumors, see e.g., Blaser, Gastroenterology 93: 371-83 (1987); Dooley et al., New Engl. J. Med. 321: 1562-66 (1989); Parsonnet et al., New Engl. J. Med. 325: 1127-31 (1991). H. pylori is believed to be transmitted by the oral route, Thomas et al., Lancet i: 340, 1194 (1992), and the risk of infection increases with age, Graham et al., Gastroenterology 100: 1495-1501 (1991), and is facilitated by crowding, Drumm et al., New Engl. J. Med. 4322: 359-63 (1990); Blaser, Clin. Infect. Dis. 15: 386-93 (1992). In developed countries, the presence of antibodies against H. pylori antigens increases from less than 20% to over 50% in people 30 and 60 years old respectively, Jones et al., Med. Microbio. 22: 57-62 (1986); Morris et al., N. Z. Med. J. 99: 657-59 (1986), while in developing countries over 80% of the population are already infected by the age of 20, Graham et al., Digestive Diseases and Sciences 36: 1084-88 (1991). H. pylori factors that have been identified so far include the flagella that are probably necessary to move across the mucus layer, see e.g., Leying et al., Mol. Microbiol. 6: 2863-74 (1992); the urease that is necessary to neutralize the acidic environment of the stomach and to allow initial colonization, see e.g., Cussac et al., J. Bacteriol. 174: 2466-73 (1992), Perez-Perez et al., J. Infect. Immun. 60: 3658-3663 (1992), Austin et al., J. Bacteriol. 174: 7470-73 (1992), PCT Publ. No. WO 90/04030; the H. pylori cytotoxin (sometimes referred to as VacA, as it causes vacuolation), see e.g., PCT Publ. No. WO 93/18150, Telford, J. L. et al., J. Exp. Med. 179: 1653-58 (1994), Cover et al., J. Bio. Chem. 267: 10570-75 (1992), Cover et al., J. Clin. Invest. 90: 913-18 (1992), Leunk, Rev. Infect. Dis. 13: 5686-89 (1991); the H. pylori heat shock protein, see e.g., PCT Publ. No. WO 93/18150, Evans et al., Infect. Immun. 60: 2125-27 (1992), Dunn et al., Infect. Immun. 60: 1946-51 (1992), Austin et al., J. Bacteriol. 174: 7470-73 (1992); and the cytotoxin-associated protein, CagA, see e.g., PCT Publ. No. WO 93/18150, Covacci, A., et al., Proc. Natl. Acad. Sci. USA 90: 5791-95 (1993), Tummuru, M. K. et al., Infect. Immun. 61: 1799-1809 (1994). Web site: http://www.delphion.com/details?pn=US05928865__ •

Feed product Inventor(s): Johansson; Marie-Louise (Lund, SE), Lonner; Clas (Eslov, SE) Assignee(s): Probi AB (Lund, SE) Patent Number: 6,537,544 Date filed: June 20, 2000 Abstract: Novel strains Lactobacillus plantarum JI:1 and Lactobacillus species AC:3 are contained in an equine feed product. An oatmeal gruel fermented with said strains can be used for the prophylaxis or treatment of disturbances in the equine intestinal microflora, as well as gastritis. Excerpt(s): The present invention refers to new strains of the genus Lactobacillus, and an equine feed product comprising one or more of said strains. Disturbances in the equine intestinal flora can bring about a deteriorated ability to take up the nutriment from the feed, a reduced efficiency, a deteriorated resistance to infections and accompanying infections of different kinds. Other symptoms are a changed consistency of the

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excrements, which are often malodorous, and an ugly coat of hair. It is well known that disturbances of the intestinal flora above all appear in stress situations, for instance during long transportations or change of stable environment, too tough training and change of feed, but also in treatment with antibiotics. Problems of a disturbed intestinal flora also occur in foals, which during their first living have to obtain an intestinal microflora of their own. Different disorders which can be associated with a change of the intestinal bacterial flora are inflammations in the intestinal mucosa and gastric ulcer, and bacterial infections giving for instance acute colitis, such as intestinal chlostridiosis, manifesting in diarrhea and toxemia and caused by i.a. Clostridium difficile, and colic, such as Baron-Gruff-disease, which is caused by Clostridium perfringens. Web site: http://www.delphion.com/details?pn=US06537544__ •

Foaming antacid suspension tablets Inventor(s): Bauer; Kurt H. (Freiburg, DE) Assignee(s): DR. Regenold GmbH (Badenweiler, DE) Patent Number: 6,589,507 Date filed: August 13, 2001 Abstract: The invention relates to antacid preparations comprising the following constituents:(i) an acid-binding active constituent (antacid) or a mixture of such active constituents,(ii) an effervescent mixture that releases CO.sub.2,(iii) a polymeric surfactant as foam-forming agent or a mixture of such surfactants,(iv) a swellable and gel-forming polymer or a mixture of such polymers, and(v) optionally conventional auxiliary substances,as well as a process for the production of such antacid preparations. In a particularly preferred embodiment the antacid preparation is formulated in the form of a chewable tablet. The antacid preparations according to the invention are suitable for the symptomatic treatment of duodenal ulcers, gastric ulcers, as well as heartburn and acid-caused gastric disorders such as hyperacidic gastritis. Excerpt(s): The present invention relates to preparations that contain one or more acidbinding active constituents (antacids), as well as a process for the production of these preparations and their use as medicaments for the regulation of gastric hyperacidity. Therapy with antacids has proved outstandingly successful for the treatment of a number of acute and chronic gastro-intestinal conditions. In particular, antacids are used for the symptomatic treatment of duodenal and gastric ulcers as well as in heartburn and acid-caused gastric disorders such as hyperacidic gastritis. The action of the antacids basically depends on the fact that the gastric hydrochloric acid is to some extent buffered so that the pH of the stomach is increased from 1 to 2 or 3, or even 4. Due to this increase in the pH value the symptoms typical of hyperacidity, such as for example a feeling of fullness or heartburn, are reduced or even eliminated. Up to now antacids have been marketed and sold in powder form, as normal tablets, predominantly as chewable tablets or as suspensions in bottles or packed in sachets. In German patent application DE 44 24 676 antacid effervescent tablets are also described. The known chewable tablets can be administered extremely easily and simply, but have the disadvantage that the patient finds that these tablets are chalky and thus unpleasant after they have been chewed. In contrast to this the known, finely dispersed suspension medicament forms are not perceived as being chalky, are well tolerated, and are furthermore characterised by a rapid and clearly detectable onset of action and effect. The disadvantage of these suspension medicament forms is however the fact that elderly patients in particular have difficulty in removing the suspensions completely

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and without too much effort from the sachet packagings. On the other hand the formulation and administration of effervescent tablets is simpler, although the effervescent tablets used up to now have to be taken with a glass of water, in which the effervescent tablets dissolve with foaming to form a liquid drinkable suspension. For this reason it is not possible to take the medicament at every opportunity. Accordingly, all the hitherto available preparation forms of antacids have certain disadvantages as regards their administration. Web site: http://www.delphion.com/details?pn=US06589507__ •

Food for inhibiting infection and treating gastritis, gastric and duodenal ulcers Inventor(s): Heo; Cheol Seong (#305 304dong Daelip hansup apt, Chunan, Chungchungnamdo 330-160, KR), Kim; Hyun Mi (#202 728-11 Pungdukchunli, Sugieup, Yongin, Kyunggido 449-840, KR), Kim; Hyung Soo (52303 Brenton Hills Dr., Granger, IN 46530), Lee; Jung Lyoul (#904 302dong Daewon apt, chowonmayeul pyungchongdong Donganku, Anyang, Kyungkido, 431-070, KR) Assignee(s): none reported Patent Number: 6,329,002 Date filed: February 7, 2000 Abstract: Live strains of Lactococcus sp. HY 49, Lactobacillus casei HY 2782, and Bifidobacterium longum HY 8001 maintained in nutritious foods, such as yogurt, imbue them with prophylactic and/or therapeutic properties. Such foods are beneficial in the prevention and/or treatment of gastritis, duodenal and gastric ulcers caused by infection from Helicobacter pylori (also referred to as H. pylori). The properties of these bacteria are boosted by the addition of egg yolk containing antibodies specific to H. pylori antigen derived from "fractionated H. pylori". Excerpt(s): A nutritional formulation in which non-toxic (to humans) bacteria thrive, is used to prevent and treat gastric disorders associated with Helicobacter pylori (also referred to as H. pylori) which are attacked by the non-toxic bacteria. Only particular strains of non-toxic comestible bacteria, when ingested by humans are effective against H. pylori. Optionally and preferably, the prophylactic and/or therapeutic effects of the comestible bacteria are boosted with egg yolk containing immunoglubins (antibodies) specific to H. pylori antigen (also referred to as "H. pylori-antibodies"). Much has been published regarding H. pylori which inhabits the human gastric mucosa. It is a gramnegative spiral rod-shaped bacterium having an outer membrane with four to six polar flagella which are sheathed and have bulbous ends; each H. pylori bacterium is about 0.85.mu.m (micrometer) in diameter with an average length of 2.9.mu.m. Known pathogenic (disease) factors of H. pylori are (i) urease which is produced by the bacteria to allow it to thrive in a strong acid environment in the range from pH 1-3, (ii) flagella which provide the bacteria with mobility, and (iii) a proteinaceous outer membrane of the cells which membrane helps the cells to stick to the gastric mucosal cells. To date, treatment to subdue secretion of gastric acid, for example with H2 isolator, is deemed unsatisfactory over the long term due to recrudescence which is now countered with medicines which act directly on the H. pylori. Presently, trends in the fight against infection by H. pylori may be categorized as follows: (a) development of antibiotics showing a direct effect against H. pylori, (b) development of vaccines for H. pylori, and (c) using anti-H. pylori antibodies which allow the live H. pylori to be terminated. For prophylaxis, (b) and (c) are preferred.

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Web site: http://www.delphion.com/details?pn=US06329002__ •

Gastroprotective flavone/flavanone inflammatory bowel disease

compounds

with

therapeutic

effect

on

Inventor(s): Ahn; Byoung Ok (Kyunggi-do, KR), Baik; Nam Gi (Kyoungki-do, KR), Kim; Dong Sung (Kyoungki-do, KR), Kim; Ik Yon (Kyoungki-do, KR), Kim; Soon Hoe (Kyoungki-do, KR), Kim; Won Bae (Seoul, KR), Lee; Sang Deuk (Seoul, KR), Lim; Geun Jho (Seoul, KR), Lim; Joong In (Seoul, KR), Oh; Tae Young (Kyunggi-do, KR), Ryu; Byung Kwon (Seoul, KR), Shin; Hee Chan (Seoul, KR), Son; Mi Won (Kyoungki-do, KR), Yang; Jae Sung (Seoul, KR), Yoo; Moohi (Seoul, KR) Assignee(s): Dong a Pharmaceutical Co., Ltd. (KR) Patent Number: 6,025,387 Date filed: January 14, 1999 Abstract: The present invention relates to novel flavone/flavanone compounds or their pharmaceutically acceptable salts and process for preparation thereof for protecting gastrointestinal tracts against gastritis, ulcers and inflammatory bowel disease. Excerpt(s): The present invention relates to novel flavone/flavanone compounds or their pharmaceutically acceptable salts, and process for preparation thereof for protecting gastrointestinal tracts against gastritis, ulcers and inflammatory bowel disease. Although the incidence of gastric ulceration, duodenal ulceration or gastritis has been declining over the last decade, about 10% of the population will develop this condition at some time during their lives. The precise cause of these diseases remains uncertain despite of intensive clinical and laboratory research, but it is explained that they are induced from imbalance in equlibrium between potentially damaging factor present in the lumen of the stomach or duodenum and the process which enable these tissues to resist autodigestion. The first line therapy for gastritis and gastric ulcer is to promote the effects of treatments by attenuating the attacking factors by administering antisecretory agents such as antacid, H2 antagonists and proton pump inhibitors. However, it has been reported that in the cases of omeprazole or long acting H2 antagonists, the duration of action was so long more than 24 hours that their long-term administration to rats caused dysplasia in epidermal cells of mucous membrane in gastrointestinal tracts (Ekman, L. et al., Scand. J. Gastroentrol.1985, 20 suppl.108: 53). And long-term administration of antisecretory agents is frequently associated with formation of gastric tumors in animals (Garner, A., Advances in Drug Therapy of Gastrointestinal Ulceration; Garner, A. and Whittle, B. J. R.(Eds.), Wiley & Sons, 1989, 275-88). Furthermore, a majority of patients with peptic ulcer disease have acid outputs within the normal range (Baron, J. H., Clinical Tests of Gastric Secretion. Macmillan, London, 1978, 86-119), so the treatments with antisecretory agents are not fundamental therapy and have a little effect on the prevention of recurrence, though they enhance acute healing of ulcer. Web site: http://www.delphion.com/details?pn=US06025387__

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Helicobacter pylori nickel binding protein Inventor(s): Gilbert-Rothstein; Joanne V. (Arlington, MA), Plaut; Andrew G. (Lexington, MA), Wright; Andrew (Lincoln, MA) Assignee(s): New England Medical Center Hospital, Inc. (Boston, MA), Tufts University School of Medicine Hospital, Inc. (Boston, MA) Patent Number: 5,780,040 Date filed: June 8, 1994 Abstract: The application discloses a nickel binding protein and its encoding DNA isolated from Helicobacter pylori. This organism is the primary cause of chronic gastritis and ensuing peptic ulcers, and has been implicated in stomach cancer. The nickel binding protein is useful to inhibit assembly of active ureases, the enzymes responsible for the pathogenic features of the bacterium. Potential uses include as a vaccine, a diagnostic, a drug target, and a therapy in itself. Excerpt(s): The field of the invention is diagnosis, prophylaxis, and treatment of gastric disease and nickel-related disorders; and non-clinical nickel detoxification The invention also relates to the bacterium Helicobacter pylori. The bacterium Helicobacter pylon was first isolated from human gastric mucosa in 1983, and was originally identified as a member of the genus Campylobacter (either C. pylori or C. pyloridis; Warren and Marshall, Lancet i:1273, 1983; Marshall and Goodwin, Int. J. Syst. Bacteriol. 37:68, 1987). H. pylori is recognized as a pathogen, and is a major cause of chronic gastritis, inflammation of the gastric mucosa, and peptic ulcers. It can also contribute to the development of gastric cancer (for review, see Sipponen et al., "Histology and Ultrastructure of Helicobacter pylori Infections: Gastritis, Duodenitis, and Peptic Ulceration, and Their Relevant Precancerous Conditions", in Helicobacter pylori: Biology and Clinical Practice 37, Goodwin and Worsley, eds., 1993). H. pylori is able to survive in the highly acidic environment of the stomach at least in part due to its high urease activity, which may raise the pH of the local environment by hydrolyzing endogenous urea into ammonia and carbon dioxide. The ammonia component affects the pH, and its local accumulation is thought to have a directly toxic effect on nearby mucosa. Web site: http://www.delphion.com/details?pn=US05780040__

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Helicobacter pylori proteins useful for vaccines and diagnostics Inventor(s): Bugnoli; Massimo (Monteriggioni, IT), Covacci; Antonello (Siena, IT), Macchia; Giovanni (Avezzano, IT), Rappuoli; Rino (Quercegrossa, IT), Telford; John (Monteriggioni, IT) Assignee(s): Chiron Corporation (Emeryville, CA) Patent Number: 6,077,706 Date filed: June 6, 1995 Abstract: Helicobacter pylori known to cause or be a cofactor in type B gastritis, peptic ulcers, and gastric tumors. In both developed and developing countries, a high percentage of people are infected with this bacterium. The present invention relates generally to certain H. pylori proteins, to the genes which express these proteins, and to the use of these proteins for diagnostic and vaccine applications. Specifically, molecular cloning, nucleotide, and amino add sequences for the H. pylori cytotoxin (CT), the

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"Cytotoxin Associated Immunodominant" (CAI) antigen, and the heat shock protein (hsp60) are described herein. Excerpt(s): The present invention relates generally to certain Helicobacter pylori proteins, to the genes which express these proteins, and to the use of these proteins for diagnostic and vaccine applications. Helicobacter pylori is a curved, microaerophilic, gram negative bacterium that has been isolated for the first time in 1982 from stomach biopsies of patients with chronic gastritis, Warren et al., Lancet i:1273-75 (1983). Originally named Campylobacter pylori, it has been recognized to be part of a separate genus named Helicobacter, Goodwin et al., Int. J. Syst. Bacteriol. 39:397-405 (1989). The bacterium colonizes the human gastric mucosa, and infection can persist for decades. During the last few years, the presence of the bacterium has been associated with chronic gastritis type B, a condition that may remain asymptomatic in most infected persons but increases considerably the risk of peptic ulcer and gastric adenocarcinoma. The most recent studies strongly suggest that H. pylori infection may be either a cause or a cofactor of type B gastritis, peptic ulcers, and gastric tumors, see e.g., Blaser, Gastroenterology 93:371-83 (1987); Dooley et al., New Engl. J. Med. 321:1562-66 (1989); Parsonnet et al., New Engl. J. Med. 325:1127-31 (1991). H. pylori is believed to be transmitted by the oral route, Thomas et al., Lancet i:340, 1194 (1992), and the risk of infection increases with age, Graham et al., Gastroenterology 100:1495-1501 (1991), and is facilitated by crowding, Drumm et al., New Engl. J. Med. 4322:359-63 (1990); Blaser, Clin. Infect. Dis. 15:386-93 (1992). In developed countries, the presence of antibodies against H. pylori antigens increases from less than 20% to over 50% in people 30 and 60 years old respectively, Jones et al., Med. Microbio. 22:57-62 (1986); Morris et al., N. Z. Med. J. 99:657-59 (1986), while in developing countries over 80% of the population are already infected by the age of 20, Graham et al., Digestive Diseases and Sciences 36:108488 (1991). The nature and the role of the virulence factors of H. pylori are still poorly understood. The factors that have been identified so far include the flagella that are probably necessary to move across the mucus layer, see e.g., Leying et al., Mol. Microbiol. 6:2863-74 (1992); the urease that is necessary to neutralize the acidic environment of the stomach and to allow initial colonization, see e.g., Cussac et al., J. Bacteriol. 174:2466-73 (1992); Perez-Perez et al., J. Infect. Immun. 60:3658-3663 (1992); Austin et al., J. Bacteriol. 174:7470-73 (1992); PCT Publ. No. WO 90/04030; and a high molecular weight cytotoxic protein formed by monomers allegedly having a molecular weight of 87 kDa that causes formation of vacuoles in eukaryotic epithelial cells and is produced by H. pylori strains associated with disease, see e.g., Cover et al., J. Bio. Chem. 267:10570-75 (1992) (referencing a "vacuolating toxin" with a specified 23 amino acid Nterminal sequence); Cover et al., J. Clin. Invest. 90:913-18 (1992); Leunk, Rev. Infect. Dis. 13:5686-89 (1991). Additionally, the following is also known. Web site: http://www.delphion.com/details?pn=US06077706__ •

Indolin-2-one derivatives Inventor(s): Emura; Takashi (Shizuoka, JP), Esaki; Toru (Shizuoka, JP), Hoshino; Eiichi (Shizuoka, JP) Assignee(s): Chugai Seiyaku Kabushiki Kaisha (Tokyo, JP) Patent Number: 6,127,544 Date filed: October 30, 1998 Abstract: A compound represented by formula (I): wherein R.sub.1 represents a halogen atom, a lower alkyl group, a lower alkoxy group, a hydroxyl group, a nitro group, a

Patents 141

trifluoromethyl group, a lower alkylthio group, an acyl group, a carboxyl group, a mercapto group or an amino group; R.sub.2 represents a hydrogen atom, a lower alkyl group, a lower alkenyl group, a lower alkynyl group, an alkoxy group, an acyl group, an aryl group or a heterocyclic group; R.sub.3 represents a lower alkyl group, a cycloalkyl group, an aryl group, or a heterocyclic group; R.sub.4 represents a hydrogen atom, a lower alkyl group, an aryl group, a heterocyclic group, --OR.sub.5, --SR.sub.5 or -NR.sub.6 R.sub.7 (wherein R.sub.5, R.sub.6, and R.sub.7 each represent a lower alkyl group, etc.); X and Y each represent --CH.sub.2 --, --NH-- or --O--; and n represents an integer of from 0 to 4, and an intermediate for synthesis thereof are disclosed. The compound of the present invention exhibits selective antagonism against gastrin receptors without causing side effects attributed to CCK-A receptor antagonism and is useful for the treatment and prevention of peptic ulcers, gastritis, reflux esophagitis, and Zollinger-Ellison syndrome, and for the treatment of neoplasm originating in the gastrointestinal system. Excerpt(s): This invention relates to an indolin-2-one derivative which exhibits selective antagonism against gastrin receptors without causing side effects attributed to CCK-A receptor antagonism and is useful for the treatment and prevention of diseases of digestive organs, such as peptic ulcers, gastritis, reflux esophagitis, and ZollingerEllison syndrome, and for the treatment of tumours originating in the gastrointestinal system. The compounds also exhibit selective antagonism against CCK-B receptors and are useful for the treatment of CCK-related disorders in the appetite control system, enhancement and prolongation of analgesia through opiate or non-opiate, induction of anesthesia or analgesia, and the treatment and prevention of symptoms of psychotic disorders including anxiety and panic disorder. Gastrin is a typical gastrointestinal hormone, like CCK, secretin, etc. It is known that gastrin accelerates secretion of gastric acid and pepsin and also accelerates growth of gastric mucous cells and especially histamine secretory cells. While gastric acid secretion is stimulated by histamine, acetylcholine, and gastrin, gastrin is the most powerful of these internal substances. Currently known drugs for controlling gastric acid secretion include muscarinic receptor antagonists such as Pirenzepine, histamine H.sub.2 receptor antagonists such as Cimetidine, and H.sup.+ --K.sup.+ ATPase inhibitors such as Omeprazole. However, it has been reported that these drugs induce hypergastrinemia during maintained administration due to the potent inhibitory activity on gastric acid secretion, and the high gastrin level induces an increase of histamine content in the gastric mucosa. The reports also reveal that discontinuation of administration of these drugs is followed by an increase of acid secretion, called rebound, and a high rate of relapses. The study of gastrin has recently been progressed, and participation of gastrin in various diseases has been elucidated. As a result, it has been suggested that a selective antagonist to gastrin receptors would be useful for the treatment and prevention of diseases induced by disorders of physiological functions related to gastrin, i.e., diseases of digestive organs, particularly peptic ulcers, gastritis, reflux esophagitis, and Zollinger-Ellison syndrome; prevention of a relapse following treatment with an H.sub.2 receptor antagonist or an H.sup.+ --K.sup.+ ATPase inhibitor; or the treatment and prevention of tumours originating in the gastrointestinal system. Web site: http://www.delphion.com/details?pn=US06127544__

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Methods for treating disorders in which docosahexaenoic acid (DHA) levels are affected Inventor(s): Alvarez; Juan G. (Boston, MA), Freedman; Steven (Brighton, MA) Assignee(s): Beth Israel Deaconess Medical Center, Inc. (Boston, MA) Patent Number: 6,180,671 Date filed: February 11, 1999 Abstract: A method of treating disorders in which DHA levels are affected is described. The method includes administering to a subject suffering from the disorder a therapeutically affective amount of DHA. This method is particularly useful in treating subjects suffering from a disorder characterized by a defect in the CF, gene, e.g. cystic fibrosis, or a chronic inflammatory disorder, e.g., ulcerative colitis, Crohn's disease, chronic pancreatitis, asthma, rheumatoid arthritis or chronic gastritis. A method of ameliorating affects of cystic fibrosis in a newborn and a method of increasing surfactant levels in a fetus are also described. Excerpt(s): Cystic Fibrosis (CF) is the most prevalent autosomal recessive disorder in the Caucasian population (Gorelick (1991) Gastroenterology 103 :681-693). Approximately 1 in 2000 live births are afflicted with CF and 5% of Caucasians in the United States are carriers of the abnormal CF gene. CF individuals rarely survive past their mid-thirties, and most mortalities are a result of recurrent pulmonary infection and, ultimately, pulmonary failure. Two other major clinical manifestations of CF are pancreatic dysfunction and male infertility. By 1989, the CF gene had been cloned and was found to code for a chloride channel. Activation of the channel in the normal pancreas activates the chloride/bicarbonate exchanger, resulting in a net secretion of bicarbonate into the lumenal space and alkalinization of the pancreatic juice. Mutations in the chloride channel like those found in CF result in a reduced chloride conductance and a reduced ability of ductal cells to secrete bicarbonate into the lumenal space. This results in the formation of inspissated plugs within the ducts leading to obstruction of the pancreatic ducts. In recent years, the focus in CF research has shifted towards the coupling of defective chloride channel function and membrane recycling. Recent research has demonstrated that membrane internalization at the apical plasma membrane of the pancreatic acinar cell is dependent on pH of the acinar lumen (Freedman et al., Eur. J Cell Biol. (1998) 75:153-63), Freedman et al., (1994) Am. J. Physiol. 267:G40-G51, and Freedman et al., (1994) Eur. J. Cell Biol. 65:354-365). Since pH of the acinar lumen is reflective of ductal bicarbonate secretion from the proximal duct cells, a phenomenon regulated via the chloride channel, a coupling may exist between duct and acinar cell function, (Freedman et al., (1994) Am. J. Physiol. 267:G40-G51, and Freedman et al., (1994) Eur. J. Cell Biol. 65:354-365). Research has also confirmed the hypothesis that lack of alkalinization of the acinar lumen leads to inhibition of apical membrane internalization and defective apical endocytosis in pancreatic acinar cells from CF mice. This block in the recycling of membranes following exocytosis leads to eventual deficiency in membranes for reformation of secretory granules. Thus, pancreatic insufficiency appears to be a result of defects in membrane recycling with obstruction of the ducts occurring as a secondary event. Web site: http://www.delphion.com/details?pn=US06180671__

Patents 143

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Monotherapy of peptic ulcers and gastritis Inventor(s): Hartmann; John F. (1 Woodmeadow Ln., Princeton Junction, NJ 08550-1323) Assignee(s): none reported Patent Number: 5,900,410 Date filed: August 12, 1997 Abstract: The present invention is directed to compositions, methods and kits for treating areas of H. pylori infection in the GI tract. The active ingredient is an antibioticbisphosphonate adduct wherein the antibiotic is selected for its ability to eradicate H. pylori. Other components include a salt of a divalent cation that is insolubilized in vivo at alkaline pH, and optionally a substrate from which the enzyme urease liberates NH.sub.3. Excerpt(s): The present invention relates to the treatment of ulcers in the upper gastrointestinal tract. The treatment of ulcers in the upper gastro-intestinal (hereafter GI) tract has heretofore been carried out by the use of bland diets, alkaline agents and gastric acid suppressors. While these methods have some effectiveness in relieving the pain and discomfort associated with such ulcers, they have only treated the symptoms and have failed to address the underlying cause which has come to be recognized as infection with Helicobacter pylori (hereafter H. pylori). Antibiotic treatments intended to eliminate the H. pylori infection have depended upon systemic distribution of the antibiotic, that is to say, absorption from the intestine, distribution into the systemic circulation, delivery to the upper GI tract, and release into the lumen. This method involves the administration of high levels of the antibiotic and, in some cases the appearance of systemic side-effects, and/or the development of a drug-resistant strain of H. pylori. It is, accordingly, an object of the present invention to provide a topical method for treating and ameliorating the infection that is responsible for gastritis and the formation of ulcers in the upper GI tract. Another object is to provide a method that does not require systemic administration of an antibiotic. A further object is to provide a kit containing the ingredients for carrying out the method of the present invention. Still another object is to provide compositions utilized in the method of the present invention. These and other objects of the present invention will be apparent from the following description. Web site: http://www.delphion.com/details?pn=US05900410__

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Prophylactic or therapeutic agent for diseases attributable to infection with helicobacters Inventor(s): Hirayama; Fumihiro (Fukuoka, JP), Sakurai; Nobuhiro (Fukuoka, JP), Sano; Mitsuharu (Fukuoka, JP), Yokoyama; Yoshito (Fukuoka, JP) Assignee(s): Welfide Corporation (Osaka, JP) Patent Number: 6,221,864 Date filed: December 23, 1999 Abstract: The present invention relates to an agent for the prophylaxis and treatment of diseases caused by Helicobacter infections, which comprises (S)-1-cyclopropyl-1,4dihydro-7-[2-(N,N-dimethylaminomethyl)morpholino]-6fluoro-8-methoxy-4oxoquinoline-3-carboxylic acid or a pharmaceutically acceptable salt thereof. The prophylactic and therapeutic agent of the present invention is effective even when used

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alone in a small dose for a short time, is almost free of problematic side effects such as tolerance and diarrhea, and is low toxic and capable of safe and ensured bacterial eradication. It is useful for the prophylaxis and treatment of diseases caused by Helicobacter infections, particularly, gastritis, gastric ulcer, duodenal ulcer, malignant lymphoma and gastric cancer. Excerpt(s): The present invention relates to a pharmaceutical agent containing (S)-1cyclopropyl-1,4-dihydro-7-[2-(N,N-dimethylaminomethyl)morpholino]-6fluoro-8methoxy-4-oxoquinoline-3-carboxylic acid or a pharmaceutically acceptable salt thereof, which agent is useful for the prophylaxis and treatment of diseases caused by Helicobacter infections, particularly gastritis, gastric ulcer, duodenal ulcer, gastric malignant lymphoma and gastric cancer. By the development of antisecretory drugs, such as histamine H.sub.2 antagonist and proton pump inhibitor, peptic ulcers, inclusive of a number of ulcers that heretofore required an operation, can now be cured by drug therapy. In view of the fact that most of the ulcers once cured are subject to recurrence and relapse, however, a maintenance therapy over a long period of time is considered to be necessary even after a complete cure, and even during the maintenance therapy, recurrence and relapse are highly frequently observed. In 1988, Marrshall B. J. et. al. (Lancet ii: 1437-42, 1988) applied eradication of Helicobacter pylori (H. pylori) to H. pylori positive gastric/duodenal ulcer cases, and reported a noticeable decrease in the relapse of duodenal ulcer. Thereafter in 1992, Graham D. Y. et. al. (Ann. Intern. Med. 116:705-708, 1992.) and in 1993, Hentschel E. et. al. (N. Engl. J. Med. 328:308-312, 1993) successively reported that relapse of peptic ulcer decreased significantly in the group subjected to eradication of H. pylori. Given the strong suggestion of the relationship between H. pylori infection, and gastritis and gastric/duodenal ulcer, a bacterial eradication therapy has been tentatively applied to patients with gastric/duodenal ulcer. Web site: http://www.delphion.com/details?pn=US06221864__ •

Specific catheter for percutaneous gastrostomy Inventor(s): Dimitri; Mauro (141, Via Delle Gondole, Rome, IT) Assignee(s): none reported Patent Number: 6,010,479 Date filed: May 21, 1996 Abstract: A specific catheter for percutaneous gastrostomy is indicated in all patients undergoing serious abdominal, general, or urologic surgical operations, or during the post-operatory period. This catheter is preferable to the naso-gastric tube which causes discomfort to patients and can be responsible for gastric erosions, gastritis, gastric bleeding, middle ear otitis, pulmonary atelectasis, and pneumonia. Moreover, this catheter is indicated for patients who require a prolonged enteral feeding. The catheter is positioned into the stomach at the end of the surgery through the abdominal wall, lateral to the abdominal incision by a percutaneous technique, and allows the best drainage of acid-mucous secretions from the stomach and duodenum. This catheter because of its material, its tip, its configuration inside the stomach, is a change from the traditional approach to patients improving their quality of life. Excerpt(s): Patients undergoing serious general and urologic surgical operations very often require a prolonged naso-gastric intubation in the post-operatory period. This intubation is performed by an anesthesiologist at the beginning of surgery by

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introducing a common naso-gastric tube (catheter). This catheter is useful for draining gastric and duodenal secretions until there are no more effects of general anesthetics on intestinal motility. This approach can cause much discomfort to patients and represents a morbidity factor by causing naso-gastric erosions, gastritis and gastric bleeding, middle ear otitis, pulmonary atelectasis, and pneumonia. The naso-gastric tube obstructs the upper airway, feels like a foreign body in the pharynx, and is not tolerated very well by the majority of patients. Percutaneous techniques for positioning gastric drainage systems have been described just recently in scientific literature starting in about 1991. The drainage of the stomach and duodenum (gastrostomy) is achieved by introducing a drainage catheter percutaneously through the abdominal wall, lateral to a surgical incision at the end of the surgery. This method presents an alternative to the nasogastric tube. Percutaneous gastrostomy is also indicated in those patients who require prolonged enteral feeding not consequent to surgery, and for whom the naso-gastric tube is not adequate. In these particular cases the gastrostomic catheter is introduced percutaneously through the abdominal wall and the gastric wall into the stomach, previously distended with air, under endoscopic guidance (gastroscopy). Smaller bladder (urethral) catheters, for draining urine, are utilized as gastrostomy catheters. Urethral catheters for bladder drainage adapted for gastrostomy have very short tips (from the distal end of the balloon to the apex of the catheter), about 3 cm, having only three holes, and are closed at their apexes. Several materials (latex rubber, polyvinyl, polyurethane, co-polymer, silicone rubber, etc.) are utilized to make catheters of different shapes for many purposes, and are already widely used all over the world, without technical difficulties. Web site: http://www.delphion.com/details?pn=US06010479__ •

Treatment of gastrointestinal ulcers or gastritis caused by microbial infection Inventor(s): Pfirrmann; Rolf W. (Lucerne, CH) Assignee(s): Ed. Geistlich Sohne AG fur chemische Industrie (CH) Patent Number: 6,117,868 Date filed: May 20, 1999 Abstract: A method and composition for the treatment of infectious gastrointestinal ulcer disease or infectious gastritis disease of microbially infected gastrointestinal tissue in a mammal involves administration of an antimicrobial amount of an antimicrobial medicament which is cell wall constituent-inactivating by chemical reaction with cell wall constituents, endotoxin non-releasing, exotoxin-inactivating or a combination thereof. Excerpt(s): The present invention relates to the field of treating patients having gastrointestinal ulcers or gastritis caused by microbial infection. The stomach's infection with the germ Heliobacter pylori (H.p.) is one of the most frequent infectious diseases in the world; in developing countries, more than 80% of the population is already infected with H.p. during childhood. In the past, chronic gastritis with prolonged dyspeptic symptoms in the upper stomach, the peptic ulcer, duodenal ulcer (UD) and ventral ulcer (UV) with pain in the upper stomach after meals or epigastric pain on empty stomach being a syndrome with unclear etiology. Its pathogenesis had not been clarified in detail. Generally, it can still be said today that there is no peptic ulcer without proteolytic gastric acid. Differential-diagnostic measures usually succeed in differentiating the peptic formation of ulcers from psychogenic gastrointestinal malfunctions. The final diagnosis depends on X-ray results.

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Web site: http://www.delphion.com/details?pn=US06117868__ •

Treatment of inflammation with 2,4,6-trihydroxy-alpha-rhomethoxyphenylacetophenone, or its pharmaceutically acceptable derivatives Inventor(s): Malaviya; Ravi (St. Paul, MN), Uckun; Fatih M. (White Bear Lake, MN) Assignee(s): Parker Hughes Institute (Roseville, MN) Patent Number: 6,248,790 Date filed: June 29, 2000 Abstract: 2,4,6-trihydroxy-.alpha.-p-methoxyphenylacetophenone (also identified herein as "D-58"), or its pharmaceutically acceptable derivatives such as salt and ester forms, is administered for inhibiting inflammatory reactions. The treatment can be remedial or prophylactic. Examples of the conditions that can be treated include acute inflammatory reactions and allergic inflammatory reactions, and specific examples include allergy, asthma, arthritis, psoriasis, skin sunburn, inflammatory pelvic disease, inflammatory bowel disease, urethritis, uvitis, senusitis, pneumonitis, encephalitis, meningitis, myocarditis, nephritis, osteomyelitis, myositis, hepatitis, gastritis, enteritis, dermatitis, gingivitis, appendicitis, pancreatitis, cholocystitis and cholangitis. The 2,4,6-trihydroxy.alpha.-p-methoxyphenylacetophenone can be administered by various routes as needed. Excerpt(s): The present invention is directed to the treatment of acute and chronic inflammatory responses, for example resulting from the presence of an allergen, injury, infection, etc. Allergic and acute inflammatory responses to injury, infection, or other tissue damage can set into motion a complex series of events. A variety of host cells that guard the host environment interface, including macrophages, mast cells, and epithelial/epidermal cells serve as the initiators of the inflammatory responses. These cells release various mediators during an inflammatory response, which include histamine, prostaglandins (PGs), leukotrienes (LTs) and proinflammatory cytokines (refs 1-4). These mediators have been implicated in the pathogenesis of a number of acute and chronic inflammatory conditions such as allergy, asthma, arthritis, psoriasis, and skin sunburn (refs 3-5). The release of inflammatory agents is mediated by a cascade of intracellular signaling events which include activation of phosphoinositide turnover (ref 6), increase in cAMP levels (ref 7), activation of protein kinase C, and an increase in intracellular calcium levels and tyrosine phosphorylation of several cytosolic proteins (refs 7 and 8). Considerable efforts have been made for identification of chemical compounds that can interrupt these signaling events as potential anti-inflammatory agents (refs 9-12). However, the need for agents providing improved inhibition continues. In accordance with the present invention, 2,4,6-trihydroxy-.alpha.-pmethoxyphenylacetophenone (also identified herein as "D-58"), or its pharmaceutically acceptable derivatives such as salt and ester forms, is administered for inhibiting inflammatory reactions to a subject in need thereof. The treatment can be remedial or prophylactic. Examples of the conditions that can be treated include acute as well as chronic inflammatory reactions and allergic inflammatory reactions, and specific examples include allergy, asthma, arthritis, psoriasis, skin sunburn, inflammatory pelvic disease, inflammatory bowel disease, urethritis, uvitis, sinusitis, pneumonitis, encephalitis, meningitis, myocarditis, nephritis, osteomyelitis, myositis, hepatitis, gastritis, enteritis, dermatitis, gingivitis, appendicitis, pancreatitis, cholocystitis and cholangititis. The 2,4,6-trihydroxy-.alpha.-p-methoxyphenylacetophenone can be administered by one of a variety of routes as needed.

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Web site: http://www.delphion.com/details?pn=US06248790__

Patent Applications on Gastritis 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 several years.) The following patent applications have been filed since December 2000 relating to gastritis: •

3-(diarylmethylene)-8-azabicyclo[3.2.1]octane derivatives Inventor(s): Boyd, Robert E.; (Horsham, PA), Carson, John R.; (Norristown, PA), Coats, Steven J.; (Quakertown, PA), Neilson, Lou Anne; (Sellersville, PA), Pitis, Philip M.; (North Wales, PA), Wu, Wu-Nan; (Lansdale, PA) Correspondence: Audley A. Ciamporcero JR.; Johnson & Johnson; One Johnson & Johnson Plaza; New Brunswick; NJ; 08933-7003; US Patent Application Number: 20020115662 Date filed: February 22, 2001 Abstract: This invention is directed to 3-(diarylmethylene)-8-azabicyclo[3.2.1]octan- e derivatives useful as.delta.-opioid or.mu.-opioid receptor modulators. Depending on their agonist or antagonist effect, the compounds are useful analgesics, immunosuppressants, antiinflammatory agents, agents for the treatment of neurological and psychiatric conditions, medicaments for drug and alcohol abuse, agents for treating gastritis and diarrhea, cardiovascular agents and agents for the treatment of respiratory diseases. Excerpt(s): The present invention is directed to compounds useful as delta-opioid and mu-opioid receptor modulators. More particularly, the present invention is directed to 3-(diarylmethylene)-8-azabicyclo[3.2.1]o- ctane derivatives useful as delta-opioid or muopioid receptor modulators. wherein R is hydrogen, methyl, propyl, hexyl, 2-ethylbutyl, allyl, 3,3-dimethallyl, cyclohexylmethyl, phenethyl, phenylpropyl, 2,2-diphenylethyl, 3,4-dimethoxyphenethyl, 4-fluorophenethyl, 2-furylmethyl, 3,4-methylenedioxybenzyl, cyano and X is N,N-dimethylamino, N,N-diethylamino, N,N-dipropylamino, N-methylN-ethylamino, N-methyl-N-propylamino, N-methyl-N-phenylamino, N-ethyl-N-(4methyl)benzylamino, N-butyl-N-ethylamino, N-butyl-N-propylamino, [N-ethyl-N-(2methyl)allyl]amino, hydroxy, O-t-butyl and 1-pyrrolidinyl; and, Y is hydrogen, methoxy and methylthio. Other selective 4-[(8-alkyl-8-azabicyclo[3.2.1] octyl-3-yl)-3-arylanilino]N,N-diethylbenzamide.delta.-opioid ligands have also been described (Thomas, J. B., Atkinson, R. N., Rothman, R. B., Burgess, J. P., Mascarella, S. W., Dersch, C. M., Xu, H. and Carroll, F. I., Biorg. Med. Chem. Lett., 2000, 10: 1281-1284). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

9

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

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•

Aminomethyl-phenyl-cyclohexanone derivatives Inventor(s): Buschmann, Helmut; (Aachen, DE), Koegel, Babette-Yvonne; (LangerweheHamich, DE), Puetz, Claudia; (Dueren, DE) Correspondence: Crowell & Moring Llp; Intellectual Property Group; P.O. Box 14300; Washington; DC; 20044-4300; US Patent Application Number: 20030096811 Date filed: July 5, 2002 Abstract: Aminomethyl-phenyl-cyclohexanone derivatives of formula I or Ia, 1their diastereomers, enantiomers and salts formed with a physiologically tolerated acid. Also disclosed are processes for preparing the same, pharmaceutical compositions comprising the same, and methods of using the same for the treatment of pain, inflammatory reaction, allergic reactions, depression, drug abuse, alcohol abuse, gastritis, cardiovascular disease, respiratory tract disease, coughing, mental illness, epilepsy, urinary incontinence, itching, and diarrhoea. Excerpt(s): The present application is a continuation of international patent application no. PCT/EP00/13282, filed Dec. 27, 2000, designating the United States of America, the entire disclosure of which is incorporated herein by reference. Priority is claimed based on Federal Republic of Germany patent application no. 100 00 311.7, filed Jan. 5, 2000. The present invention relates to aminomethyl-phenyl-cyclohexanone derivatives and processes for their preparation, the use of aminomethyl-phenyl-cyclohexanone derivatives for the preparation of medicaments and medicaments comprising aminomethyl-phenyl-cyclohexanone derivatives. Treatment of chronic and non-chronic states of pain is of great importance in medicine. There is a worldwide need for pain treatments with a good action for target-orientated treatment of chronic and non-chronic states of pain appropriate for the patient, by which is to be understood successful and satisfactory pain treatment for the patient. This manifests itself in the large number of scientific works which have been published in the field of applied analgesia and basic research in nociception in recent years. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

•

ANTI-HELICOBACTER VACCINE COMPLEX Inventor(s): TOROSSIAN, FERNAND NARBEY; (TOULOUSE, FR) Correspondence: John A Artz; Lyon & Artz; 28333 Telegraph Road; Suite 250; Southfield; MI; 48034 Patent Application Number: 20020032152 Date filed: August 25, 1998 Abstract: A therapeutical vaccine complex having activity specific for Helicobacter bacteria as well as non-specific immunomodulation activity for regulating the natural defences of the body, is disclosed. The drug is also useful for preventing relapses, particularly in cases of resistance to conventional treatment. The drug essentially consists of RNA, selective membrane fractions of microbial germs, particular amino acid sequences, sodium chloride and a steroidal anti-inflammatory in predetermined proportions enabling simultaneous delivery of antibiotics and frenosecretories. Said drug is particularly suitable for treating digestive tract diseases caused by Helicobacter (antral gastritis, duodenal ulcers, gastric ulcers, oesophagitis, hepatitis) and preventing

Patents 149

stomach cancer and degenerative infectious MALT (mucosa-associated lymphoid tissue) lymphoma, as well as coronary diseases directly or indirectly dependent on Helicobacter infections. Excerpt(s): The present invention relates to a therapeutic and preventive anti-bacterial vaccine complex which possesses a vaccinating power linked to the presence of specific antigens against Helicobacter pylori (previously called Campylobacter pylori), Helicobacter hepaticus, Helicobacter coronari, and nonspecific antigens providing immunomodulation. [MARSHALL B. J., WARREN Jr., Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration Lancet 1984: i:1311-4)]. [MGRAUD F., Helicobacter pylori, the most important bacterium among the mucus bacteria, La lettre de l'infectiologue 1993; 8 (suppl. 4): 151-9]. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Antimicrobial agent Inventor(s): Hadano, Makoto; (Tokyo, JP), Sato, Masaru; (Saitama, JP) Correspondence: Nixon & Vanderhye P.C.; 8th Floor; 1100 North Glebe Road; Arlington; VA; 22201-4714; US Patent Application Number: 20030069279 Date filed: May 15, 2002 Abstract: The present invention relates to an antimicrobial agent for preventing, ameliorating and treating diseases attributable to Helicobacter pylori, for example peptic ulcer and gastritis, particularly recurring peptic ulcer and recurring gastritis, and provides (1) an antimicrobial agent comprising oxethazaine represented by the following formula as an active ingredient, (2) an antimicrobial agent comprising oxethazaine and a proton pump inhibitor as active ingredients, and (3) an antimicrobial agent comprising oxethazaine and an antibiotic as active ingredients. 1 Excerpt(s): The present invention relates to an antimicrobial agent for preventing, ameliorating and treating diseases caused by the microaerophilic Gram-negative spiral and short bacillus Helicobacter pylori (H. pylori), for example peptic ulcer and gastritis, particularly recurring peptic ulcer and gastritis. Conventionally, a large number of medicines have been used as anti-ulcer agents for preventing, ameliorating and treating peptic ulcer such as gastric ulcer and duodenal ulcer, and recently, histamine H.sub.2receptor antagonists among these medicines are mainly used. By the advent of histamine H.sub.2-receptor antagonists, it became possible to rapidly ameliorate and treat peptic ulcer and gastritis, particularly with respect to subjective symptoms. However, in the treatment of peptic ulcer or gastritis by the conventional anti-ulcer agents containing histamine H.sub.2-receptor antagonists, there is the problem that ulcer recurs highly frequently when chemotherapy is suspended after the recovery. Because the reason for this recurrence has not been revealed for a long time, none of effective prophylactic and therapeutic methods have been established. Meanwhile, it was shown from 1979 onward that the microaerophilic Gram-negative spiral and short bacillus H. pylori is present in gastric mucosa of patients suffering from peptic ulcer and bacterium has a close relationship with gastritis and gastric ulcer. It, formerly classified as Campylobacter pylori (C. pylori), was newly designated H. pylori in re-consideration in microbial taxonomy in 1989, and thus C. pylori and H. pylori are the same bacterium although it may be referred to as C. pylori in some literatures. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Apparatus and method for debilitating or killing microorganisms within the body Inventor(s): Ganz, Robert A.; (Minnetonka, MN), Melgaard, Hans L.; (North Oaks, MN) Correspondence: James V. Harmon; Pillsbury Center, Suite 2000; 220 South Sixth Street; Minneapolis; MN; 55402; US Patent Application Number: 20030191459 Date filed: April 9, 2002 Abstract: A surgical apparatus has a body portion that includes a shaft terminating in a distal head or tip and a means for directing light radiation from the apparatus onto the lining of a body cavity for treating an ailment in a body cavity of a patient as for example a gastrointestinal ailment of a patient such as gastritis, gastric ulcer, duodenal ulcer, gastric cancer, gastric lymphoma, ulcerative colitis, or Crohn's disease as well as for treating diseases of the circulatory system, urogenital systems and other body cavities. The method of use of the apparatus comprises inserting the shaft of the apparatus into a body cavity, e.g., stomach or colon, of the patient to place the distal tip of the shaft in the desired position. The body cavity of the patient is then irradiated with light radiation so as to kill or debilitate microorganisms lining the body cavity without serious destruction of the body tissue of the patient to thereby improve or alleviate one or more of the symptoms of the ailment. A probiotic comprising innocuous bacteria can be administered to the patient to reestablish the growth of normal microbial flora when used in the gastrointestinal tract. Excerpt(s): This invention relates to an apparatus and method for the destruction of micro-organisms on or within a body cavity of a patient through the use of radiation. Infections involving the human gastrointestinal tract are extremely common, involving many millions of people on an annual basis. These infections include bacteria, viruses, and fungi, and are responsible for significant illness, morbidity and, in many cases, death. While the invention has utility in destroying microorganisms in various parts of the body, e.g., the stomach, bowel, lungs, peritoneal cavity, urinary tract, etc., it is particularly useful in the treatment of gastrointestinal infections. It has recently been shown that the most common gastrointestinal infection in the world is due to Helicobacter pylori, a bacterial pathogen that infects the stomach and duodenum. In the United States, for example, Helicobacter pylori is found in approximately 20% of the adult population. It is a chronic gut infection and, once acquired, is notoriously difficult to cure. Most infectious bacteria can be readily destroyed by the human immune system; however, Helicobacter pylori lives in the lumen of the stomach and on the surfaces of the stomach and duodenal cells, making it relatively resistant to a host immune response, even if vigorous. Its position has, however, been taken advantage of in the treatment method and apparatus employed in the present invention. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Benzamidine derivatives Inventor(s): Baxter, Ellen W.; (Glenside, PA), Nortey, Samuel O.; (Elkins Park, PA), Reitz, Allen B.; (Lansdale, PA) Correspondence: Audley A. Ciamporcero JR.; Johnson & Johnson; One Johnson & Johnson Plaza; New Brunswick; NJ; 08933-7003; US Patent Application Number: 20020123489 Date filed: December 11, 2001

Patents 151

Abstract: Benzamidine derivatives are useful delta-opioid receptor modulators, agonists useful as analgesics and antagonists useful as immunosuppressants, antiinflammatory agents, agents for the treatment of neurological and psychiatric conditions, medicaments for drug and alcohol abuse, agents for treating gastritis and diarrhea, cardiovascular agents and agents for the treatment of respiratory diseases. Excerpt(s): The present invention is directed to delta-opioid receptor modulators and methods for use thereof. More particularly, the present invention is directed to benzamidine derivatives which are delta-opioid receptor agonists or antagonists and methods for use thereof. The foregoing reference compounds have been described as either.delta.-opioid or.mu.-opioid receptor agonists or antagonists. wherein R and R' are hydrogen, lower alkyl, hydroxy, lower alkoxy, halogen or trifluoromethyl and may be the same or different; R" is lower alkyl, lower alkenyl, cycloalkyl, or phenyl, and R'" is hydrogen, lower alkyl, lower alkenyl, carboalkoxy, carboalkoxyalkyl, formyl, phenyl, halophenyl, cinnamyl, benzyl or benzhydryl as having hypoglycemic activity. The lower alkyl, lower alkoxy and lower alkenyl groups may be branched or straight chained and contain up to 6 carbon atoms. The cycloalkyl groups contain from 3 to 7 carbon atoms in the ring which may also carry a lower alkyl substituent. The carboalkoxy groups contain alkyl groups having from 1 to 5 carbon atoms and include carbomethoxy, carbethoxy, carbopropoxy, carbobutoxy and the like. Desirably, R and R' are lower alkyl, preferably methyl, or halogen, preferably chloro; R may be hydrogen and R' is then chloro, lower alkyl, preferably methyl, or trifluoromethyl; R" is lower alkyl, preferably isobutyl, and R'" is carbethoxy. Exemplified compounds include those wherein R is selected from hydrogen, chlorine, fluorine or methyl; R' is selected from hydrogen, chlorine, fluorine, methyl, methoxy, hydroxy or trifluoromethyl; R" is selected from hydrogen, chlorine, fluorine, methyl, ethyl, n-propyl, n-butyl, i-butyl, i-amyl, n-hexyl, allyl, cyclohexyl, phenyl or 3,4-dimethylphenyl; R'" is selected from hydrogen, methyl, ethyl, n-hexyl, allyl, phenyl, 4-Cl-phenyl, benzhydryl, benzyl, 2,4-Cl.sub.2-benzyl, 2,3,4-(MeO).sub.3benzyl, COOEt or CHO. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Chelate compound-containing antibacterial agent for helicobacter pylori Inventor(s): Nagai, Toshiro; (Tsukuba-shi, JP), Oita, Shigeru; (Zentsuji-shi, JP) Correspondence: Frishauf, Holtz, Goodman; Langer & Chick, P.C.; 25th Floor; 767 Third Avenue; New York; NY; 10017; US Patent Application Number: 20020058696 Date filed: March 8, 2001 Abstract: An antibacterial agent is provided, which has an action for inhibiting growth of Helicobacter pylori participating to occurrence of chronic gastritis and gastric ulcer, and a highly safe substance is used as an effective component therein. An antibacterial agent for Helicobacter pylori is characterized in that at least one substance selected from the group consisting of ethylenediaminetetraacetic acid and its metal salts is contained as an effective component. Excerpt(s): The present invention relates to an antibacterial agent for Helicobacter pylori, in more detail, to an antibacterial agent for Helicobacter pylori, said agent contains as an effective component a chelate compound, safety of which against human bodies is confirmed. Recently, it has been found that Helicobacter pylori is much participated to occurrence of chronic gastritis and gastric ulcer. In Japan, it is said that

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about 60 millions people corresponding to an about half of total populations are infected with Helicobacter pylori (Shokunokagaku, Vol. 265, pages 87-99, 2000). Cure of chronic gastritis and gastric ulcer can be attained by removing the bacterium from stomach by means of administration of antibiotics etc. However, there are some cases wherein the bacterium is hard to be removed depending on patients. Further, as to antibiotics, there are some problems concerning appearance of resistant bacteria and side effects. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Circulating epstein-barr virus DNA in the serum of patients with gastric carcinoma Inventor(s): Chan, Wing Yee; (Tuen Mun, CN), Lo, Yuk Ming Dennis; (Kowloon, CN), Ng, Kwok Wai; (Tai Po, CN) Correspondence: Townsend And Townsend And Crew, Llp; Two Embarcadero Center; Eighth Floor; San Francisco; CA; 94111-3834; US Patent Application Number: 20020192642 Date filed: January 25, 2002 Abstract: The present invention features methods for diagnosing, detecting, monitoring and determining the prognosis of gastric cancer, non-head and neck and lymphoid malignancies, and gastritis in a patient by detecting or measuring EBV DNA present in the serum or plasma of the patient. The present invention also features diagnostic kits comprising suitable reagents for detecting EBV DNA in the serum or plasma of a patient. Excerpt(s): This invention relates to the discovery that Epstein Barr virus may be found in the cell free fluid of a patient's blood and when such virus is found and the patient suffers from gastritis, that patient has a predisposition to progress from gastritis to gastric cancer. It is known that tumour-derived DNA can be released by cancer cells of a variety of tumours (Anker et al., Cancer Metastasis Rev. 18: 65-73 (1999)). Examples include oncogene mutations from pancreatic carcinoma (Anker et al., Gastroenterology. 112: 4-1120 (1997)), microsatellite alterations in lung cancer (Chen et al., Nature Medicine. 2: 3-1035 (1996)) and epigenetic changes from liver cancer (Wong et al., Cancer Res. 59: 3 (1999)). In addition, virus DNA has been found in the circulation of a number of cancers known to be associated with virus infection. Examples include Epstein-Barr virus (EBV) DNA from nasopharyngeal cancer (Mutirangura et al., Clin Cancer Res. 4: 665-9 (1998); Lo et al., Cancer Res. 59: 1188-91 (1999)) and certain lymphomas (Lei et al., Br J Haematol. 111:239-46 (2000); Gallagher et al., Int J Cancer. 84: 442-8 (1999); Drouet et al., J Med Virol. 57: 383-9 (1999)), and human papillomavirus DNA from head and neck cancer (Capone et al., Clin Cancer Res. 6: 4171-5 (2000)). Recently, much interest has been focused on the presence of tumor-derived DNA in the plasma and serum of cancer patients (Chen, X. Q. et al., Nat. Med., 2:1033-1035 (1996); Nawroz, H. et al., Nat. Med., 2:1035-1037 (1996)). For virally-associated cancers, cell-free tumor-associated viral DNA has been detected in the plasma and serum of patients (Mutirangura, A. et al., Cancer Res., 4:665-669 (1998); Lo, Y. M. D. et al., Clin. Cancer Res., 59:1188-1191 (1999); Capone, R. B. Clin. Cancer Res., 6:4171-4175 (2000)). One important virus which has been associated with many types of malignancy is the Epstein-Barr virus (EBV) (Cohen, J. I. N. Engl. J Med., 343:481-492 (2000)). Epstein-Barr virus (EBV) is a human herpesvirus that infects the majority of the human population. EBV is commonly transmitted by saliva and established latent infection in B lymphocytes where it persists for the lifetime of the host. In this regard, circulating EBV DNA has been detected in the plasma and serum of patients with nasopharyngeal

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carcinoma (NPC) (Mutirangura, A. et al., Cancer Res., 4:665-669 (1998); Lo, Y. M. D. et al., Clin. Cancer Res., 59:1188-1191 (1999)) and certain lymphoid malignancies (Lei, K. I. et al., Br. J Haematol., 111:239-246 (2000); Drouet, E. et al., J. Med. Virol., 57:383-389 (1999); Gallagher, A. et al., Int. J. Cancer, 84:442-448 (1999)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Compositions for preventing and treating digestive organs diseases Inventor(s): Araki, Hiromasa; (Yamatokoriyama-shi, JP), Kakehi, Kazuaki; (Nara-shi, JP), Kawabata, Atsufumi; (Yamatotakada-shi, JP), Kawai, Kenzo; (Matsubara-shi, JP), Kuroda, Ryotaro; (Osaka-shi, JP), Nishikawa, Hiroyuki; (Kashiba-shi, JP), Nishimura, Sachiyo; (Sakurai-shi, JP), Tanaka, Shuichi; (Sennan-gun, JP) Correspondence: Browdy And Neimark, P.L.L.C.; 624 Ninth Street, NW; Suite 300; Washington; DC; 20001-5303; US Patent Application Number: 20030166553 Date filed: August 22, 2002 Abstract: The present invention provides a composition for safely and effectively preventing and treating digestive organs diseases, particularly, gastric ulcer, duodenal ulcer, gastritis, diarrhea, enteritis and the like. There is also provided a composition having a novel mechanism of action in order to solve the problems which was difficult to be solved by the side effect previously known mechanisms of action. More particularly, there is provided a pharmaceutical composition containing an ingredient which activates PAR-2 as an essential ingredient, which is useful for inhibiting gastric acid secretion, promoting digestive tract mucus secretion, protecting digestive tract mucosa, repairing tissue of digestive organs, and preventing and treating digestive organs diseases. Excerpt(s): The present invention relates to compositions for preventing and treating digestive organs diseases, especially, compositions for preventing and/or treating gastric ulcer, duodenal ulcer, gastritis, diarrhea, enteritis and the like. Peptic ulcer such as gastric ulcer, duodenal ulcer and the like are resulted from the disruption of a balance between aggressive factors and protective factors. Example of disruption-inducing factors include drugs (e.g., non-steroidal anti-inflammatory agents, adrenocortical hormone agents, antibiotics, anti-cancer agents, oral hypoglycemic agents), stress, alcohols, corrosive drugs, cirrhosis, anisakid spp., eating habits and the like. At present, aggressive factor inhibitors, protective factor enhancers, and combinations thereof are clinically used. As the aggressive factor inhibitors, there are clinically used antacids (e.g., sodium bicarbonate and aluminum hydroxide gel, magnesium oxide etc.), anticholinergics (e.g., atropine sulfate, pirenzepine hydrochloride etc.), H2-receptor antagonists (e.g., cimetidine, ranitidine, famotidine, nizatidine, roxatidine etc.), proton pump inhibitors (e.g., omepurazor, ransoprazol, ransoprazol sodium etc.), anti-gastrin drugs (e.g., proglumide, secretin, urogastorone), and anti-pepsin drugs (sucrose sulfate ester, sucralfate etc.) and the like. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Food containing active strains for inhibiting infection and treating gastritis, gastric and duodenal ulcers Inventor(s): Baek, Young Jin; (Seoul, KR), Heo, Cheol Seong; (Chunan, KR), Kim, Hyung Soo; (Granger, IN), Lee, Jeong Jun; (Suwon, KR) Correspondence: Alfred D. Lobo, ESQ.; Lobo & CO., L.P.A.; 933 The Leader Building; 526 Superior Avenue; Cleveland; OH; 44114-1401; US Patent Application Number: 20020037341 Date filed: October 10, 2001 Abstract: Live strains of Lactobacillus acidophilus HY2177 and Lactobacillus casei HY2743 maintained in nutritious foods, such as yogurt, imbue them with prophylactic and/or therapeutic properties. Such foods are beneficial in the prevention and/or treatment of gastritis, duodenal and gastric ulcers caused by infection from Helicobacter pylori (also referred to as H. pylori). The properties of these bacteria are boosted by the addition of egg yolk containing antibodies specific to H. pylori antigen derived from "fractionated H. pylori" and may be administered as active strains alone in a food supplement, or the active strains may be combined with H. pylori-antibodies (IgY). Excerpt(s): This application is a continuation-in-part application of Ser. No. 09/498,668 filed on Feb. 7, 2000. A nutritional formulation in which non-toxic (to humans) bacteria thrive, is used to prevent and treat gastric disorders associated with Helicobacter pylori (also referred to as H. pylori) which are believed to be attacked by the non-toxic bacteria. Only particular strains of non-toxic comestible bacteria, when ingested by humans are effective against H. pylori. Optionally and preferably, the prophylactic and/or therapeutic effects of the comestible bacteria are boosted with egg yolk containing immunoglubins (antibodies) specific to H. pylori antigen (also referred to as "H. pylori-antibodies"). Much has been published regarding H. pylori which inhabits the human gastric mucosa. It is a gram-negative spiral rod-shaped bacterium having an outer membrane with four to six polar flagella which are sheathed and have bulbous ends; each H. pylori bacterium is about 0.85.mu.m (micrometer) in diameter with an average length of 2.9.mu.m. Known pathogenic (disease) factors of H. pylori are (i) urease (urea aminohydrolase) which is produced by the bacteria to allow it to thrive in a strong acid environment in the range from pH 1-3, (ii) flagella which provide the bacteria with mobility, and (iii) a protein-aceous outer membrane of the cells which membrane helps the cells to stick to the gastric mucosal cells. Survival of H. pylori relies upon creation of a relatively non-acidic microenvironment in the vicinity of the bacteria, and a relatively basic microenvironment is provided by the enzyme urease; the more basic the better, and the closer to neutral pH, the more difficult it is for the H. pylori to thrive. The ability to command a near-neutral microenvironment is an essential property of bacteria which effectively prevent and treat gastric disorders. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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METHOD FOR PREVENTING GASTRITIS USING AMYLIN OR AMYLIN AGONISTS Inventor(s): BEYNON, GARETH W.; (BRIGHTWELL-CUM SOTWELL, UA), GEDULIN, BRONISLAVA; (SAN DIEGO, CA), YOUNG, ANDREW A.; (SAN DIEGO, CA) Correspondence: Bradford J. Duft, Esq; Brobeck, Phleger & Harrison Llp; 12390 EL Camino Real; San Diego; CA; 92130; US Patent Application Number: 20020010133 Date filed: May 6, 1997 Abstract: Methods for treating or preventing gastritis or gastric injury are disclosed, comprising administering a therapeutically effective amount of an amylin or an amylin agonist. Methods are also disclosed for the treatment of pain, fever, inflammation, arthritis, hypercoagulability, or other conditions for which a non-steroidal antiinflammatory drug would be indicated, comprising administering an amylin or amylin agonist in conjunction with administering a therapeutically effective amount of a nonsteroidal anti-inflammatory agent. Pharmaceutical compositions comprising an amylin or amylin agonist and a non-steroidal anti-inflammatory drug are also disclosed. Excerpt(s): The present invention relates to methods for treating or preventing gastritis or gastric injury by administering an amylin or an amylin agonist. The present invention also relates to the treatment of pain, fever, inflammation, arthritis, hypercoagulability, or other conditions for which a non-steroidal anti-inflammatory drug would be indicated, comprising administering an amylin or an amylin agonist in conjunction with a nonsteroidal anti-inflammatory drug. Pharmaceutical compositions comprising an amylin or an amylin agonist and a non-steroidal anti-inflammatory agent are also described by the present invention. Publications and other materials including patents and patent applications used to illuminate the specification are hereby incorporated by reference. The structure and biology of amylin have previously been reviewed. See, for example, Rink et al., Trends in Pharmaceutical Sciences, 14:113-118 (1993); Gaeta and Rink, Med. Chem. Res., 3:483-490 (1994); and, Pittner et al., J. Cell. Biochem., 55S:19-28 (1994). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Method for the production of the egg containing anti-pathogenic bacteria specific antbodies(igy) and the yogurt and ice cream containing the igy Inventor(s): Baek, Ban-Suk; (Gyeonggi-do, KR), Jung, Kwnag-Yong; (Daejeon, KR), Lee, Nam-Hyung; (Seoul, KR), Ryu, Jung-Soo; (Daejeon, KR), Sunwoo, Sun-Young; (Seoul, KR) Correspondence: Fleshner & Kim; PO Box 221200; Chantilly; VA; 20153-1200; US Patent Application Number: 20030185856 Date filed: November 27, 2002 Excerpt(s): The present invention provides the method for the production of the egg containing anti-pathogenic bacteria specific antibodies (IgY) preventing gastritis, diarrhea, and food poisoning by immunizing young hens with antigen proteins of E. coli causing enteritis, Helicobacter pylori causing gastritis, and Salmonella enteritidis and Salmonella typhimurium, causing food poisoning, simultaneously, the composition containing the protein powders of the specific antibodies described above, mixed in the appropriate ratio, which produced by immunization with the four antigens separately,

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and the foodstuff processed with milk, such as the yogurt and ice cream, containing the anti-pathogenic bacteria specific antibodies (IgY). Additionally, as the method for isolating the protein powders of the specific antibodies, the method for separating protein and phospholipid, particularly, proceeded in a process of diluting egg yolk with distilled water in 1:1 ratio, adding the appropriate amount of ammonium sulfate which enable water-soluble protein and phospholipid to separate, and the method for separating the pigment of egg-yolk and water-soluble protein, proceeded in a process of diluting those separated solution with distilled water, sitting in the certain temperature to precipitate and purify the proteins. The prior art related to patent of E.1coli is summarized as following. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

METHODS FOR TREATMENT AND PREVENTION OF HELICOBACTER PYLORI INFECTION USING LACTOFERRIN Inventor(s): CONNEELY, ORLA M.; (HOUSTON, TX), HEADON, DENIS R.; (HOUSTON, TX), WARD, PAULINE P.; (HOUSTON, TX) Correspondence: Howrey Simon Arnold & White, Llp; Box 34; 301 Ravenswood AVE.; Menlo Park; CA; 94025; US Patent Application Number: 20020016289 Date filed: February 25, 1999 Abstract: The present invention is directed to methods for using lactoferrin as a therapeutic and/or prophylactic compound to treat and/or prevent infections caused by enteropathogens such as H. pylori. The present invention is directed to the treatment or prevention of diseases and disorders resulting from infection by enteropathogens such as H. pylori including histological gastritis, functional dyspepsia, duodenal ulcers, gastric ulcers, gastric cancer, chronic renal failure, HIV, pernicious anemia, ZollingerEllison syndrome and colonic polyps. The present invention is further directed to novel formulations and compositions comprising lactoferrin and pharmaceutically acceptable carriers, excipients and/or adjunct companion therapies such as one or more antibiotics. Excerpt(s): The present invention is in the field of molecular biology, biochemistry and medicine. Specifically, the present invention provides methods for treating bacterial infections, especially Helicobacter pylori infections using lactoferrin alone or in combination with another agent such as an antibiotic. Helicobacter pylori is an etiologic agent of gastric and peptic ulcer disease which infects over 50% of the human adult population. Diseases such as histological gastritis, functional dyspepsia, duodenal ulcers, gastric ulcers, gastric cancer, chronic renal failure, HIV, pernicious anemia, Zollinger-Ellison syndrome and colonic polyps have been associated with H. pylori infection. The present invention is directed to methods for treating and/or preventing infection with such organisms as H. pylori and related diseases resulting from infections with the same using lactoferrin alone or in combination with an antibiotic. The present invention is further directed to novel formulations and compositions comprising lactoferrin and pharmaceutically acceptable carriers, excipients and/or adjunct companion therapies. Helicobacter is a member of the superfamily VI of Gram-negative bacteria. Vandamme et al., Int. J. Syst. Bacteriol., 1991, 41:88-103. It is a microaerobe having an asaccharolytic metabolism, a membrane bound urease and an aptitude for living in mucus. There are at least 9 known species of Helicobacter. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Naphthyloxy acetic acid derivatives and a pharmaceutical composition comprising them as an active ingredient Inventor(s): Hamanaka, Nobuyuki; (Mishima-gun, JP), Nagao, Yuuki; (Mishima-gun, JP), Torisu, Kazuhiko; (Mishima-gun, JP) Correspondence: Stevens, Davis, Miller & Mosher, L.L.P.; Suite 850; 1615 L Street, N.W.; Washington; DC; 20036; US Patent Application Number: 20010005760 Date filed: January 22, 2001 Abstract: The naphthyloxyacetic acid derivatives of the formula (I) 1wherein A is H, -(alkylene)COOR', --(alkylene)CONR.sup.2R.sup.3, --(alkylene)OH, --(alkylene)tetrazole, --(alkylene)CN; E is single bond or alkylene; G is --S--, --SO--, --SO.sub.2--, --O--or -NR.sup.4--; L is alkylene, --(CH.sub.2).sub.m--CH.dbd.CH--(CH.sub.2).sub.n--or --(C (CH.sub.2).sub.y--; M is phenyl, phenyl(thio, oxy, amino), diphenylmethyl, diphenylmethyl(thio, oxy, amino), and pharmaceutical composition comprising them as an active ingradient.The compounds of the formula (I) can combine PGE.sub.2 receptor and exhibit the activity to antagonize or agonize for PGE.sub.2 receptor. Therefore, they are useful as anti-hyperlipemia, for the prevention of abortion, for analgesics, as antidiarrheals, sleep inducer, diuretic, anti-diabetes, abortient, cathartics, antiulcer, antigastritis or antihypertensive etc. Excerpt(s): (2) a pharmaceutical composition (Prostaglandin E.sub.2 (PGE.sub.2) antagonists or agonists) which comprises them as an active ingredient. Therefor, to antagonize PGE.sub.2 receptor means to suppress the effects above mentioned, so such an activity is linked to inhibit diuretic, to inhibit hyperlipemia, to inhibit reduce of blood sugar, to inhibit uterine contraction, to have analgesic action, to inhibit digestive peristalsis, to induce sleep. Therefor, PGE.sub.2 receptor antagonists are considered to be useful as anti-hyperlipemia, for the prevention of abortion, for analgesics, or as antidiarrheals or sleep inducer. To agonize for PGE.sub.2 receptor means to promote the effects above mentioned, so such an activity is linked to have diuretic, to promote hyperlipemia, to promote reduce of blood sugar, to contractile uterine, to promote digestive peristalsis, to suppress gastric acid secretion or to reduce blood pressure. Therefor, PGE.sub.2 receptor agonists are considered to be useful for diuretic, antidiabetes, abortient, cathartics, antiulcer, anti-gastritis or antihypertensive. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Novel lactobacillus paracasei subsp. paracasei strain antibacterial against helicobacter pyroli and escherichia coli 0157:h7 Inventor(s): Cho, Seong-Kun; (Kyonggi-do, KR) Correspondence: George M Kaplan; Dilworth & Barrese; 333 Earle Ovington Boulevard; Uniondale; NY; 11553; US Patent Application Number: 20030138406 Date filed: August 23, 2002 Abstract: The present invention relates to novel lactic microorganism, method for preparation and uses thereof. Particularly, the present invention relates to novel Lactobacillus paracasei strain (lactobacillus paracasei subsp. paracasei CSK 01) which is prepared by the process comprising the steps: (1) administering lactic bacteria derived

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from gastric mucus of pig to patients of gastritis and enteritis; (2) separating lactic bacteria from the patients' feces again after their complete recovery; and (3) identifying the bacteria strain by performing 16S rRNA sequencing and RAPD polymerase chain reaction. The Lactobacillus strain of the present invention can attach to and proliferate on gastric and intestinal mucosa, resist to acidic and bilious conditions outstandingly and have excellent antibacterial properties. Therefore, the Lactobacillus strain and its antibacterial substance can be utilized widely to develop new drugs, functional food, health promoting additives and the like. Excerpt(s): The present invention relates to a novel lactic microorganism, its antibacterial substance and methods for preparation thereof. Particularly, the present invention relates to a novel Lactobacillus paracasei strain (Lactobacillus paracasei subsp. paracasei CSK 01) which is prepared by the process comprising the steps: (1) administering lactic bacteria derived from gastric mucus of pig to patients of gastritis and enteritis; (2) separating lactic bacteria from the patients' feces again after their complete recovery; and (3) identifying the bacterial strain by performing 16S rRNA sequencing and RAPD polymerase chain reaction. The Lactobacillus strain of the present invention can attach to and proliferate on gastric and intestinal mucosa, resist to acidic and bilious conditions outstandingly and have excellent antibacterial properties and thus can be utilized widely to develop new drugs, functional food, health promoting additives and the like. Generally, Lactobacillus sp. has a high affinity for epithelial cells of alimentary organs which contain a lot of lectin material. Thus, lactic bacteria coming from outer environment to inner body are prone to attach to and proliferate on this region. Also, the lactic bacteria which are settled habitually in the inner body make colonies onto this affiliated surface. Various kinds of Lactobacillus sp. inhabit aboriginally epithelial cells and make symbiosis to survive mutually, which gives host animals functional benefits consistently. Especially, each species plays a different role and thus has a peculiar function of probiotics, for example A bacterium strain makes colonies, B strain secretes antibacterial substance, C strain secretes highly acidic lactates, D strain helps digestive activities and the like. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Nutritional composition Inventor(s): Anantharaman, Helen Gillian; (Bridgewater, CT), Fuchs, Eileen C.; (Gaylordsville, CT), Garcia-Rodenas, Clara L.; (Forel, CH), Guigoz, Yves; (Epalinges, CH), Leathwood, Peter; (Blonay, CH), Mallangi, Chandrasekhara R.; (New Milford, CT), Reiffers-Magnani, Kristel; (La Tour-de-Peilz, CH), Turini, Marco; (Epalinges, CH) Correspondence: Bell, Boyd & Lloyd Llc; P.O. Box 1135; Chicago; IL; 60690-1135; US Patent Application Number: 20020044957 Date filed: March 29, 2001 Abstract: A composition for a nutritional supplement for convalescing patients recovering from illness or surgery, those with limited appetite such as the elderly, children or anorexic patients, or those who have impaired ability to digest other sources of protein such as persons having chronic gastritis who have a reduced gastric pepsin digestion. The supplement comprises: (i) a protein source which provides at least about 8% total calories of the composition and which includes at least about 50% by weight whey protein; (ii) a lipid source having an omega 3:6 fatty acid ratio of about 5:1 to about 10:1 and which provides at least about 18% total calories of the composition; (iii) a carbohydrate source; and (iv) a balanced macronutrient profile comprising at least

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vitamin E and vitamin C. The supplement has reduced capacity to induce satiety. Also disclosed are a method of production of the composition; use of the composition in the manufacture of a functional food or medicament; and a method of treatment which comprises administering an effective amount of the composition. Excerpt(s): This application claims the benefit of U.S. Provisional Application Ser. No. 60/227,117 filed on Aug. 22, 2000. The present invention relates to a composition for a nutritional supplement; a method of production of the composition; use of the composition in the manufacture of a functional food or medicament for the nutrition, prevention or treatment of convalescing patients recovering from illness or surgery, those with limited appetite such as the elderly, or anorexic patients, or those who have impaired ability to digest other sources of protein such as persons having chronic gastritis who have a reduced gastric pepsin digestion; and a method of providing nutrition or treatment which comprises administering an effective amount of the composition. Many people do not take in sufficient nutrients for a nutritionally complete diet. In order to assist these people, nutritional supplements have been developed. Nutritional supplements are usually not intended to provide all the nutrients necessary for a nutritionally complete diet; instead they are generally intended to supplement the diet such that it becomes more nutritionally complete. However, in some instances they may provide complete nutrition. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Pharmaceutical composition for preventing and/or curing digestive disorders Inventor(s): Ito, Mikio; (Aichi, JP) Correspondence: Armstrong,westerman, Hattori,; Mcleland & Naughton, Llp; 1725 K Street, Nw, Suite 1000; Washington; DC; 20006; US Patent Application Number: 20020001628 Date filed: July 30, 2001 Abstract: The invention provides a pharmaceutical composition for preventing and/or curing digestive disorders such as digestive ulcers, gastritis, etc. The pharmaceutical composition contains, as the active ingredient, an aluminosilicate having silver and zinc ions, and it has an excellent effect for protecting gastric mucous membrane and an excellent effect of promoting the curing of a gastric ulcer. Excerpt(s): The present invention relates to a pharmaceutical composition for preventing and/or curing digestive disorders such as digestive ulcers, gastritis, etc. It is said that digestive disorders such as typically gastric ulcers are so-called national diseases much seen in Japan, and the rate of the diseases in Japan is higher than that in other countries. Accordingly, various medicines for such digestive disorders have heretofore been developed and put into practical use. At present, however, better medicines for digestive disorders are desired. The object of the present invention is to provide a pharmaceutical composition for preventing and/or curing digestive disorders such as digestive ulcers, gastritis, etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Salts of bicyclic, N-acylated imidazo-3-amines and imidazo-5-amines Inventor(s): Gerlach, Matthias; (Brachttal, DE), Sundermann, Corinna; (Aachen, DE) Correspondence: Crowell & Moring Llp; Intellectual Property Group; P.O. Box 14300; Washington; DC; 20044-4300; US Patent Application Number: 20030119842 Date filed: October 18, 2002 Abstract: Salts of a bicyclic, N-acylated imidazo-3-amine or an imidazo-5-amine of the formula: 1addition products thereof with acids, and methods for preparing the salts and addition products. Also disclosed are pharmaceutical compositions comprising the same and methods using the pharmaceutical compositions for the treatment or prophylaxis of pain, drug or alcohol abuse, diarrhoea, gastritis, ulcers, urinary incontinence, depression, narcolepsy, overweight, asthma, glaucoma, tinnitus, itching, hyperkinetic syndrome, epilepsy, or schizophrenia, for inducing anesthesia, and for anxiolysis. Excerpt(s): The present application is a continuation of international patent application no. PCT/EP01/03772, filed Apr. 3, 2001, designating the United States of America, and published in German as WO 01/81344, the entire disclosure of which is incorporated herein by reference. Priority is claimed based on Federal Republic of Germany patent application no. 100 19 714.0, filed Apr. 20, 2000. The present invention relates to salts of bicyclic, N-acylated imidazo-3-amines and imidazo-5-amines, to a process for producing them, to their use for producing pharmaceutical compositions and to pharmaceutical compositions containing these compounds. Individual compounds from the category of non-acylated bicyclic imidazo-3-amines and imidazo-5-amines which form the basis of the compounds according to the present invention are known to have interesting pharmacological properties. Thus, certain imidazo[1,2-a]pyridines are described as blood pressure-reducing active ingredients (GB-B-1,135,893), as anthelmintics and antimycotics (J. Med. Chem. 1972, 15, 982-985) and as anti-secretory active ingredients for the treatment of inflammatory diseases (EP-A-0 068 378). EP-A-0 266 890 and J. Med. Chem. 1987, 30, 2031-2046 also describe an effect of individual imidazopyridines against inflammatory diseases, in particular of the stomach. Further pharmacological effects described for individual representatives of the category of non-acylated imidazo-3amines and imidazo-5-amines are antibacterial properties (Chem. Pharm. Bull. 1992, 40, 1170), antiviral properties (J. Med. Chem. 1998, 41 5108-5112) and the effect as benzodiazepine-receptor antagonist (J. Heterocyclic Chem. 1998, 35, 1205-1217). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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SPECIFIC ANTIBODIES FOR USE IN PREPARATION OF PHARMACEUTICAL COMPOSITIONS USEFUL IN THE PREVENTION OR TREATMENT OF GASTRITIS, GASTRIC ULCERS AND DUODENAL ULCERS Inventor(s): ARIGA, MASATO; (SAITAMA-KEN, JP), ICATLO, FAUSTINO C. JR.; (GIFU-SHI, JP), KIMURA, NOBUTAKE; (SAITAMA-KEN, JP), KODAMA, YOSHIKATSU; (GIFU-SHI, JP) Correspondence: Burns Doane Swecker & Mathis L L P; Post Office Box 1404; Alexandria; VA; 22313-1404; US Patent Application Number: 20010021393 Date filed: April 8, 1998

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Abstract: The present invention provides specific antibodies obtained from eggs laid by hens which have been immunized against urease of Helicobacter pylori as an antigen, and specific antibodies obtained from eggs laid by hens which have been immunized against flagella of Helicobacter pylori as an antigen. These antibodies are useful for the prevention or treatment of gastritis, gastric ulcers and duodenal ulcers caused by infection of Helicobacter pylori. At least one organism selected from lactic acid bacteria, Enterococcuses, yeasts, and Baillus can be used along with the antibodies. Excerpt(s): The present invention relates to specific antibodies for use in preparing pharmaceutical compositions useful for the prevention or treatment of gastritis, gastric ulcers and duodenal ulcers caused by infection of Helicobacter pylori (hereinafter referred to as H. pylori or Hp), and for use as an additive to foods useful for the prevention of gastritis, gastric ulcers and duodenal ulcers. At present it is believed that eradication of H. pylori in the stomach is essential for treating peptic ulcers fully. The combination of antibiotics and suppressors of gastric acid secretion has been generally proposed as a therapy for effective eradication of H. pylori as described below. H. pylori is a gram-negative spiral rod-shaped bacterium having some flagella at one end and inhabiting the human gastric mucosa. Marshall, B. J. and Warren, J. R. in Australia reported in 1983 that this bacterium was frequently detected in stomach biopsy specimens from patients with gastric ulcers. At that time this bacterium was named Campylobacter pylori since it resembles Campylobacter in morphology and growth characteristics. Later, it was found that the bacterium is different from Campylobacter in the fatty acid composition of its outer membrane and sequence of ribosome 16S-RNA. Therefore, the bacterium is now referred to as Helicobacter pylori and belongs to a newly established genus of Helicobacter. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Substituted pyrrole mannich bases to combat pain and allergic reactions Inventor(s): Gerlach, Matthias; (Brachttal, DE), Maul, Corinna; (Aachen, DE) Correspondence: Oblon Spivak Mcclelland Maier & Neustadt PC; Fourth Floor; 1755 Jefferson Davis Highway; Arlington; VA; 22202; US Patent Application Number: 20030023100 Date filed: June 25, 2002 Abstract: The invention relates to substituted pyrrole Mannich bases of general formula (I), wherein R.sup.1=H, a C.sub.1-10-alkyl-, aryl, a heteroaryl- or an aryl, heteroaryl-, CN, Br--, Cl or OH radical bound by a C.sub.1-6 alkylene group, R.sup.2=CH(R.sup.4)N(R.sup.5)(R.sup.6), R3, R3', R3" identically or individually represent H, F, Cl, Br, CF.sub.3, CN, NO.sub.2, SO.sub.2NH.sub.2, NHR', SR.sup.8, OR.sup.9, CO(OR.sup.10), CH.sup.2CO(OR.sup.11), COR.sup.15, a C.sub.1-10-alkyl-, aryl-, heteroaryl- aryl radical or a heteroalkyl radical bound by a C.sub.1-6 alkylene group, R.sup.4=an unsubstituted phenyl radical or a phenyl radical substituted at least with C.sub.1-4 alkyl, C.sub.1-3-alkoxy-, halogen-, a method for the production of the above-mentioned compounds, medicaments containing said compounds, and the use of said compounds in the production of medicaments. Said active ingredients are particularly suitable for pain therapy, and for treating inflammatory and allergic reactions, drug or alcohol abuse, diarrhoea, gastritis, ulcers, cardiovascular diseases, urinary incontinence, depressions, states of shock, migranes, narcolepsy, overweight, asthma, glaucoma, hyperkinetic syndrome, lack of drive, bulimia, anorexia, catalepsia, anxiolysis increasing vigilance and/or increasing libido.

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Excerpt(s): The invention relates to substituted pyrrole Mannich bases, processes for their preparation, medicaments comprising these compounds and the use of these compounds for the preparation of medicaments. Pain is one of the basic clinical symptoms. There is a worldwide need for effective pain treatments. The urgent need for action for target-orientated treatment of chronic and non-chronic states of pain appropriate for the patient, by which is to be understood successful and satisfactory pain treatment for the patient, is documented in the large number of scientific works which have been published in the field of applied analgesia and basic research in nociception in recent years. Conventional opioids, such as e.g. morphine, are effective in the treatment of severe to very severe pain. However, they have as undesirable concomitant symptoms, inter alia, respiratory depression, vomiting, sedation, constipation and development of tolerance. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Treatment of helicobacter with isothiocyanates Inventor(s): Fahey, Jed W.; (Eldersburg, MD) Correspondence: Richard C. Peet; Foley & Lardner; Washington Harbour; 3000 K Street, N.W., Suite 500; Washington; DC; 20007-5109; US Patent Application Number: 20020151505 Date filed: August 21, 2001 Abstract: The present invention relates to methods of preventing or inhibiting the growth of Helicobacter through the use of a composition that comprises a glucosinolate, an isothiocyanate or a derivative or metabolite thereof. The present invention also relates to methods of preventing or treating persistent chronic gastritis, ulcers and/or stomach cancer in subjects at risk for, or in need of treatment thereof. Excerpt(s): Stomach cancer is the second most common form of cancer worldwide. Helicobacter pylori is a microaerophilic, gram-negative bacterium of cosmopolitan distribution that causes persistent chronic gastritis. Carriers of H. pylori (in gastric mucosa) are at 3 to 6 times the risk for developing stomach cancer (gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma) as non-carriers (J. Danesh et al., Cancer Surveys, 33:263-289 (1999); D. Forman et al., Br Med Bull, 54:71-78 (1998); S. Hansen et al., Scand J Gastroenterol, 34:353-360 (1999); J-Q Huang et al., Gastroenterology, 114:1169-1179(1998)). H. pylori causes inflammation of stomach tissue in carriers, resulting in increased blood flow, swelling and irritation. Inflammation of the lower part of the stomach leads to ulcers in about 10% of carriers. Inflammation of the upper part of the stomach leads to impaired acid secretion and ultimate die-off of acid-producing cells and leads to reduced stomach function and ultimately to cancer. Helicobacter pylori was only first described following its cultivation from human gastric biopsy specimens in 1982 (J R Warren et al., Lancet, (1983), 1:1273-1275; B J Marshall et al., Microbios Lett. (1984), 25:83-88). Since then, as many as 26 related Helicobacter species have been described colonizing the mucosal surfaces of humans and other animals (J V Solnick, D B Schauer, Clin Microbiol Rev, (2001), 14:59-97). These organisms not only colonize gastric tissues of mammals, but are found in the intestinal tract and the liver of birds, as well as in mammals including humans, mice, ferrets, gerbils, dogs and cats. They have been implicated as agents responsible for inflammation, and in malignant transformation in immunocompetent hosts as well as immunocompromised humans and animals. However, H. pylori is now well-documented as one of the most prevalent human pathogens worldwide (R M Genta et al., Virchows Arch, 425:339-347

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(1994)), and the causal agent for most gastric and duodenal ulcers, as well as a risk factor for the development of gastric cancer (J Danesh, Cancer Surveys, 33:263-289 (1999)). The human stomach is the only known natural reservoir for H. pylori, although many mammalian species can be infected by related species. Antibiotic therapy aimed at eradication of H. pylori (e.g. amoxycillin and clarithromycin plus the H.sub.2 inhibitor omeprazol for 10-14 days) is now recommended for infected patients who have verified peptic ulcerations of the stomach or duodenum or who have gastric mucosa-associated lymphoid tissue lymphomas, and cure rates are on the order of 90% (Helicobacter Foundation, "Treatment of Helicobacter pylori, p. 1-5 (1998)). However, a complex antibiotic therapy as described above may not be available in developing countries, where H. pylori infection rates can be as high as 70% of the population. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Treatment of inflammation with 2,4,6-trihydroxy-alpha-para-methoxyphenylacetophenone, or its pharmaceutically acceptable derivatives Inventor(s): Malaviya, Ravi; (St. Paul, MN), Uckun, Fatih M.; (White Bear Lake, MN) Correspondence: Merchant & Gould PC; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20020010217 Date filed: June 19, 2001 Abstract: 2,4,6-trihydroxy-.alpha.-p-methoxyphenylacetophenone (also identified herein as "D-58"), or its pharmaceutically acceptable derivatives such as salt and ester forms, is administered for inhibiting inflammatory reactions. The treatment can be remedial or prophylactic. Examples of the conditions that can be treated include acute inflammatory reactions and allergic inflammatory reactions, and specific examples include allergy, asthma, arthritis, psoriasis, skin sunburn, inflammatory pelvic disease, inflammatory bowel disease, urethritis, uvitis, senusitis, pneumonitis, encephalitis, meningitis, myocarditis, nephritis, osteomyelitis, myositis, hepatitis, gastritis, enteritis, dermatitis, gingivitis, appendicitis, pancreatitis, cholocystitis and cholangitis. The 2,4,6-trihydroxy.alpha.-p-methoxyphenylacetophenone can be administered by various routes as needed. Excerpt(s): The present invention is directed to the treatment of acute and chronic inflammatory responses, for example resulting from the presence of an allergen, injury, infection, etc. Allergic and acute inflammatory responses to injury, infection, or other tissue damage can set into motion a complex series of events. A variety of host cells that guard the host environment interface, including macrophages, mast cells, and epithelial epidermal cells serve as the initiators of the inflammatory responses. These cells release various mediators during an inflammatory response, which include histamine, prostaglandins (PGs), leukotrienes (LTs) and proinflammatory cytokines (refs 1-4). These mediators have been implicated in the pathogenesis of a number of acute and chronic inflammatory conditions such as allergy, asthma, arthritis, psoriasis, and skin sunburn (refs 3-5). The release of inflammatory agents is mediated by a cascade of intracellular signaling events which include activation of phosphoinositide turnover (ref 6), increase in cAMP levels (ref 7), activation of protein kinase C, and an increase in intracellular calcium levels and tyrosine phosphorylation of several cytosolic proteins (refs 7 and 8). Considerable efforts have been made for identification of chemical compounds that can interrupt these signaling events as potential anti-inflammatory agents (refs 9-12). However, the need for agents providing improved inhibition

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continues. In accordance with the present invention, 2,4,6-trihydroxy-.alpha.-- pmethoxyphenylacetophenone (also identified herein as "D-58"), or its pharmaceutically acceptable derivatives such as salt and ester forms, is administered for inhibiting inflammatory reactions to a subject in need thereof. The treatment can be remedial or prophylactic. Examples of the conditions that can be treated include acute as well as chronic inflammatory reactions and allergic inflammatory reactions, and specific examples include allergy, asthma, arthritis, psoriasis, skin sunburn, inflammatory pelvic disease, inflammatory bowel disease, urethritis, uvitis, sinusitis, pneumonitis, encephalitis, meningitis, myocarditis, nephritis, osteomyelitis, myositis, hepatitis, gastritis, enteritis, dermatitis, gingivitis, appendicitis, pancreatitis, cholocystitis and cholangititis. The 2,4,6-trihydroxy-.alpha.-p-methoxyphenylacetophenone can be administered by one of a variety of routes as needed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Urease inhibitors Inventor(s): Kajiwara, Masahiro; (Saitama, JP) Correspondence: Finnegan, Henderson, Farabow, Garrett &; Dunner Llp; 1300 I Street, NW; Washington; DC; 20006; US Patent Application Number: 20030060482 Date filed: September 5, 2002 Abstract: A urease inhibitor and an anti-Helicobacter pylori agent, which contain, as an active ingredient, an isothiazole derivative represented by the general formula (1): 1wherein R.sup.1 represents a hydrogen atom or an amino group, R.sup.2 represents a hydrogen atom, a lower alkyl group, or an acetyl group, and X represents a carbon atom or a nitrogen atom. These drugs are effective to prevent and treat gastrointestinal diseases caused by urease of Helicobacter pylori, such as chronic gastritis and gastroduodenal ulcer. Excerpt(s): The present invention relates to a novel urease inhibitor and a novel antiHelicobacter pylori agent. It has recently been made clear that urease produced by Helicobacter pylori has a close relation to the development of gastrointestinal diseases such as chronic gastritis and gastroduodenal ulcer. The mechanism of gastric mucosa injury due to urease is considered as follows. Urea secreted from the gastric parietal is hydrolyzed by urease to produce ammonia and carbon dioxide. Ammonia has a strong mucosa injurious effect, thereby to cause a blood flow disorder of the gastric mucosa, and also neutralizes gastric acid, thereby to enable habitation of Helicobacter pylori within the stomach under a severe acidic environment. In case Helicobacter pylori adheres to the gastric mucosa, epithelial cells of the gastric mucosa produce Interleukin8 (IL-8) as a kind of cytokines, while IL-8 acts on neutrophils, thereby to cause migration and activation of neutrophils. The activated neutrophils form phagocytosis and phagosome and also cause production of active oxygen and degranulation. The produced active oxygen itself causes a mucosa injury and induced to hypochlorous acid through an action of chlorine and myeloperoxidase in the stomach, and is also converted into monochloramine by means of ammonia, thus causing a cell injury. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Keeping Current In order to stay informed about patents and patent applications dealing with gastritis, 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 “gastritis” (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 gastritis. You can also use this procedure to view pending patent applications concerning gastritis. 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 6. BOOKS ON GASTRITIS Overview This chapter provides bibliographic book references relating to gastritis. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on gastritis 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 “gastritis” (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 gastritis: •

Diseases of the Gastroesophageal Mucosa: The Acid-Related Disorders Source: Totowa, NJ: The Humana Press, Inc. 2001. 199 p. Contact: Humana Press, Inc. 999 Riverview Dr., Suite 208 Totowa, NJ 07512. (973) 2561699. Fax (973) 256-8341. E-mail: [email protected] PRICE: $99.50, plus shipping and handling. ISBN: 089603965X. Summary: Gastric acid-related diseases are among the most commonly encountered disorders in clinical practice. The last decade has witnessed profound changes in the clinical approach to this family of conditions, which includes gastroesophageal reflux disease (GERD), peptic ulcers of all etiologies (causes), and dyspepsia (heartburn). This text emphasizes the diagnosis and treatment of these conditions, with subtext on epidemiology and pathophysiology (where their understanding is important for management conditions). Eleven chapters cover the management of peptic ulcer disease; the epidemiology, demographics and pathophysiology of Helicobacter pylori-related

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diseases, including gastritis, ulcers, and cancer; the diagnosis and treatment of Helicobacter-pylori related diseases; the management of nonsteroidal antiinflammatory drug (NSAID) related ulcers; nonvariceal upper gastrointestinal bleeding; ZollingerEllison syndrome and other acid-hypersecretory states; dyspepsia and nonulcer dyspepsia; the epidemiology and pathophysiology of gastroesophageal reflux disease (GERD); the diagnosis and treatment of GERD; Barrett's esophagus and adenocarcinoma; and extraesophageal manifestations of GERD. Each chapter includes a list of references and a subject index concludes the text. •

PDR for Herbal Medicines. 1st ed Source: Montvale, NJ: Medical Economics Company. 1998. 1244 p. Contact: Available from Medical Economics Publishing Inc. P.O. Box 10689, Des Moines, IA 50336. (800) 922-0937. Fax (515) 284-6714. Website: www.medecbookstore.com. PRICE: $59.99. ISBN: 1563632926. Summary: Most of today's herbal remedies exhibit varying degrees of therapeutic value. Some, such as ginkgo, valerian, and saw palmetto, seem genuinely useful, while others, such as ephedra, tansy, and nightshade, can actually be dangerous. As the use of unfamiliar botanicals spreads, the need to steer patients toward the few truly useful preparations and warn them away from ineffective, dangerous alternatives is becoming an increasingly significant priority. This volume, from the publishers of Physicians Desk Reference, brings together the findings of the German Regulatory Authority's herbal watchdog agency (commonly caused Commission E). This agency conducted an intensive assessment of the peer-reviewed literature on some 300 common botanicals, weighing the quality of the clinical evidence and identifying the uses for which the herb can reasonably be considered effective. This reference book contains profiles of over 600 medicinal herbs. Each entry contains up to 9 standard sections: name(s), description, actions and pharmacology, indications and usage, contraindications, precautions and adverse reactions, overdosage, dosage, and literature. The entries have also been indexed by scientific and common name, indications, therapeutic category, and side effects. To assist in identification, the reference book includes a section of full-color plates of the plants included. The book concludes with a glossary of the specialized botanical nomenclature and other unfamiliar terminology, a list of poison control centers, and a list of drug information centers. Some of the herbs are listed for use for abdominal cramps or distress, acid indigestion, appetite stimulation, rectal bleeding, various bowel disorders, stomach cancer, cholelithiasis (gallstones), colic, colitis, constipation, dehydration, diarrhea, digestive disorders, dysentery, enteritis, anal fissure, flatulence (intestinal gas), gastritis, gastroenteritis, gastrointestinal disorders, gout, helminthiasis, hemorrhage, hemorrhoids, hepatitis, hypercholesterolemia, jaundice, liver and gall bladder complaints, liver disorders, malaria, nausea, abdominal pain, and vomiting.

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Helicobacter Pylori Handbook Source: Oxford, England: Blackwell Science Ltd. 1995. 56 p. Contact: Available from Blackwell Science, Inc. 238 Main Street, Cambridge, MA 02142. (800) 215-1000 or (617) 876-7000. Fax (617) 492-5263. PRICE: $9.95. ISBN: 0865426597. Summary: The link between Helicobacter pylori infection and ulcer disease has been one of the most significant discoveries in gastroenterology in the past decade. The role of this organism in the development of nonulcer dyspepsia, gastric cancer, and lymphoma is also attracting interest. This monograph is designed to keep health care professionals

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whose specialty lies outside the field of gastroenterology abreast of this rapidly changing area. The author provides a concise, up to date review of H. pylori infection, current approaches to its diagnosis and treatment, and the position of H. pylori eradication in the management of gastrointestinal disorders. Written in outline format, the monograph covers epidemiology, transmission, the host response to infection, classification of gastritis, H. pylori and peptic ulcer disease or gastric cancer, H. pylori in children, diagnostic tests used to confirm infection, drug therapy, patient selection, and patients with dyspepsia. A list of further reading and a subject index appear at the end. 17 figures. 16 tables. 8 references. (AA-M). •

Gastroenterology and Hepatology: The Comprehensive Visual Reference. Volume 3: Stomach and Duodenum 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: 0443078432. 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 12 chapters on the stomach and duodenum, each written by experts in their respective fields. The first chapter reviews the current concepts of regulation of gastric acid secretion; the second chapter reviews the complex endocrinology of the stomach and duodenum. Chapter 3 presents a pictorial of the gastrointestinal immune system, covering the basic science of gut immunology and using the examples of H. pylori gastritis and celiac sprue as examples of immunopathic disorders of the stomach and duodenum, respectively. Chapters 4 to 8 summarize in some detail the current concepts and risk factors for ulcerative and inflammatory diseases of the stomach and duodenum. Chapter 9 covers bleeding lesions of the stomach and duodenum, both benign and malignant. Chapter 10 illustrates the many types of neoplasms of the stomach and duodenum with emphasis on gastric adenocarcinoma; Chapter 11 depicts the various surgical procedures on the stomach and duodenum available for the treatment of benign and malignant disorders, including morbid obesity. The volume concludes with a chapter on the dermatologic manifestations of gastrointestinal diseases as well as cutaneous lesions that, when present, are markers for disease of the gastrointestinal tract, liver, biliary tree, or pancreas. 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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Medical Advisor Home Edition: The Complete Guide to Alternative and Conventional Treatments Source: Alexandria, VA: Time-Life Books. 1997. 960 p. Contact: Available from Time-Life Books. 400 Keystone Industrial Park, Dunsmore, PA 18512. PRICE: $20.00. ISBN: 0783552505. Summary: This book offers information about 300 health problems, ranging from relatively benign conditions to the most serious diseases. There are symptoms charts which name several related problems and help readers decide which ailment entry to look up. Ailment entries provide a more complete list of symptoms, plus guidelines to discern whether the condition is potentially serious or requires a doctor's attention. Each entry describes the ailment and how it affects the body. Next, the entry outlines the

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underlying causes of the ailment and the tests and procedures a doctor may use to confirm the diagnosis. The treatment segment presents conventional and alternative recommendations for curing the problem or alleviating the symptoms. Most ailment entries conclude with advice on preventive measures that can be used to maintain health. Alternative treatments discussed include bodywork, acupuncture and acupressure, herbal therapies, homeopathy, lifestyle changes, and nutrition and diet. The book begins with a section on emergency medicine. Also included is a visual diagnostic guide, an atlas to the body, a medicine chest section (describing herbs, homeopathic remedies, and over the counter drugs), a glossary, a subject index, a bibliography, and a list of health associations and organizations. Topics related to digestive diseases include abdominal pain, AIDS, allergies, anal bleeding, anal fissure, anorexia nervosa, bad breath, bowel movement abnormalities, bulimia, celiac disease, cholesterol problems, colitis, colorectal cancer, constipation, Crohn's disease, diarrhea, diverticulitis, flu, food poisoning, gallstones, gas and gas pains, gastritis, gastroenteritis, heartburn, hiatal hernia, hiccups, incontinence, indigestion, irritable bowel syndrome, lactose intolerance, lupus, obesity, pancreatic cancer, pancreatic problems, stomach cancer, stomach ulcers, swallowing difficulty, trichomoniasis, vomiting, and worms. The book is illustrated with line drawings and full-color photographs. •

Good Food for Bad Stomachs Source: New York, NY: Oxford University Press. 1997. 240 p. Contact: Available from Oxford University Press. Order Department, 2001 Evans Road, Cary, NC 27513. (800) 451-7556. Fax (919) 677-1303. PRICE: $12.95 plus shipping and handling. ISBN: 0195126556. Summary: This book presents a detailed look at present knowledge about the role of eating habits in preventing, causing, and treating the many disorders that plague the gastrointestinal tract and its associated digestive glands, the liver, the gallbladder, and the pancreas. The author begins with three chapters that discuss nutrition and digestion, focusing on the elements of a realistic, reasonable diet. Other portions of the book are devoted to intestinal gas, constipation, diarrhea, the effect of aging, the effects of food on drug absorption, and the many effects of drugs on food absorption. The bulk of the chapters treat the kinds of disorders that can and do occur from one end of the digestive tract to the other, and the role of diet in these disorders. The author covers esophagitis, swallowing disorders, inflammation and ulcers of the stomach and duodenum (including peptic ulcer and gastritis), gallstones, pancreatitis, acute and chronic liver disease, traveler's diarrhea, constipation, inflammation and defects of the small intestine, celiac disease (gluten enteropathy), kidney oxalate stones, and the role of diet in colonic polyps and colon and rectal cancer. The author also discusses food intolerances, allergies, and reactions. The book concludes with a subject index. 14 tables.

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Diagnosis and Management of Peptic Ulcer Disease. 2nd ed Source: West Islip, NY: Professional Communications, Inc. 1997. 203 p. Contact: Available from Professional Communications, Inc. 400 Center Bay Drive, West Islip, NY 11795. (800) 337-9838. PRICE: $17.95. ISBN: 1884735304. Summary: This handbook reviews the diagnosis and management of peptic ulcer disease. The author emphasizes its functional and structural setting, causes, complications, and therapy, with particular attention to H. pylori, the worldwide infection known to account for the majority of duodenal and gastric ulcers. Both of these types of ulcers are now seen as common chronic diseases which are multifactorial,

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involving both genetic and environmental factors. The handbook, in pocket-size for ease of reference, includes 17 chapters in six sections: gastrointestinal structure and function, including etiology; the role of H. pylori, including epidemiology and natural history; NSAIDs (nonsteroidal anti-inflammatory drugs) and stress-induced ulcers; diagnostic considerations, including clinical presentation, laboratory tests, and radiology and endoscopy; treatment, including general therapeutic measures and drug therapy; and complications, including bleeding ulcers, perforation, penetration, and gastric outlet obstruction. The association of both duodenal and gastric ulcers with antral inflammation and, perhaps most influential, the discovery of Helicobacter pylori as a cause of antral gastritis has alerted clinicians to the importance of mucosal inflammation in the pathogenesis and recurrent nature of peptic ulceration. The finding that H. pylori can usually be eliminated by antibiotics carries potentially revolutionary therapeutic implications. Black and white photographs and charts illustrate the handbook, each chapter includes references, and a subject index concludes the volume. 30 figures. 13 tables. (AA-M). •

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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Foods That Harm, Foods That Heal: An A-Z Guide to Safe and Healthy Eating Source: Pleasantville, NY: Reader's Digest. 1997. 400 p. Contact: Available from Customer Service, Reader's Digest. Pleasantville, NY 10570. (800) 846-2100. PRICE: $30.00. ISBN: 0895779129. Summary: This nutrition reference book features more than 400 photographs and illustrations with more than 400 A to Z entries on a vast range of foods and health concerns, include caffeine, cancer, diabetes, fast food, garlic, heart disease, influenza, osteoporosis, pregnancy, sexually transmitted diseases, and vegetarianism. The book is designed to provide families with information to help understand the close links between foods and wellness. Each food entry provides at-a-glance information on its nutrients (or lack of) and its benefits and drawbacks. Each ailment is accompanied by a list of foods and beverages that are considered safe, and what foods or beverages should be cut down or avoided altogether. Personalized case studies help to illustrate various topics. There are special features on eating during different life stages, from infancy to old age, as well as such issues as genetically altered foods, irradiation, pesticides, and pollution. Other topics include how to cook foods to achieve maximum nutritional benefits; which dietary supplements really work; tips on exercising, storing food, and reading food labels; an instructive analysis of the most popular diet regimens; and controversial foods and additives such as eggs, nitrites, bran, cheese, milk, fat, wine, and alcohol. A glossary defines unfamiliar or technical terms; there is also a listing of organizations that can provide further information and resources. Topics specifically related to digestive diseases include allergic reactions to food, anorexia nervosa, antioxidants, appetite loss, basic food groups, carbohydrates, celiac disease, childhood and adolescent nutrition, cholesterol, constipation, convenience foods, Crohn's disease, diarrhea, dieting and weight control, digestive and malabsorption disorders, diverticulitis, fats, fiber, food poisoning, gastritis, gastroenteritis, gout, hiatal hernia, indigestion and heartburn, intolerance to milk and other foods, irritable bowel syndrome, malnutrition, medicine-food interactions, minerals, obesity, organic and health foods, preparation and storage of food, restaurants and eating out, smoking and diet, sports nutrition, supplements, traveler's health, ulcers, vitamins, and worms and other parasites.

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Instructions for Patients. 5th ed Source: Philadelphia, PA: W.B. Saunders Company. 1994. 598 p. Contact: Available from W.B. Saunders Company. Book Order Fulfillment, 6277 Sea Harbor Drive, Orlando, FL 32887-4430. (800) 545-2522. Fax (800) 874-6418. PRICE: $49.95. ISBN: 0721649300 (English); 0721669972 (Spanish). Summary: This paper-bound book presents a number of patient instruction fact sheets. Each fact sheet includes three sections: basic information on signs and symptoms, causes, risk factors, etc.; treatment; and when to contact one's health care provider. Digestive system topics include food allergy, anal fissure, celiac disease, appendicitis, Crohn's disease, constipation, ulcerative colitis, cirrhosis of the liver, cholecystitis or cholangitis, diarrhea, diverticular disease, gallstones, gastritis, hiatal hernia, hemorrhoids, heartburn, irritable bowel syndrome, and lactose intolerance, among others. The fact sheets are designed to be photocopied and distributed to patients as a reinforcement of oral instructions and as a teaching tool. The book is available in English or Spanish.

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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 “gastritis” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “gastritis” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “gastritis” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

Advances in Gastroenterology: 4. Chronic Atrophic Gastritis by F. Di Mario (1991); ISBN: 8829909971; http://www.amazon.com/exec/obidos/ASIN/8829909971/icongroupinterna

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Campylobacter Pylori in Gastritis and Peptic Ulcer Disease by Martin J. Blaser (Editor); ISBN: 0896401626; http://www.amazon.com/exec/obidos/ASIN/0896401626/icongroupinterna

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Campylobacter Pylori in Gastritis and Peptic Ulcer Disease; ISBN: 4260141627; http://www.amazon.com/exec/obidos/ASIN/4260141627/icongroupinterna

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Chronic Gastritis and Hypochlorhydria in the Elderly by Peter R. Holt, Robert M. Russell (Editor); ISBN: 0849369703; http://www.amazon.com/exec/obidos/ASIN/0849369703/icongroupinterna

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Gastritis by David Y. Graham (Editor), et al; ISBN: 0397516754; http://www.amazon.com/exec/obidos/ASIN/0397516754/icongroupinterna

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Gastritis by Robert A. Kozol (Editor); ISBN: 0849354978; http://www.amazon.com/exec/obidos/ASIN/0849354978/icongroupinterna

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Gastritis Y Colitis by Abel, Dr Cruz (2001); ISBN: 9706433880; http://www.amazon.com/exec/obidos/ASIN/9706433880/icongroupinterna

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Gastritis: A Critical Review by R. Cheli, et al (1987); ISBN: 0387174664; http://www.amazon.com/exec/obidos/ASIN/0387174664/icongroupinterna

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Helicobacter Pylori in Peptic Ulceration and Gastritis by Barry J. Marshall, et al; ISBN: 0865421080; http://www.amazon.com/exec/obidos/ASIN/0865421080/icongroupinterna

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Helicobacter Pylori, Gastritis and Peptic Ulcer by P. Malfertheiner (Editor), et al (1990); ISBN: 0387520309; http://www.amazon.com/exec/obidos/ASIN/0387520309/icongroupinterna

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Helicobacter Pylori, Gastritis and Peptic Ulcer (1990); ISBN: 3540520309; http://www.amazon.com/exec/obidos/ASIN/3540520309/icongroupinterna

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La Gastritis de Platon by Antonio Tabucchi (1999); ISBN: 8433905783; http://www.amazon.com/exec/obidos/ASIN/8433905783/icongroupinterna

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The Official Patient's Sourcebook on Gastritis: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 0597832773; http://www.amazon.com/exec/obidos/ASIN/0597832773/icongroupinterna

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The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “gastritis” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:10 •

A family study of chronic gastritis; histological, immunological, and functional aspects. Author: Varis, Kalle.; Year: 9999; Helsinki, 1971

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Aspects of chronic atrophic gastritis: with special reference to serum gastrin and antral gastrin cells Author: Stockbrügger, Reinhold.; Year: 1971; Göteborg [Sweden: s.n.], 1976

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Campylobacter pylori: defining a cause of gastritis and peptic ulcer disease: proceedings from a symposium on the occasion of the 13th International Congress of Gastroenterology, Rome, 7 September 1988 Author: Tytgat, G. N. J.; Year: 1964; Oslo, Norway: Universitetsforlaget, c1989

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Duodenogastric reflux in patients with upper abdominal complaints or gastric ulcer: with particular reference to reflux-associated gastritis Author: Niemelä, Seppo.; Year: 1972; Oslo: Universitetsforlaget, c1985

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Gastritis, peptic ulcer, and gastric cancer Author: Kekki, M.; Year: 1978; Oslo, Norway: Universitetsforlaget, c1991

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Irradiated guinea-pig gastric mucosa: morphological and functional aspects connected with the gastritis-cancer problem Author: Capoferro, Renato.; Year: 1967; Oslo: [s.n.], 1974

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Third International Sucralfate Symposium: peptic ulcer disease and gastritis: a worldwide review Author: Marks, I. N.; Year: 1974; New York, N.Y.: Technical Pub., c1985

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

10

In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.

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Helicobacter Pylori-Related Diseases: Demographics, Epidemiology, and Pathophysiology of Gastritis, Ulcers, and Cancer Source: in Freston, J.W. Diseases of the Gastroesophageal Mucosa: The Acid-Related. Totowa, NJ: The Humana Press, Inc. 2001. p.29-41. Contact: Humana Press, Inc. 999 Riverview Dr., Suite 208 Totowa, NJ 07512. (973) 2561699. Fax (973) 256-8341. E-mail: [email protected] PRICE: $99.50, plus shipping and handling. ISBN: 089603965X. Summary: Gastric acid-related diseases are among the most commonly encountered disorders in clinical practice. This chapter on the demographics, epidemiology, and pathophysiology of gastritis, ulcers and cancer is from a text that emphasizes the diagnosis and treatment of these conditions. Helicobacter pylori is a common bacterial infection of the gastric mucosa. The infection is generally asymptomatic, but it may cause a variety of gastrointestinal diseases that are associated with significant morbidity and mortality. In some cases, increased acid secretion can lead to the formation of duodenal ulcers. In other hosts, acid secretion may be reduced, leading to an association with gastric ulcers as well as gastric carcinoma and lymphoma. Topics include prevalence of H. pylori in developing countries, host factors, route of transmission, reinfection, bacteriology, virulence factors, acute versus chronic gastritis, the pathogenesis of ulcer formation, and the pathogenesis of H. pylori and gastric cancer. 1 table. 45 references.

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Gastritis and Peptic Ulcer Disease in Children Source: in Brandt, L., et al., eds. Clinical Practice of Gastroenterology. Volume Two. Philadelphia, PA: Current Medicine. 1999. p. 1294-1300. 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: Gastritis in children remains underrecognized and poorly characterized. This chapter on gastritis and peptic ulcer disease in children is from a lengthy textbook that brings practitioners up to date on the complexities of gastroenterology practice, focusing on the essentials of patient care. This chapter covers anatomy and physiology; etiology, pathology and clinical features; nonerosive, nonspecific gastritis or chronic active gastritis; specific and distinctive types of gastritis; peptic ulcer disease (PUD), and duodenitis. Specific types of gastritis covered include Crohn's disease, chronic granulomatous disease, eosinophilic gastropathy, allergic gastropathy, Menetrier's disease, chronic varioliform gastritis, graft versus host disease, and cytomegalovirus. The author notes that in children with chronic peptic ulcer disease, duodenal ulcers are far more prevalent than are gastric ulcers. Secondary PUD usually occurs in association with an identifiable ulcerogenic agent or circumstance, including ulcers caused by physiologic stress, drugs, and those associated with other diseases. The ulcers are more often acute and are more prevalent in the stomach than in the duodenum. The treatment of specific disorders in children is similar to that in adults. The difference in treatment results from the issues specific to children: the management of fluid and electrolyte balance in resuscitation; dosage, palatability and appropriate form of medications; and the potential adverse effects of medications. 3 tables. 34 references.

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Gastritis and Other Gastropathies Source: in Feldman, M.; Friedman, L.S.; Sleisenger, M.H. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 7th ed. [2-volume set]. St. Louis, MO: Saunders. 2002. p. 810-827. Contact: Available from Elsevier. 11830 Westline Industrial Drive, St. Louis, MO 63146. (800) 545-2522. Fax (800) 568-5136. Website: www.us.elsevierhealth.com. PRICE: $229.00 plus shipping and handling. ISBN: 0721689736. Summary: Gastritis is defined as microscopic inflammation of the stomach, thus biopsy is required for definitive diagnosis. This chapter on gastritis and other gastropathies is from a comprehensive and authoritative textbook that covers disorders of the gastrointestinal tract, biliary tree, pancreas, and liver, as well as the related topics of nutrition and peritoneal disorders. Topics include classification; chronic, nonspecific gastritides, including diffuse antral-predominant gastritis, multifocal atrophic gastritis, and diffuse corporal atrophic gastritis; infectious gastritis, including that due to viruses, bacteria, fungi, or parasites; granulomatous gastritides, including sarcoidosis and xanthogranulomatous gastritis; distinctive forms of gastritis, including collagenous gastritis, lymphocytic gastritis, and eosinophilic gastritis; miscellaneous forms of gastritis, including gastritis cystica profound and gastric graft-versus-host disease (GVHD); reactive gastropathies (acute erosive gastritis), including medications, alcohol, cocaine, stress, radiation, bile reflux, ischemia, bezoar, prolapse gastropathy, linear gastric erosions in a hiatal hernia (Cameron's ulcer), and congestive gastropathy (portal hypertensive gastropathy); and hyperplastic gastropathies, notably Menetrier's disease and hyperplastic, hypersecretory gastropathy. The chapter includes a mini-outline with page citations, full-color illustrations, and extensive references. 11 figures. 1 table. 217 references.

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Gastritis and Ulcers in Children Source: in Wyllie, R. and Hyams, J.S., eds. Pediatric Gastrointestinal Disease. 2nd ed. Philadelphia, PA: W.B. Saunders Company. 1999. p. 221-243. 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) 568-5136 or (314) 453-7095. E-mail: [email protected]. Website: customerservice.wbsaunders.com. PRICE: $155.00 plus shipping and handling. ISBN: 0721674615. Summary: This chapter on gastritis and ulcers in children is from a medical textbook that covers all facets of clinical pediatric gastrointestinal disease. The text emphasizes a clinical focus and incorporates anatomy and physiology considerations into each chapter rather than a separate section. The authors of this chapter maintain that although the overall prevalence of gastritis in children is not defined, an understanding of the causes of pediatric gastritis and mucosal ulceration is critical for the management of children with abdominal pain. The authors review the pathogenesis of gastritis, including acid secretion, the bicarbonate mucus barrier, and genetic factors; and causes of secondary peptic ulcer disease (PUD), including excessive acid secretion (due to Zollinger Ellison syndrome, or gastrinoma), other disorders of acid hypersecretion, Crohn's disease, eosinophilic gastroenteritis, Menetrier's disease (hypertrophic gastritis), autoimmune gastritis, and stress related gastritis and ulcers. The authors then discuss drug related gastritis and ulcers, primarily those due to nonsteroidal antiinflammatory agents. The role of Helicobacter pylori is explored next, including its epidemiology, pathogenesis, microbiology, methods for detection, H. pylori associated gastroduodenal

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disease in children (including gastric cancer and gastric lymphomas), treatment of H. pylori infection and vaccine development, and indications for treatment (patient selection). The authors then review the clinical findings (including diagnosis, histopathology, classification) of primary and secondary gastritis and primary and secondary peptic ulcer disease. The chapter concludes with a brief discussion of treatment strategies for gastric inflammation, including mucosal cytoprotection, enhancement of mucosal barrier function, and acid secretion inhibition and acid neutralization. 7 figures. 4 tables. 348 references.

Directories In addition to the references and resources discussed earlier in this chapter, a number of directories relating to gastritis have been published that consolidate information across various sources. The Combined Health Information Database lists the following, which you may wish to consult in your local medical library:11 •

1998-1999 Complete Directory for People with Rare Disorders Source: Lakeville, CT: Grey House Publishing, Inc. 1998. 726 p. Contact: Available from Grey House Publishing, Inc. Pocket Knife Square, Lakeville, CT 06039. (860) 435-0868. Fax (860) 435-0867. PRICE: $190.00. ISBN: 0939300982. Summary: This directory, from the National Organization for Rare Disorders (NORD) provides a wealth of information on diseases and organizations. The directory offers four sections: disease descriptions, disease specific organizations, umbrella organizations, and government agencies. In the first section, the directory includes descriptions of 1,102 rare diseases in alphabetical order. Each entry defines the disorder, then refers readers to the organizations that might be of interest. Diseases related to digestive diseases include achalasia, Addison's disease, Alagille syndrome, Barrett's esophagus, Budd Chiari syndrome, Caroli disease, celiac sprue, cholangitis, cholecystitis, cirrhosis, colitis, Crohn's disease, Cushing syndrome, cystic fibrosis, diverticulitis, Dubin Johnson syndrome, fructose intolerance, galactosemia, gastritis, gastroesophageal reflux, hepatitis, Hirschprung's disease, Hurler syndrome, imperforate anus, irritable bowel syndrome, jejunal atresia, Korsakoff's syndrome, lipodystrophy, maple syrup urine disease, Morquio syndrome, polyposis, porphyria, proctitis, prune belly syndrome, sarcoidosis, Stevens Johnson syndrome, Tropical sprue, tyrosinemia, valinemia, vitamin E deficiency, Whipple's disease, Wilson's disease, and Zollinger Ellison syndrome. Each of the 445 organizations listed in the second section is associated with a specific disease or group of diseases. In addition to contact information, there is a descriptive paragraph about the organization and its primary goals and program activities. Entries include materials published by the organization as well as the diseases

11

You will need to limit your search to “Directory” and “gastritis” using the "Detailed Search" option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find directories, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Select your preferred language and the format option “Directory.” Type “gastritis” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months.

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the organizations cover, which refer readers to Section I. The third section lists 444 organizations that are more general in nature, serving a wide range of diseases (for example, the American Liver Foundation). The final section describes 74 agencies that are important federal government contacts that serve the diverse needs of individuals with rare disorders. A name and key word index concludes the volume.

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CHAPTER 7. MULTIMEDIA ON GASTRITIS Overview In this chapter, we show you how to keep current on multimedia sources of information on gastritis. 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 gastritis is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “gastritis” 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 “gastritis” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on gastritis: •

Clinical Case Reviews: Management of H. Pylori in Gastrointestinal Disease Source: Secaucus, NJ: Network for Continuing Medical Education. 1995. (videocassette). Contact: Available from Network for Continuing Medical Education. 1425 Broad Street, Clifton, NJ 07013. (800) 223-0272 or (973) 473-9500. Fax (973) 591-1224. Order Number: S102. PRICE: Call for pricing information. Summary: Helicobacter pylori (H. pylori) is now known to be an etiology in more than 90 percent of peptic ulcer cases. This knowledge has led to the evolution of therapies that make it possible to cure nearly all ulcers. This medical continuing education program reviews the management of H. pylori in gastrointestinal disease and presents three case studies involving H. pylori in peptic ulcer disease. The first section explores the discovery of H. pylori as an etiologic factor in peptic ulcer, including the history and evolution of this discovery (Marshall and Warren's research). The next section discusses the three possible mechanisms of gastric mucosal injury caused by H. pylori (ammonia, cytotoxins, and mucosal immune response). The instructional portion of the videotape

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also covers the types of illnesses related to H. pylori (from asymptomatic gastritis to PUD), the incidence and other epidemiologic factors of the infection, transmission, the role of H. pylori infection in ulcer recurrence rates, diagnostic tests, drug therapy regimens, and patient selection issues. The remaining portion of the tape presents three case studies. The video features live action of real physicians and patients, and graphics and anatomic illustrations.

Bibliography: Multimedia on Gastritis The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in gastritis (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on gastritis: •

Atrophic gastritis [sound recording]: recorded at DDW 1990, San Antonio. Year: 1990; Format: Sound recording; [Bethesda, Md.]: American Gastroenterological Association, c1990

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Campylobacter pyloridis as a cause of gastritis and peptic ulcer [videorecording]: fact or fiction Source: with Harold C. Neu; Year: 1987; Format: Videorecording; Secaucus, N.J.: Network for Continuing Medical Education, 1987

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Correction of Alkaline reflux gastritis [videorecording] Source: Stephen B. Vogel; Year: 1999; Format: Videorecording; Woodbury, CT: Cine-Med, 1999

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New magic bullets and the fight against gastritis [sound recording] Source: Barry Marshall; Year: 1996; Format: Sound recording; [Bethesda, Md.: National Institutes of Health, 1996]

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CHAPTER 8. PERIODICALS AND NEWS ON GASTRITIS Overview In this chapter, we suggest a number of news sources and present various periodicals that cover gastritis.

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

Helicobacter-induced gastritis increases hyperglycemia in diabetic mice Source: Reuters Medical News Date: June 12, 2002

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Soluble transferrin receptor levels identify anemia, gastritis in diabetics Source: Reuters Medical News Date: September 25, 2000

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Corpus gastritis protects against reflux esophagitis Source: Reuters Medical News Date: July 28, 1999

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H pylori vaccine protection correlates with secretory IgA, gastritis in mice Source: Reuters Medical News Date: May 12, 1999

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H. pylori infection linked to atrophic gastritis Source: Reuters Medical News Date: February 25, 1999

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Severe corpus gastritis may identify patients at increased risk of gastric cancer Source: Reuters Medical News Date: August 05, 1998

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Focal Gastritis May Be Early Warning Of Crohn's Disease Source: Reuters Medical News Date: March 19, 1997

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H. Pylori: "The Major Risk Factor For Atrophic Gastritis" Source: Reuters Medical News Date: May 20, 1996

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Omeprazole Increases Risk Of Atrophic Gastritis In Subset Of Patients With Reflux Esophagitis Source: Reuters Medical News Date: April 18, 1996

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H. Pylori May Cause Atrophic Gastritis And Increase Gastric Cancer Risk Source: Reuters Medical News Date: December 06, 1995

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Atrophic Gastritis A "Direct" Result Of Helicobacter Pylori Infection Source: Reuters Medical News Date: June 16, 1995 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.

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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 “gastritis” (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 “gastritis” (or synonyms). If you know the name of a company that is relevant to gastritis, 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 “gastritis” (or synonyms).

Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “gastritis” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on gastritis: •

Younger Adults at Risk for Low B12, Too Source: Tufts University Health and Nutrition Letter. 18(7):7. September 2000. Contact: 10 High St., Suite 706, Boston, MA 02110. [email protected] www.healthletter.tufts.edu. Summary: A new study by Tufts University researchers suggests that adults in their 20s, 30s, and 40s may be at risk for low vitamin B12 levels. People over 50 are known to be at increased risk for this vitamin deficiency because they are more likely to have atrophic gastritis, a condition in which there is too little stomach acid to allow for proper absorption of the nutrient. A lack of vitamin B12 levels, if it is severe enough, can cause

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neurologic damage ranging from tingling sensations to a lack of balance, memory changes, and disorientation. Tufts researchers measured blood levels of B12 in 3,000 men and women aged 26 to 83. While overall blood levels of the vitamin did decline with age, the percentage of people whose blood levels fell below the cutoff point for suspected deficiency was not any greater among the older participants. More research needs to be conducted before scientists know precisely why B12 deficiency risk appears to be more common among younger adults than previously thought. Researchers theorize that the people with low B12 levels in the study used antacids which if taken habitually, could cause the same drop in stomach acid as atrophic gastritis. Vitamin B12 is found in meat, fish, poultry, dairy products, and fortified cereal. •

Helicobacter Pylori Infection and Gastric Cancer in the Asia Pacific Region Source: Asian Pacific Gastroenterology News. Issue 4: 11. June 2000. Contact: Available from Blackwell Science Asia. 54 University Street, Carlton, Victoria 3053, Australia. 61 3 9347 0300. Fax 61 3 9347 5001. E-mail: [email protected]. Summary: Helicobacter pylori infection causes histological gastritis; chronic gastritis from long term H. pylori infection results in gastric mucosal atrophy, which eventually progresses to intestinal metaplasia and sometimes to gastric (stomach) cancer. This brief article reviews the problem of H. pylori infection and gastric cancer in the Asia Pacific region. The author reports data that show just over 10 percent of H. pylori infected persons in Japan may develop gastric cancer. The prevalence of asymptomatic H. pylori infection differs greatly between countries, being low in developed countries and high in developing countries. Because H. pylori is transmitted via the fecal to oral route, and children are more readily infected than adults, the author notes that conducting a survey on H. pylori infection is the same as assessing the water supply and sewage systems of a country. The present prevalence of H. pylori infection in Japan is extremely low at an early age, as in other developed countries, and subsequently shows a rapid increase until it reaches a plateau of approximately 70 percent at 50 years of age. The author also explores the different incidence of gastric cancer as it varies between countries. It is suggested that H. pylori infection leads to histological chronic gastritis, regardless of the strain of the organism, and after that the course of the disease depends on environmental factors (diet, age), virulence of H. pylori strains, and host factors including genetics. The author concludes by calling for additional research collaboration between countries in the Asia Pacific region. 1 figure.

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Is Cyclic Vomiting Different from Chronic Vomiting? Source: Code V. p. 5. Spring 1994. Contact: Available from Cyclic Vomiting Syndrome Association. 13180 Caroline Court, Elm Grove, WI 53122. (414) 784-6842. Fax (414) 821-5494. E-mail: [email protected]. PRICE: Single copy free. Summary: In this brief letter, a physician reviews the differences between cyclic vomiting and chronic vomiting. The author reports on his observations that, of children who were vomiting repeatedly for more than three months duration, one-third had the cyclic pattern and two-thirds had the chronic pattern. He goes on to describe the differences, including the criteria used to separate the cyclic from chronic groups; addresses the problem of dehydration; and notes the different etiologies of the two types of vomiting. Children with cyclic vomiting were more likely to have disorders outside the gastrointestinal tract, such as abdominal migraine, sinus infection, or metabolic

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disorders. Children with chronic vomiting were more likely to have diseases within the gastrointestinal tract, including esophagitis, gastritis (Helicobacter infection), duodenitis (acid-induced), Giardia, and irritable bowel syndrome (IBS). •

Sjogren's Syndrome and the Gastrointestinal Tract Source: Moisture Seekers Newsletter. 17(2): 1, 4-5. March 1999. Contact: Available from Sjogren's Syndrome Foundation, Inc. 8120 Woodmont Avenue, Suite 530, Bethesda, MD 20814-1437. (301) 718-0300 or (800) 475-6473. Fax (301) 718-0322. Website: www.sjogrens.org. Summary: This article on Sjogren's syndrome (SS) and the gastrointestinal tract is from a patient education newsletter for people with SS. The author outlines the areas where the gastroenterologist may play a role in caring for the person with SS, such as dealing with swallowing difficulties, dyspepsia (indigestion), diarrhea, and jaundice (usually due to primary biliary cirrhosis, or scarring). Difficulty in swallowing is usually due to the lack of saliva associated with SS, but occasionally it may be due to a blockage (postcricoid web) or a weakness of the muscle contractions involved in swallowing. In addition, those patients with SS are vulnerable to acid reflux, which causes heartburn symptoms. Children with SS are prone to achalasia, a type of muscle problem involving the lower esophageal sphincter. Dyspepsia (indigestion) is relatively common in patients with SS, as is inflammation of the stomach (gastritis). The author briefly discusses the role of the bacterium Helicobacter pylori in gastritis. There are at least two diseases associated with SS and diarrhea: chronic pancreatitis and celiac disease (gluten intolerance). The author notes that the link between SS and gastroenterological conditions is often via abnormal autoantibodies.

•

Malnutrition in the Hemodialysis Patient Source: Renal Nutrition Forum. 14(4): 1-4. Fall 1995. Contact: Available from Renal Nutrition Forum. 2246 Poinciana Road, Winter Park, FL 32792. (407) 774-0631. Summary: This article presents a brief overview of research addressing nutritional status in the hemodialysis (HD) patient and the relationship between malnutrition, morbidity, and mortality. The article is also intended to help the dietitian in preventing malnutrition in the HD patient by offering suggestions for therapy. Dialysis factors which may contribute to malnutrition include an increase in muscle protein degradation caused by blood contact with the dialyzer membrane; inadequate dialysis resulting in a uremic state which leads to nausea, vomiting, and loss of appetite; and loss of amino acids and peptides in dialysate. Hormonal disturbances include insulin resistance, increased circulating levels of catabolic hormones such as insulin and parathyroid hormone, and decreased levels of anabolic hormones such as growth factor and erythropoietin caused by deterioration of kidney function. Gastrointestinal factors include gastroparesis, malabsorption, gastritis, esophagitis, and constipation. The author reports on studies documenting that malnutrition greatly increases morbidity and mortality in the HD patient. HD patients should ingest 1.2 grams of protein per kilogram of actual body weight, where 50 percent is high biological value protein. An adequate energy intake is vital for the efficient utilization of dietary protein. The most important factor in improving malnutrition in this population is to assure adequate dialysis. The author concludes with a section on interventions for patients who continue to have poor appetites, even if dialysis delivery is optimal. 1 table. 15 references.

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Academic Periodicals covering Gastritis Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to gastritis. In addition to these sources, you can search for articles covering gastritis 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 9. 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 gastritis. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI® Advice for the Patient® can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with gastritis. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The

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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to gastritis: Caffeine •

Systemic - U.S. Brands: Cafcit; Caffedrine Caplets; Dexitac Stay Alert Stimulant; Enerjets; Keep Alert; Maximum Strength SnapBack Stimulant Powders; NoDoz Maximum Strength Caplets; Pep-Back; Quick Pep; Ultra Pep-Back; Vivarin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202105.html

Clarithromycin •

Systemic - U.S. Brands: Biaxin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202667.html

Metronidazole •

Systemic - U.S. Brands: Flagyl; 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

Misoprostol •

Systemic - U.S. Brands: Cytotec http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202375.html

Omeprazole •

Systemic - U.S. Brands: Prilosec http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202423.html

Orlistat •

Oral--Local - U.S. Brands: Xenical http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500006.html

Orphenadrine •

Systemic - U.S. Brands: Antiflex; Banflex; Flexoject; Mio-Rel; Myolin; Myotrol; Norflex; Orfro; Orphenate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202426.html

Orphenadrine and Aspirin •

Systemic - U.S. Brands: Norgesic; Norphadrine; Orphenagesic http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202427.html

Penicillins •

Systemic - U.S. Brands: Amoxil; Bactocill; Beepen-VK; Betapen-VK; Bicillin L-A; Cloxapen; Crysticillin 300 A.S.; Dycill; Dynapen; Geocillin; Geopen; Ledercillin VK; Mezlin; Nafcil; Nallpen; Omnipen; Omnipen-N; Pathocil; Pen Vee K; Pentids; Permapen; Pfizerpen; Pfizerpen-AS; Pi http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202446.html

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Ranitidine Bismuth Citrate •

Systemic - U.S. Brands: http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202427.html

Sucralfate •

Oral - U.S. Brands: Carafate http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202533.html

Urea •

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

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

Mosby’s Drug Consult™ Mosby’s Drug Consult™ database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.

PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.

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APPENDICES

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

NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •

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

•

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/

12

These publications are typically written by one or more of the various NIH Institutes.

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•

National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm

•

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.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •

Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html

•

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

13

Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.

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•

Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html

•

Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database

A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “gastritis” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “gastritis” (or synonyms) into the “For these words:” box. The following is a sample result: •

Gastritis, Ulcers and Helicobacter Pylori Source: Overland Park, KS: Tri-Med Specialties, Inc. 199x. 2 p. Contact: Available from Tri-Med Specialties, Inc. P.O. Box 23306, Overland Park, KS 66223. (800) 874-6331. PRICE: Free. Available only to medical professionals. Summary: This brochure provides information for patients about helicobacter pylori (H. pylori) infections. It defines H. pylori infection, describes its symptoms, and explains the relationship between H. pylori and ulcers. It then discusses diagnosis and treatment. A list of references for further information is included.

The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “gastritis” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category.

15 16

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

The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH).

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Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total

Items Found 17535 145 331 53 4 18068

HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “gastritis” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.

17

Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html.

18

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

19

Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 20 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 21 The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.

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Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •

CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.

•

Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.

The Genome Project and Gastritis In the following section, we will discuss databases and references which relate to the Genome Project and gastritis. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).23 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “gastritis” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for gastritis: •

Cystic Fibrosis with Helicobacter Pylori Gastritis, Megaloblastic Anemia, and Subnormal Mentality Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?219721

•

Gastritis, Familial Giant Hypertrophic Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?137280 Genes and Disease (NCBI - Map)

The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of 23 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.

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important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •

Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html

•

Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html

•

Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html

•

Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html

•

Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html

•

Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html

•

Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez

Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases:

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•

3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo

•

Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books

•

Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome

•

NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/

•

Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide

•

OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM

•

PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset

•

ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo

•

Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein

•

PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed

•

Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure

•

Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy

To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “gastritis” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database24 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. 24

Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html.

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The Genome Database25 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “gastritis” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).

25

Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.

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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 gastritis 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 gastritis. 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 gastritis. 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 “gastritis”:

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•

Other guides Digestive Diseases http://www.nlm.nih.gov/medlineplus/digestivediseases.html Food Contamination/Poisoning http://www.nlm.nih.gov/medlineplus/foodcontaminationpoisoning.html Peptic Ulcer http://www.nlm.nih.gov/medlineplus/pepticulcer.html Stomach Cancer http://www.nlm.nih.gov/medlineplus/stomachcancer.html Stomach Disorders http://www.nlm.nih.gov/medlineplus/stomachdisorders.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 gastritis. 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: •

Helicobacter Pylori Infection (Gastritis) Source: in Sodeman, W.A., Jr. Instructions for Geriatric Patients. Philadelphia, PA: W.B. Saunders Company. 1995. p. 110-111. 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. PRICE: $38.95. ISBN: 0721643353. Summary: This chapter, from a book of instructions for geriatric patients, provides a basic information sheet on Helicobacter pylori infection (gastritis). H. pylori infections tend to become chronic or long lasting, although they usually cause no complaints or symptoms. But in some people, this chronic infection can lead to the development of stomach and duodenal ulcers. H. pylori infections are not difficult to eradicate, but they do require the use of two or three drugs. The fact sheet outlines the drugs commonly used, including omeprazole (Prilosec), amoxicillin, metronidazole (Flagyl), and bismuth (Pepto-Bismol). The author notes that the timing of treatment for H. pylori infections will take into consideration other health care problems that may need more urgent or immediate treatment. The information sheet concludes by reminding readers to contact their health care provider if they miss more than a single dose of a drug regimen to

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eradicate H. pylori. The instructions are designed to supplement and reinforce physician instructions to their patients. (AA-M). •

Gastritis Source: Camp Hill, PA: Chek-Med Systems, Inc. 199x. [2 p.]. Contact: Available from Chek-Med Systems, Inc. 200 Grandview Avenue, Camp Hill, PA 17011-1706. (800) 451-5797 or (717) 761-1170. Fax (717) 761-0216. PRICE: $22.00 per pack of 50 brochures; 3 pack minimum. Summary: This patient education brochure describes gastritis, a condition defined as inflammation of the stomach. In gastritis, white blood cells move into the wall of the stomach as a response to some type of injury. The brochure discusses the causes (etiology) of gastroparesis, including helicobacter pylori (a bacteria that can live in the mucous lining of the stomach), autoimmune gastritis (which results in pernicious anemia because the body can no longer absorb vitamin B12), side effects of aspirin and nonsteroidal antiinflammatory drugs (NSAIDs), alcohol and other chemicals, and hypertrophic gastritis. The symptoms of gastritis depend on how acute the illness is and how long it has been present. In the acute phase, there may be pain or gnawing in the upper abdomen, nausea, and vomiting. In the chronic phase, the pain may be dull and there may be loss of appetite with a feeling of fullness after several bites of food. The brochure cautions that often there are no symptoms at all. Diagnosis is made from the patient's medical history, in conjunction with endoscopy and biopsy of the stomach lining. An upper gastrointestinal (GI) x-ray exam and certain blood tests may also be helpful. Treatment depends on the cause; for most types of gastritis, reduction of stomach acid by medication is often helpful. Serious complications of gastritis are unusual. One exception is the H. pylori infection which, when present for a long time, may lead to stomach cancer in some individuals. 2 figures. Healthfinder™

Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •

Gastritis Summary: An inflammation of the lining of the stomach. Gastritis can be caused by infection, irritation, autoimmune disorders, or backflow of bile into the stomach (bile reflux). Source: National Library of Medicine, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6874 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 gastritis. 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

206 Gastritis

and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats

•

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 gastritis. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with gastritis. 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 gastritis. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/.

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Simply type in “gastritis” (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 “gastritis”. 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 “gastritis” (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 “gastritis” (or a synonym) into the search box, and click “Submit Query.”

209

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.26

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

26

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)27: •

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/

27

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/

•

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

•

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

•

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

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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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

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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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

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•

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

•

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

•

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

•

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

215

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

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

•

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

•

Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/

•

Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html

•

On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/

•

Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp

•

Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm

Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on gastritis: •

Basic Guidelines for Gastritis Gastritis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001150.htm Gastritis - acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000240.htm Gastritis - chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000232.htm Helicobacter pylori Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000229.htm Peptic ulcer Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000206.htm

216 Gastritis

•

Signs & Symptoms for Gastritis Abdominal indigestion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003260.htm Abdominal pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm Anemia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000560.htm Dark stools Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003130.htm Emesis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Erosion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003225.htm Erythema Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003220.htm Hematemesis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003118.htm Hiccups Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003068.htm Indigestion Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003260.htm Loss of appetite Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003121.htm Nausea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Stress gastritis Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000225.htm Vomiting Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003117.htm Vomiting blood Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003118.htm

Online Glossaries 217

•

Diagnostics and Tests for Gastritis ANA Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003535.htm Biopsy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003416.htm CBC Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003642.htm EGD Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003888.htm EGD (esophagogastroduodenoscopy) Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003888.htm Endoscopy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003338.htm Esophagogastroduodenoscopy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003888.htm Gastric acid Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003883.htm Gastroscopy Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003728.htm GI series Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003816.htm HCT Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm Stool guaiac Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003393.htm Upper GI and small bowel series Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003816.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm

•

Nutrition for Gastritis Vitamin B12 Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002403.htm

218 Gastritis

•

Background Topics for Gastritis Acute Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002215.htm Aggravated by Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002227.htm Alcohol use Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001944.htm Bile Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002237.htm Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Head trauma Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000028.htm Helicobacter pylori Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000229.htm Helicobacter pylori gastritis (chronic gastritis) Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000229.htm Incidence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002387.htm Lymph system Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002247.htm Respiratory Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002290.htm

Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •

Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical

•

MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

•

Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

•

Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

219

GASTRITIS 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 Cramps: Abdominal pain due to spasmodic contractions of the bowel. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Ablation: The removal of an organ by surgery. [NIH] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [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] Acetaldehyde: A colorless, flammable liquid used in the manufacture of acetic acid, perfumes, and flavors. It is also an intermediate in the metabolism of alcohol. It has a general narcotic action and also causes irritation of mucous membranes. Large doses may cause death from respiratory paralysis. [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] Acetone: A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis. [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] Achlorhydria: A lack of hydrochloric acid in gastric juice despite stimulation of gastric secretion. [NIH] Acoustic: Having to do with sound or hearing. [NIH] Acrylonitrile: A highly poisonous compound used widely in the manufacture of plastics, adhesives and synthetic rubber. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acute leukemia: A rapidly progressing cancer of the blood-forming tissue (bone marrow). [NIH]

Acyl: Chemical signal used by bacteria to communicate. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH]

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Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adduct: Complex formed when a carcinogen combines with DNA or a protein. [NIH] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenoma: A benign epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of adenosine to inosine with the elimination of ammonia. Since there are wide tissue and species variations in the enzyme, it has been used as a tool in the study of human and animal genetics and in medical diagnosis. EC 3.5.4.4. [NIH] Adherens Junctions: Anchoring points where the cytoskeleton of neighboring cells are connected to each other. They are composed of specialized areas of the plasma membrane where bundles of microfilaments attach to the membrane through the transmembrane linkers, cadherins, which in turn attach through their extracellular domains to cadherins in the neighboring cell membranes. In sheets of cells, they form into adhesion belts (zonula adherens) that go all the way around a cell. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adolescent Nutrition: Nutrition of children aged 13-18 years. [NIH] Adoptive Transfer: Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (immunotherapy, adoptive). [NIH] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy.

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[EU]

Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]

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] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] 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] Alkalinization: The process by which a substance becomes an alkali. An alkali is the opposite of an acid. [NIH] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allograft: An organ or tissue transplant between two humans. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] 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

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herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Aluminum Compounds: Inorganic compounds that contain aluminum as an integral part of the molecule. [NIH] Aluminum Hydroxide: Hydrated aluminum. A compound with many biomedical applications: as a gastric antacid, an antiperspirant, in dentifrices, as an emulsifier, as an adjuvant in bacterins and vaccines, in water purification, etc. [NIH] Amebiasis: Infection with any of various amebae. It is an asymptomatic carrier state in most individuals, but diseases ranging from chronic, mild diarrhea to fulminant dysentery may occur. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amenorrhea: Absence of menstruation. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Alcohols: Compounds possessing both a hydroxyl (-OH) and an amino group (NH2). [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Ammonium Sulfate: Sulfuric acid diammonium salt. It is used in fractionation of proteins. [NIH]

Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to ampicillin except that its resistance to gastric acid permits higher serum levels with oral administration. [NIH] Amphetamines: Analogs or derivatives of amphetamine. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopression, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation. [NIH] Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broadspectrum antibiotic. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH]

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Ampulla: A sac-like enlargement of a canal or duct. [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anaemia: A reduction below normal in the number of erythrocytes per cu. mm., in the quantity of haemoglobin, or in the volume of packed red cells per 100 ml. of blood which occurs when the equilibrium between blood loss (through bleeding or destruction) and blood production is disturbed. [EU] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Anal Fissure: A small tear in the anus that may cause itching, pain, or bleeding. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [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] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anergic: 1. Characterized by abnormal inactivity; inactive. 2. Marked by asthenia or lack of energy. 3. Pertaining to anergy. [EU] Anergy: Absence of immune response to particular substances. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general anesthesia, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH]

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Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]

Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Anorexia Nervosa: The chief symptoms are inability to eat, weight loss, and amenorrhea. [NIH]

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] Anthelmintics: Agents destructive to parasitic worms. They are used therapeutically in the treatment of helminthiasis in man and animal. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]

Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticholinergics: Medicines that calm muscle spasms in the intestine. Examples are dicyclomine (dy-SY-kloh-meen) (Bentyl) and hyoscyamine (HY-oh-SY-uh-meen) (Levsin). [NIH]

Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidiarrheals: Miscellaneous agents found useful in the symptomatic treatment of diarrhea. They have no effect on the agent(s) that cause diarrhea, but merely alleviate the condition. [NIH] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Antihypertensive: An agent that reduces high blood pressure. [EU] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH]

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Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] 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] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Anti-Ulcer Agents: Various agents with different action mechanisms used to treat or ameliorate ulcers or irritation of the gastrointestinal tract. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Anxiety Disorders: Disorders in which anxiety (persistent feelings of apprehension, tension, or uneasiness) is the predominant disturbance. [NIH] Aplastic anemia: A condition in which the bone marrow is unable to produce blood cells. [NIH]

Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Appendicitis: Acute inflammation of the vermiform appendix. [NIH] Approximate: Approximal [EU] Aptitude: The ability to acquire general or special types of knowledge or skill. [NIH] Aqueous: Having to do with water. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginase: A ureahydrolase that catalyzes the hydrolysis of arginine or canavanine to yield L-ORNITHINE and urea. Deficiency of this enzyme causes hyperargininemia. EC 3.5.3.1. [NIH]

Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriography: A procedure to x-ray arteries. The arteries can be seen because of an injection of a dye that outlines the vessels on an x-ray. [NIH]

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Arthrography: Roentgenography of a joint, usually after injection of either positive or negative contrast medium. [NIH] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aspergillus: A genus of mitosporic fungi containing about 100 species and eleven different teleomorphs in the family Trichocomaceae. [NIH] Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Asthenia: Clinical sign or symptom manifested as debility, or lack or loss of strength and energy. [NIH] Astrovirus: A genus of small, circular RNA viruses in the family Astroviridae. They cause gastroenteritis and are found in the stools of several vertebrates including humans. Transmission is by the fecal-oral route. There are at least seven human serotypes and the type species is human astrovirus 1. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atelectasis: Incomplete expansion of the lung. [NIH] Atresia: Lack of a normal opening from the esophagus, intestines, or anus. [NIH] Atrial: Pertaining to an atrium. [EU] Atrial Fibrillation: Disorder of cardiac rhythm characterized by rapid, irregular atrial impulses and ineffective atrial contractions. [NIH] Atrophic Gastritis: Chronic irritation of the stomach lining. Causes the stomach lining and glands to wither away. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Atropine: A toxic alkaloid, originally from Atropa belladonna, but found in other plants, mainly Solanaceae. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autacoids: A chemically diverse group of substances produced by various tissues in the body that cause slow contraction of smooth muscle; they have other intense but varied pharmacologic activities. [NIH]

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Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmune Hepatitis: A liver disease caused when the body's immune system destroys liver cells for no known reason. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Axonal: Condition associated with metabolic derangement of the entire neuron and is manifest by degeneration of the distal portion of the nerve fiber. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Bacillus: A genus of Bacillaceae that are spore-forming, rod-shaped cells. Most species are saprophytic soil forms with only a few species being pathogenic. [NIH] Bacteremia: The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bacterial Proteins: Proteins found in any species of bacterium. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH]

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Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its subdivisions is the basal (basement) lamina. [NIH] 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] Belladonna: A species of very poisonous Solanaceous plants yielding atropine (hyoscyamine), scopolamine, and other belladonna alkaloids, used to block the muscarinic autonomic nervous system. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Beta carotene: A vitamin A precursor. Beta carotene belongs to the family of fat-soluble vitamins called carotenoids. [NIH] Beta-Defensins: Defensins found mainly in epithelial cells. [NIH] Beta-Thromboglobulin: A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, preeclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders. [NIH] Bezoar: A ball of food, mucus, vegetable fiber, hair, or other material that cannot be digested in the stomach. Bezoars can cause blockage, ulcers, and bleeding. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile Ducts: Tubes that carry bile from the liver to the gallbladder for storage and to the small intestine for use in digestion. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Bile Reflux: Reflux of bile mainly into the upper digestive tract, but also into the pancreas. [NIH]

Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH]

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Biliary Tract: The gallbladder and its ducts. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Bioassay: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] 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] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biopsy specimen: Tissue removed from the body and examined under a microscope to determine whether disease is present. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Bismuth: A metallic element that has the atomic symbol Bi, atomic number 83 and atomic weight 208.98. [NIH] Bladder: The organ that stores urine. [NIH] Blast phase: The phase of chronic myelogenous leukemia in which the number of immature, abnormal white blood cells in the bone marrow and blood is extremely high. Also called blast crisis. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [NIH] Blood Cell Count: A count of the number of leukocytes and erythrocytes per unit volume in a sample of venous blood. A complete blood count (CBC) also includes measurement of the hemoglobin, hematocrit, and erythrocyte indices. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood 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]

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Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]

Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Body Regions: Anatomical areas of the body. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]

Breakdown: A physical, metal, or nervous collapse. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Bronchial: Pertaining to one or more bronchi. [EU] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Cadherins: A group of functionally related glycoproteins responsible for the calciumdependent cell-to-cell adhesion mechanism. They are divided into subclasses E-, P-, and Ncadherins, which are distinct in immunological specificity and tissue distribution. They promote cell adhesion via a homophilic mechanism. These compounds play a role in the construction of tissues and of the whole animal body. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in

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the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium Oxalate: The calcium salt of oxalic acid, occurring in the urine as crystals and in certain calculi. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoid: A type of tumor usually found in the gastrointestinal system (most often in the appendix), and sometimes in the lungs or other sites. Carcinoid tumors are usually benign. [NIH]

Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]

Cardia: That part of the stomach surrounded by the esophagogastric junction, characterized by the lack of acid-forming cells. [NIH] Cardiac: Having to do with the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carotenoids: Substance found in yellow and orange fruits and vegetables and in dark green, leafy vegetables. May reduce the risk of developing cancer. [NIH]

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Carrier State: The condition of harboring an infective organism without manifesting symptoms of infection. The organism must be readily transmissable to another susceptible host. [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] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Catheters: A small, flexible tube that may be inserted into various parts of the body to inject or remove liquids. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Causality: The relating of causes to the effects they produce. Causes are termed necessary when they must always precede an effect and sufficient when they initiate or produce an effect. Any of several factors may be associated with the potential disease causation or outcome, including predisposing factors, enabling factors, precipitating factors, reinforcing factors, and risk factors. [NIH] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Caustic: An escharotic or corrosive agent. Called also cauterant. [EU] Celiac Disease: A disease characterized by intestinal malabsorption and precipitated by gluten-containing foods. The intestinal mucosa shows loss of villous structure. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell motility: The ability of a cell to move. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell

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division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] 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] Cerebellar: Pertaining to the cerebellum. [EU] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] 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] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemoprevention: The use of drugs, vitamins, or other agents to try to reduce the risk of, or delay the development or recurrence of, cancer. [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] Chemotaxis: The movement of cells or organisms toward or away from a substance in response to its concentration gradient. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chest Pain: Pressure, burning, or numbness in the chest. [NIH] Chlorine: A greenish-yellow, diatomic gas that is a member of the halogen family of elements. It has the atomic symbol Cl, atomic number 17, and atomic weight 70.906. It is a powerful irritant that can cause fatal pulmonary edema. Chlorine is used in manufacturing, as a reagent in synthetic chemistry, for water purification, and in the production of chlorinated lime, which is used in fabric bleaching. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholecystectomy: Surgical removal of the gallbladder. [NIH]

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Cholecystitis: Inflammation of the gallbladder. [NIH] Cholelithiasis: Presence or formation of gallstones. [NIH] Cholera: An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is vibrio cholerae. This condition can lead to severe dehydration in a matter of hours unless quickly treated. [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] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Cholic Acid: A major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic lymphocytic leukemia: A slowly progressing disease in which too many white blood cells (called lymphocytes) are found in the body. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic phase: Refers to the early stages of chronic myelogenous leukemia or chronic lymphocytic leukemia. The number of mature and immature abnormal white blood cells in the bone marrow and blood is higher than normal, but lower than in the accelerated or blast phase. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Cimetidine: A histamine congener, it competitively inhibits histamine binding to H2 receptors. Cimetidine has a range of pharmacological actions. It inhibits gastric acid secretion, as well as pepsin and gastrin output. It also blocks the activity of cytochrome P450. [NIH] 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] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH]

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Clarithromycin: A semisynthetic macrolide antibiotic derived from erythromycin that is 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] Clathrin: The main structural coat protein of coated vesicles which play a key role in the intracellular transport between membranous organelles. Clathrin also interacts with cytoskeletal proteins. [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] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coated Vesicles: Vesicles formed when cell-membrane coated pits invaginate and pinch off. The outer surface of these vesicles are covered with a lattice-like network of coat proteins, such as clathrin, coat protein complex proteins, or caveolins. [NIH] Coca: Any of several South American shrubs of the Erythroxylon genus (and family) that yield cocaine; the leaves are chewed with alum for CNS stimulation. [NIH] Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [NIH] Cochlear: Of or pertaining to the cochlea. [EU] Cochlear Diseases: Diseases of the cochlea, the part of the inner ear that is concerned with hearing. [NIH] Codons: Any triplet of nucleotides (coding unit) in DNA or RNA (if RNA is the carrier of primary genetic information as in some viruses) that codes for particular amino acid or signals the beginning or end of the message. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Colic: Paroxysms of pain. This condition usually occurs in the abdominal region but may occur in other body regions as well. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in

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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] Colonic Polyps: Pedunculated or sessile growths arising from the mucous membrane of the colon. [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] Commensal: 1. Living on or within another organism, and deriving benefit without injuring or benefiting the other individual. 2. An organism living on or within another, but not causing injury to the host. [EU] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complement Activation: The sequential activation of serum components C1 through C9, initiated by an erythrocyte-antibody complex or by microbial polysaccharides and properdin, and producing an inflammatory response. [NIH] 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]

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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] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjugation: 1. The act of joining together or the state of being conjugated. 2. A sexual process seen in bacteria, ciliate protozoa, and certain fungi in which nuclear material is exchanged during the temporary fusion of two cells (conjugants). In bacterial genetics a form of sexual reproduction in which a donor bacterium (male) contributes some, or all, of its DNA (in the form of a replicated set) to a recipient (female) which then incorporates differing genetic information into its own chromosome by recombination and passes the recombined set on to its progeny by replication. In ciliate protozoa, two conjugants of separate mating types exchange micronuclear material and then separate, each now being a fertilized cell. In certain fungi, the process involves fusion of two gametes, resulting in union of their nuclei and formation of a zygote. 3. In chemistry, the joining together of two compounds to produce another compound, such as the combination of a toxic product with some substance in the body to form a detoxified product, which is then eliminated. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: 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] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of

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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] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]

Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary Disease: Disorder of cardiac function due to an imbalance between myocardial function and the capacity of the coronary vessels to supply sufficient flow for normal function. It is a form of myocardial ischemia (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels. [NIH] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Coronary Vessels: The veins and arteries of the heart. [NIH] Corpus: The body of the uterus. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Corticosteroids: Hormones that have antitumor activity in lymphomas and lymphoid leukemias; in addition, corticosteroids (steroids) may be used for hormone replacement and for the management of some of the complications of cancer and its treatment. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Crowding: Behavior with respect to an excessive number of individuals, human or animal, in relation to available space. [NIH]

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Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] Cyanosis: A bluish or purplish discoloration of the skin and mucous membranes due to an increase in the amount of deoxygenated hemoglobin in the blood or a structural defect in the hemoglobin molecule. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytochrome b: Cytochromes (electron-transporting proteins) with protoheme or a related heme as the prosthetic group. The prosthetic group is not covalently bound to the protein moiety. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] 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] Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents. [NIH] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Cytotoxins: Substances elaborated by microorganisms, plants or animals that are specifically toxic to individual cells; they may be involved in immunity or may be contained in venoms. [NIH]

Dairy Products: Raw and processed or manufactured milk and milk-derived products. These are usually from cows (bovine) but are also from goats, sheep, reindeer, and water buffalo. [NIH]

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Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] 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] Defense Mechanisms: Unconscious process used by an individual or a group of individuals in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydration: The condition that results from excessive loss of body water. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]

Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]

Dental Plaque: A film that attaches to teeth, often causing dental caries and gingivitis. It is composed of mucins, secreted from salivary glands, and microorganisms. [NIH] Dentifrices: Any preparations used for cleansing teeth; they usually contain an abrasive, detergent, binder and flavoring agent and may exist in the form of liquid, paste or powder; may also contain medicaments and caries preventives. [NIH] Depersonalization: Alteration in the perception of the self so that the usual sense of one's own reality is lost, manifested in a sense of unreality or self-estrangement, in changes of body image, or in a feeling that one does not control his own actions and speech; seen in

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depersonalization disorder, schizophrenic disorders, and schizotypal personality disorder. Some do not draw a distinction between depersonalization and derealization, using depersonalization to include both. [EU] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Derealization: Is characterized by the loss of the sense of reality concerning one's surroundings. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialysate: A cleansing liquid used in the two major forms of dialysis--hemodialysis and peritoneal dialysis. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] 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] Diarrhoea: Abnormal frequency and liquidity of faecal discharges. [EU] Diastolic: Of or pertaining to the diastole. [EU] Dicyclomine: A muscarinic antagonist used as an antispasmodic and in urinary incontinence. It has little effect on glandular secretion or the cardiovascular system. It does have some local anesthetic properties and is used in gastrointestinal, biliary, and urinary tract spasms. [NIH] Dietitian: An expert in nutrition who helps people plan what and how much food to eat. [NIH]

Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH]

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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: The act of dilating. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diuretic: A drug that increases the production of urine. [NIH] Diverticula: Plural form of diverticulum. [NIH] Diverticulitis: Inflammation of a diverticulum or diverticula. [NIH] Diverticulum: A pathological condition manifested as a pouch or sac opening from a tubular or sacular organ. [NIH] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] 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] Duodenal Ulcer: An ulcer in the lining of the first part of the small intestine (duodenum).

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[NIH]

Duodenitis: An irritation of the first part of the small intestine (duodenum). [NIH] Duodenogastric Reflux: Reflux of duodenal contents into the stomach. [NIH] Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dysentery: Any of various disorders marked by inflammation of the intestines, especially of the colon, and attended by pain in the abdomen, tenesmus, and frequent stools containing blood and mucus. Causes include chemical irritants, bacteria, protozoa, or parasitic worms. [EU]

Dyspepsia: Impaired digestion, especially after eating. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] Echography: Ultrasonography; the use of ultrasound as a diagnostic aid. Ultrasound waves are directed at the tissues, and a record is made, as on an oscilloscope, of the waves reflected back through the tissues, which indicate interfaces of different acoustic densities and thus differentiate between solid and cystic structures. [EU] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [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] Egg Yolk: Cytoplasm stored in an egg that contains nutritional reserves for the developing embryo. It is rich in polysaccharides, lipids, and proteins. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]

Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Emboli: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embolism: Blocking of a blood vessel by a blood clot or foreign matter that has been transported from a distant site by the blood stream. [NIH]

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Embolization: The blocking of an artery by a clot or foreign material. Embolization can be done as treatment to block the flow of blood to a tumor. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emergency Medicine: A branch of medicine concerned with an individual's resuscitation, transportation and care from the point of injury or beginning of illness through the hospital or other emergency treatment facility. [NIH] Emergency Treatment: First aid or other immediate intervention for accidents or medical conditions requiring immediate care and treatment before definitive medical and surgical management can be procured. [NIH] Empiric: Empirical; depending upon experience or observation alone, without using scientific method or theory. [EU] Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] Encephalitis, Viral: Inflammation of brain parenchymal tissue as a result of viral infection. Encephalitis may occur as primary or secondary manifestation of Togaviridae infections; Herpesviridae infections; Adenoviridae infections; Flaviviridae infections; Bunyaviridae infections; Picornaviridae infections; Paramyxoviridae infections; Orthomyxoviridae infections; Retroviridae infections; and Arenaviridae infections. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH] Endocrinology: A subspecialty of internal medicine concerned with the metabolism, physiology, and disorders of the endocrine system. [NIH] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [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] Endosomes: Cytoplasmic vesicles formed when coated vesicles shed their clathrin coat. Endosomes internalize macromolecules bound by receptors on the cell surface. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph

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vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium, Lymphatic: Unbroken cellular lining (intima) of the lymph vessels (e.g., the high endothelial lymphatic venules). It is more permeable than vascular endothelium, lacking selective absorption and functioning mainly to remove plasma proteins that have filtered through the capillaries into the tissue spaces. [NIH] Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components from interstitium to lumen; this function has been most intensively studied in the blood capillaries. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Energy Intake: Total number of calories taken in daily whether ingested or by parenteral routes. [NIH] Enhancers: Transcriptional element in the virus genome. [NIH] Enteric bacteria: Single-celled microorganisms that lack chlorophyll. Some bacteria are capable of causing human, animal, or plant diseases; others are essential in pollution control because they break down organic matter in the air and in the water. [NIH] Enteric Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Enteritis: Inflammation of the intestine, applied chiefly to inflammation of the small intestine; see also enterocolitis. [EU] Enterochromaffin-like Cells: Irregular-shaped argyrophilic cells which produce histamine, chromogranin A/pancreastatin, and an as yet unidentified peptide hormone. They are the predominant endocrine cell type of the oxyntic (acid-producing) mucosa of the stomach. ECL cells respond to gastrin by releasing their secretory products and this source of histamine acts as the positive paracrine stimulator of the release of hydrochloric acid from the parietal cell. [NIH] Enterocolitis: Inflammation of the intestinal mucosa of the small and large bowel. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [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] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH] Eosinophilic Gastroenteritis: Infection and swelling of the lining of the stomach, small intestine, or large intestine. The infection is caused by white blood cells (eosinophils). [NIH]

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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] Epidemiologic Factors: Events, characteristics, or other definable entities that have the potential to bring about a change in a health condition or other defined outcome. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitopes: Sites on an antigen that interact with specific antibodies. [NIH] Epstein: Failure of the upper eyelid to move downward on downward movement of the eye, occurring in premature and nervous infants. [NIH] Epstein-Barr virus: EBV. A common virus that remains dormant in most people. It has been associated with certain cancers, including Burkitt's lymphoma, immunoblastic lymphoma, and nasopharyngeal carcinoma. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [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] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Escherichia: A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria whose organisms occur in the lower part of the intestine of warm-blooded animals. The species are either nonpathogenic or opportunistic pathogens. [NIH] Escherichia coli: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce diarrhea and pyogenic infections. [NIH]

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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] Esophagogastroduodenoscopy: Exam of the upper digestive tract using an endoscope. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]

Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excipients: Usually inert substances added to a prescription in order to provide suitable consistency to the dosage form; a binder, matrix, base or diluent in pills, tablets, creams, salves, etc. [NIH] Excitability: Property of a cardiac cell whereby, when the cell is depolarized to a critical level (called threshold), the membrane becomes permeable and a regenerative inward current causes an action potential. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] 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] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exotoxin: Toxic substance excreted by living bacterial cells. [NIH] Expert Systems: Computer programs based on knowledge developed from consultation with experts on a problem, and the processing and/or formalizing of this knowledge using these programs in such a manner that the problems may be solved. [NIH] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]

External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH]

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Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Faecal: Pertaining to or of the nature of feces. [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] Fallopian Tubes: Two long muscular tubes that transport ova from the ovaries to the uterus. They extend from the horn of the uterus to the ovaries and consist of an ampulla, an infundibulum, an isthmus, two ostia, and a pars uterina. The walls of the tubes are composed of three layers: mucosal, muscular, and serosal. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Famotidine: A competitive histamine H2-receptor antagonist. Its main pharmacodynamic effect is the inhibition of gastric secretion. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Feasibility Studies: Studies to determine the advantages or disadvantages, practicability, or capability of accomplishing a projected plan, study, or project. [NIH] Febrile: Pertaining to or characterized by fever. [EU] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH] Ferrets: Semidomesticated variety of European polecat much used for hunting rodents and/or rabbits and as a laboratory animal. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH]

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Filtration: The passage of a liquid through a filter, accomplished by gravity, pressure, or vacuum (suction). [EU] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flaccid: Weak, lax and soft. [EU] Flagellin: A protein with a molecular weight of 40,000 isolated from bacterial flagella. At appropriate pH and salt concentration, three flagellin monomers can spontaneously reaggregate to form structures which appear identical to intact flagella. [NIH] Flatulence: Production or presence of gas in the gastrointestinal tract which may be expelled through the anus. [NIH] Flatus: Gas passed through the rectum. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride to prevent dental caries. [NIH] Focus Groups: A method of data collection and a qualitative research tool in which a small group of individuals are brought together and allowed to interact in a discussion of their opinions about topics, issues, or questions. [NIH] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Follicles: Shafts through which hair grows. [NIH] Foramen: A natural hole of perforation, especially one in a bone. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH]

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Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Fructose: A type of sugar found in many fruits and vegetables and in honey. Fructose is used to sweeten some diet foods. It is considered a nutritive sweetener because it has calories. [NIH] Fructose Intolerance: An autosomal recessive fructose metabolism disorder due to deficient fructose-1-phosphate aldolase (EC 2.1.2.13) activity, resulting in accumulation of fructose-1phosphate. The accumulated fructose-1-phosphate inhibits glycogenolysis and gluconeogenesis, causing severe hypoglycemia following ingestion of fructose. Prolonged fructose ingestion in infants leads ultimately to hepatic failure and death. Patients develop a strong distaste for sweet food, and avoid a chronic course of the disease by remaining on a fructose- and sucrose-free diet. [NIH] Fulminant Hepatic Failure: Liver failure that occurs suddenly in a previously healthy person. The most common causes of FHF are acute hepatitis, acetaminophen overdose, and liver damage from prescription drugs. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Galactosemia: Buildup of galactose in the blood. Caused by lack of one of the enzymes needed to break down galactose into glucose. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallstones: The solid masses or stones made of cholesterol or bilirubin that form in the gallbladder or bile ducts. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Ganglioside: Protein kinase C's inhibitor which reduces ischemia-related brain damage. [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] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastric atrophy: A condition in which the stomach muscles shrink and become weak. The digestive (peptic) glands may also shrink, resulting in a lack of digestive juices. [NIH] Gastric Emptying: The evacuation of food from the stomach into the duodenum. [NIH]

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Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]

Gastric Mucosa: Surface epithelium in the stomach that invaginates into the lamina propria, forming gastric pits. Tubular glands, characteristic of each region of the stomach (cardiac, gastric, and pyloric), empty into the gastric pits. The gastric mucosa is made up of several different kinds of cells. [NIH] Gastric Outlet Obstruction: The hindering of output from the stomach to the small intestine. The source varies: peptic ulcer, foreign bodies, aging, neoplasms, etc. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastrinoma: A gastrin-secreting tumor of the non-beta islet cells. It is usually located in the pancreas but is also found at other sites, as in the antrum of the stomach, hilus of the spleen, and regional lymph nodes. The presence of gastrinoma is one of three requirements to be met for identification of Zollinger-Ellison syndrome, which sometimes occurs in families with multiple endocrine neoplasia type 1 (MEN-1). Gastrinomas in patients with MEN-1 are usually diffuse in nature. [NIH] Gastritis: Inflammation of the stomach. [EU] Gastritis, Atrophic: Chronic gastritis with mucosal atrophy. [NIH] Gastroduodenal: Pertaining to or communicating with the stomach and duodenum, as a gastroduodenal fistula. [EU] Gastroenteritis: An acute inflammation of the lining of the stomach and intestines, characterized by anorexia, nausea, diarrhoea, abdominal pain, and weakness, which has various causes, including food poisoning due to infection with such organisms as Escherichia coli, Staphylococcus aureus, and Salmonella species; consumption of irritating food or drink; or psychological factors such as anger, stress, and fear. Called also enterogastritis. [EU] Gastroenterologist: A doctor who specializes in diagnosing and treating disorders of the digestive system. [NIH] Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas). [NIH] 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 tract: The stomach and intestines. [NIH] Gastrointestinal Transit: Passage of food (sometimes in the form of a test meal) through the gastrointestinal tract as measured in minutes or hours. The rate of passage through the intestine is an indicator of small bowel function. [NIH] Gastroparesis: Nerve or muscle damage in the stomach. Causes slow digestion and emptying, vomiting, nausea, or bloating. Also called delayed gastric emptying. [NIH] Gastroscopy: Endoscopic examination, therapy, or surgery of the interior of the stomach.

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[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]

Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Pool: The total genetic information possessed by the reproductive members of a population of sexually reproducing organisms. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Techniques: Chromosomal, biochemical, intracellular, and other methods used in the study of genetics. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genitourinary: Pertaining to the genital and urinary organs; urogenital; urinosexual. [EU] Genomics: The systematic study of the complete DNA sequences (genome) of organisms. [NIH]

Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geriatric: Pertaining to the treatment of the aged. [EU] Germ-free: Free of bacteria, disease-causing viruses, and other organisms that can cause infection. [NIH] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Giardiasis: An infection of the small intestine caused by the flagellated protozoan Giardia lamblia. It is spread via contaminated food and water and by direct person-to-person contact. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]

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Glomeruli: Plural of glomerulus. [NIH] Glomerulonephritis: Glomerular disease characterized by an inflammatory reaction, with leukocyte infiltration and cellular proliferation of the glomeruli, or that appears to be the result of immune glomerular injury. [NIH] Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Gluconeogenesis: The process by which glucose is formed from a non-carbohydrate source. [NIH]

Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]

Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]

Gluten: The protein of wheat and other grains which gives to the dough its tough elastic character. [EU] 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] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or Nacetylgalactosamine. [NIH] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH]

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Government Agencies: Administrative units of government responsible for policy making and management of governmental activities in the U.S. and abroad. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]

Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Graft Survival: The survival of a graft in a host, the factors responsible for the survival and the changes occurring within the graft during growth in the host. [NIH] Graft-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granule: A small pill made from sucrose. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Granulomatous Disease, Chronic: A recessive X-linked defect of leukocyte function in which phagocytic cells ingest but fail to digest bacteria, resulting in recurring bacterial infections with granuloma formation. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [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] Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or

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as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [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] Helminthiasis: Infestation with parasitic worms of the helminth class. [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] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemorrhoids: Varicosities of the hemorrhoidal venous plexuses. [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]

Heparin: Heparinic acid. A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood

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clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatic: Refers to the liver. [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 Encephalopathy: A condition that may cause loss of consciousness and coma. It is usually the result of advanced liver disease. Also called hepatic coma. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocyte: A liver cell. [NIH] Hepatocyte Growth Factor: Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is proto-oncogene protein C-met. [NIH] Hepatomegaly: Enlargement of the liver. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Herpes Zoster: Acute vesicular inflammation. [NIH] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]

Heterotrophic: Pertaining to organisms that are consumers and dependent on other organisms for their source of energy (food). [NIH] Hiatal Hernia: A small opening in the diaphragm that allows the upper part of the stomach to move up into the chest. Causes heartburn from stomach acid flowing back up through the opening. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Homeobox: Distinctive sequence of DNA bases. [NIH] Homeopathic remedies: Small doses of medicines, herbs, or both that are believed to stimulate the immune system. [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]

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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] Host: Any animal that receives a transplanted graft. [NIH] Human growth hormone: A protein hormone, secreted by the anterior lobe of the pituitary, which promotes growth of the whole body by stimulating protein synthesis. The human gene has already been cloned and successfully expressed in bacteria. [NIH] Human papillomavirus: HPV. A virus that causes abnormal tissue growth (warts) and is often associated with some types of cancer. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hydrochloric Acid: A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. Gastric acid is the hydrochloric acid component of gastric juice. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxides: Inorganic compounds that contain the OH- group. [NIH] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypercholesterolemia: Abnormally high levels of cholesterol in the blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersecretion: Excessive secretion. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions

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upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypochlorous Acid: HClO. An oxyacid of chlorine containing monovalent chlorine that acts as an oxidizing or reducing agent. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]

Hypoglycemic Agents: Agents which lower the blood glucose level. [NIH] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Ice Cream: A frozen dairy food made from cream or butterfat, milk, sugar, and flavorings. Frozen custard and French-type ice creams also contain eggs. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Image Cytometry: A technique encompassing morphometry, densitometry, neural networks, and expert systems that has numerous clinical and research applications and is particularly useful in anatomic pathology for the study of malignant lesions. The most common current application of image cytometry is for DNA analysis, followed by quantitation of immunohistochemical staining. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]

effects

of

foreign

Immunity, Mucosal: Nonsusceptibility to the pathogenic effects of foreign microorganisms or antigenic substances as a result of antibody secretions of the mucous membranes. Mucosal epithelia in the gastrointestinal, respiratory, and reproductive tracts produce a form of IgA (IgA, secretory) that serves to protect these ports of entry into the body. [NIH] Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH]

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Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunophenotyping: Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort Tlymphocytes into subsets based on CD antigens by the technique of flow cytometry. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Imperforate Anus: A birth defect in which the anal canal fails to develop. The condition is treated with an operation. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] Impotence: The inability to perform sexual intercourse. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [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] Incision: A cut made in the body during surgery. [NIH] Incompetence: Physical or mental inadequacy or insufficiency. [EU] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubated: Grown in the laboratory under controlled conditions. (For instance, white blood cells can be grown in special conditions so that they attack specific cancer cells when

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returned to the body.) [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indigestion: Poor digestion. Symptoms include heartburn, nausea, bloating, and gas. Also called dyspepsia. [NIH] Indolent: A type of cancer that grows slowly. [NIH] Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes. [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] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]

Infectious Mononucleosis: A common, acute infection usually caused by the Epstein-Barr virus (Human herpesvirus 4). There is an increase in mononuclear white blood cells and other atypical lymphocytes, generalized lymphadenopathy, splenomegaly, and occasionally hepatomegaly with hepatitis. [NIH] Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]

Influenza: An acute viral infection involving the respiratory tract. It is marked by inflammation of the nasal mucosa, the pharynx, and conjunctiva, and by headache and severe, often generalized, myalgia. [NIH] Information Centers: Facilities for collecting and organizing information. They may be specialized by subject field, type of source material, persons served, location, or type of services. [NIH] Informed Consent: Voluntary authorization, given to the physician by the patient, with full

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comprehension of the risks involved, for diagnostic or investigative procedures and medical and surgical treatment. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called 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] Inoculum: The spores or tissues of a pathogen that serve to initiate disease in a plant. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insertional: A technique in which foreign DNA is cloned into a restriction site which occupies a position within the coding sequence of a gene in the cloning vector molecule. Insertion interrupts the gene's sequence such that its original function is no longer expressed. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] 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]

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Interleukin-8: A cytokine that activates neutrophils and attracts neutrophils and Tlymphocytes. It is released by several cell types including monocytes, macrophages, Tlymphocytes, fibroblasts, endothelial cells, and keratinocytes by an inflammatory stimulus. IL-8 is a member of the beta-thromboglobulin superfamily and structurally related to platelet factor 4. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestinal Flora: The bacteria, yeasts, and fungi that grow normally in the intestines. [NIH] Intestinal Polyps: Pedunculated or sessile growths arising from the intestinal mucosa and extending into the lumen. The disease includes intestinal polyposis. [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] Intracellular Membranes: Membranes of subcellular structures. [NIH] Intracranial Hypertension: Increased pressure within the cranial vault. This may result from several conditions, including hydrocephalus; brain edema; intracranial masses; severe systemic hypertension; pseudotumor cerebri; and other disorders. [NIH] Intraepithelial: Within the layer of cells that form the surface or lining of an organ. [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] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]

Involuntary: Reaction occurring without intention or volition. [NIH] Iohexol: An effective non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Its low systemic toxicity is the combined result of low chemotoxicity and low osmolality. [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] Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill

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cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Irritable Bowel Syndrome: A disorder that comes and goes. Nerves that control the muscles in the GI tract are too active. The GI tract becomes sensitive to food, stool, gas, and stress. Causes abdominal pain, bloating, and constipation or diarrhea. Also called spastic colon or mucous colitis. [NIH] Irritants: Drugs that act locally on cutaneous or mucosal surfaces to produce inflammation; those that cause redness due to hyperemia are rubefacients; those that raise blisters are vesicants and those that penetrate sebaceous glands and cause abscesses are pustulants; tear gases and mustard gases are also irritants. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Islet: Cell producing insulin in pancreas. [NIH] Isothiocyanates: Organic compounds with the general formula R-NCS. [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]

Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [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] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated

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with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH] Kidney stone: A stone that develops from crystals that form in urine and build up on the inner surfaces of the kidney, in the renal pelvis, or in the ureters. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactates: Salts or esters of lactic acid containing the general formula CH3CHOHCOOR. [NIH] Lactobacillus: A genus of gram-positive, microaerophilic, rod-shaped bacteria occurring widely in nature. Its species are also part of the many normal flora of the mouth, intestinal tract, and vagina of many mammals, including humans. Pathogenicity from this genus is rare. [NIH] Lactose Intolerance: The disease state resulting from the absence of lactase enzyme in the musocal cells of the gastrointestinal tract, and therefore an inability to break down the disaccharide lactose in milk for absorption from the gastrointestinal tract. It is manifested by indigestion of a mild nature to severe diarrhea. It may be due to inborn defect genetically conditioned or may be acquired. [NIH] Laminin: Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]

Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense

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reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]

Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Linkages: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipodystrophy: A collection of rare conditions resulting from defective fat metabolism and characterized by atrophy of the subcutaneous fat. They include total, congenital or acquired, partial, abdominal infantile, and localized lipodystrophy. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] 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 Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH]

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Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] 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]

Lucida: An instrument, invented by Wollaton, consisting essentially of a prism or a mirror through which an object can be viewed so as to appear on a plane surface seen in direct view and on which the outline of the object may be traced. [NIH] Lumen: The cavity or channel within a tube or tubular organ. [EU] Luminol: 5-Amino-2,3-dihydro-1,4-phthalazinedione. Substance that emits light on oxidation. It is used in chemical determinations. [NIH] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]

Lymphadenopathy: Disease or swelling of the lymph nodes. [NIH] Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphoproliferative Disorders: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes

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dead cells, and stimulates the action of other immune system cells. [NIH] Magnesium Hydroxide: Magnesium hydroxide (Mg(OH)2). An inorganic compound that occurs in nature as the mineral brucite. It acts as an antacid with cathartic effects. [NIH] Magnesium Oxide: Magnesium oxide (MgO). An inorganic compound that occurs in nature as the mineral periclase. In aqueous media combines quickly with water to form magnesium hydroxide. It is used as an antacid and mild laxative and has many nonmedicinal uses. [NIH] Maintenance therapy: Treatment that is given to help a primary (original) treatment keep working. Maintenance therapy is often given to help keep cancer in remission. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malabsorption syndrome: A group of symptoms such as gas, bloating, abdominal pain, and diarrhea resulting from the body's inability to properly absorb nutrients. [NIH] Malaria: A protozoan disease caused in humans by four species of the genus Plasmodium (P. falciparum (malaria, falciparum), P. vivax (malaria, vivax), P. ovale, and P. malariae) and transmitted by the bite of an infected female mosquito of the genus Anopheles. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high fever, sweating, shaking chills, and anemia. Malaria in animals is caused by other species of plasmodia. [NIH] Malaria, Falciparum: Malaria caused by Plasmodium falciparum. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations. [NIH] Malaria, Vivax: Malaria caused by Plasmodium vivax. This form of malaria is less severe than malaria, falciparum, but there is a higher probability for relapses to occur. Febrile paroxysms often occur every other day. [NIH] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

MALT lymphoma: Mucosa-associated lymphoid tissue lymphoma. A type of cancer that arises in cells in mucosal tissue that are involved in antibody production. [NIH] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mannich Bases: Ketonic amines prepared from the condensation of a ketone with formaldehyde and ammonia or a primary or secondary amine. A Mannich base can act as the equivalent of an alpha,beta unsaturated ketone in synthesis or can be reduced to form physiologically active amino alcohols. [NIH] Maple Syrup Urine Disease: A genetic disorder involving deficiency of an enzyme necessary in the metabolism of branched-chain amino acids, and named for the characteristic odor of the urine. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH]

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Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]

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] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megaloblastic: A large abnormal red blood cell appearing in the blood in pernicious anaemia. [EU] 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] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metaplasia: A condition in which there is a change of one adult cell type to another similar

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adult cell type. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Methylmalonic Acid: A malonic acid derivative which is a vital intermediate in the metabolism of fat and protein. Abnormalities in methylmalonic acid metabolism lead to methylmalonic aciduria. This metabolic disease is attributed to a block in the enzymatic conversion of methylmalonyl CoA to succinyl CoA. [NIH] Metronidazole: Antiprotozoal used in amebiasis, trichomoniasis, giardiasis, and as treponemacide in livestock. It has also been proposed as a radiation sensitizer for hypoxic cells. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985, p133), this substance may reasonably be anticipated to be a carcinogen (Merck, 11th ed). [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microfilaments: The smallest of the cytoskeletal filaments. They are composed chiefly of actin. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitosporic Fungi: A large and heterogenous group of fungi whose common characteristic is the absence of a sexual state. Many of the pathogenic fungi in humans belong to this group. [NIH]

Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH]

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Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]

Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] 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] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucociliary: Pertaining to or affecting the mucus membrane and hairs (including eyelashes, nose hair, .): mucociliary clearing: the clearance of mucus by ciliary movement ( particularly in the respiratory system). [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucosal Ulceration: Skin ulceration in workers who work with lime and lime solutions. [NIH]

Mucositis: A complication of some cancer therapies in which the lining of the digestive system becomes inflamed. Often seen as sores in the mouth. [NIH] 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]

Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH]

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Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Musculature: The muscular apparatus of the body, or of any part of it. [EU] Musculoskeletal Diseases: Diseases of the muscles and their associated ligaments and other connective tissue and of the bones and cartilage viewed collectively. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Myalgia: Pain in a muscle or muscles. [EU] Mycophenolate mofetil: A drug that is being studied for its effectiveness in preventing graft-versus-host disease and autoimmune disorders. [NIH] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelography: X-ray visualization of the spinal cord following injection of contrast medium into the spinal arachnoid space. [NIH] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocarditis: Inflammation of the myocardium; inflammation of the muscular walls of the heart. [EU] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Myositis: Inflammation of a voluntary muscle. [EU] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Naive: Used to describe an individual who has never taken a certain drug or class of drugs (e. g., AZT-naive, antiretroviral-naive), or to refer to an undifferentiated immune system

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cell. [NIH] Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors. [NIH] Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of naloxone. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence. [NIH] Narcolepsy: A condition of unknown cause characterized by a periodic uncontrollable tendency to fall asleep. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephropathy: Disease of the kidneys. [EU] Nephrotoxic: Toxic or destructive to kidney cells. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [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] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU]

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Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neurotic: 1. Pertaining to or characterized by neurosis. 2. A person affected with a neurosis. [EU]

Neutralization: An act or process of neutralizing. [EU] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophil: A type of white blood cell. [NIH] Neutrophil Activation: The process in which the neutrophil is stimulated by diverse substances, resulting in degranulation and/or generation of reactive oxygen products, and culminating in the destruction of invading pathogens. The stimulatory substances, including opsonized particles, immune complexes, and chemotactic factors, bind to specific cellsurface receptors on the neutrophil. [NIH] Neutrophil Infiltration: The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions. [NIH] Niche: The ultimate unit of the habitat, i. e. the specific spot occupied by an individual organism; by extension, the more or less specialized relationships existing between an organism, individual or synusia(e), and its environment. [NIH] Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme urease. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]

Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nizatidine: A histamine H2 receptor antagonist with low toxicity that inhibits gastric acid secretion. The drug is used for the treatment of duodenal ulcers. [NIH] Nonulcer Dyspepsia: Constant pain or discomfort in the upper GI tract. Symptoms include burning, nausea, and bloating, but no ulcer. Possibly caused by muscle spasms. [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]

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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] 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] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleolus: A small dense body (sub organelle) within the nucleus of eukaryotic cells, visible by phase contrast and interference microscopy in live cells throughout interphase. Contains RNA and protein and is the site of synthesis of ribosomal RNA. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritional Status: State of the body in relation to the consumption and utilization of nutrients. [NIH] 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] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Oesophagitis: Inflammation of the esophagus. [EU] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in

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eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Ornithine: An amino acid produced in the urea cycle by the splitting off of urea from arginine. [NIH] Ornithine Decarboxylase: A pyridoxal-phosphate protein, believed to be the rate-limiting compound in the biosynthesis of polyamines. It catalyzes the decarboxylation of ornithine to form putrescine, which is then linked to a propylamine moiety of decarboxylated Sadenosylmethionine to form spermidine. EC 4.1.1.17. [NIH] Osmolality: The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per kilogram of solvent. The osmolality is directly proportional to the colligative properties of solutions; osmotic pressure, boiling point elevation, freezing point depression, and vapour pressure lowering. [EU] Osteomyelitis: Inflammation of bone caused by a pyogenic organism. It may remain localized or may spread through the bone to involve the marrow, cortex, cancellous tissue, and periosteum. [EU] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Otitis: Inflammation of the ear, which may be marked by pain, fever, abnormalities of hearing, hearing loss, tinnitus, and vertigo. [EU] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Overdosage: 1. The administration of an excessive dose. 2. The condition resulting from an excessive dose. [EU] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Oxalate: A chemical that combines with calcium in urine to form the most common type of kidney stone (calcium oxalate stone). [NIH] Oxazolone: Immunologic adjuvant and sensitizing agent. [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 metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic

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nerve. [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 cancer: Cancer of the pancreas, a salivary gland of the abdomen. [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 Insufficiency: Absence of or reduced pancreatic exocrine secretion into the duodenum and resultant poor digestion of lipids, vitamins, nitrogen, and carbohydrates. [NIH]

Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Panic: A state of extreme acute, intense anxiety and unreasoning fear accompanied by disorganization of personality function. [NIH] Panic Disorder: A type of anxiety disorder characterized by unexpected panic attacks that last minutes or, rarely, hours. Panic attacks begin with intense apprehension, fear or terror and, often, a feeling of impending doom. Symptoms experienced during a panic attack include dyspnea or sensations of being smothered; dizziness, loss of balance or faintness; choking sensations; palpitations or accelerated heart rate; shakiness; sweating; nausea or other form of abdominal distress; depersonalization or derealization; paresthesias; hot flashes or chills; chest discomfort or pain; fear of dying and fear of not being in control of oneself or going crazy. Agoraphobia may also develop. Similar to other anxiety disorders, it may be inherited as an autosomal dominant trait. [NIH] Papilla: A small nipple-shaped elevation. [NIH] Papillomavirus: A genus of Papovaviridae causing proliferation of the epithelium, which may lead to malignancy. A wide range of animals are infected including humans, chimpanzees, cattle, rabbits, dogs, and horses. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [NIH]

Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parasitic Diseases: Infections or infestations with parasitic organisms. They are often

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contracted through contact with an intermediate vector, but may occur as the result of direct exposure. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Parathyroid hormone: A substance made by the parathyroid gland that helps the body store and use calcium. Also called parathormone, parathyrin, or PTH. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parenteral Nutrition: The administering of nutrients for assimilation and utilization by a patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously). [NIH] Paresthesias: Abnormal touch sensations, such as burning or prickling, that occur without an outside stimulus. [NIH] Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parietal Cells: Cells in the stomach wall that make hydrochloric acid. [NIH] Parietal Lobe: Upper central part of the cerebral hemisphere. [NIH] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Particle: A tiny mass of material. [EU] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]

Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] 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 Compliance: Voluntary cooperation of the patient in following a prescribed regimen. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

Patient Selection: Criteria and standards used for the determination of the appropriateness

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of the inclusion of patients with specific conditions in proposed treatment plans and the criteria used for the inclusion of subjects in various clinical trials and other research protocols. [NIH] Pediatrics: A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence. [NIH] Peer Review: An organized procedure carried out by a select committee of professionals in evaluating the performance of other professionals in meeting the standards of their specialty. Review by peers is used by editors in the evaluation of articles and other papers submitted for publication. Peer review is used also in the evaluation of grant applications. It is applied also in evaluating the quality of health care provided to patients. [NIH] Pelvic: Pertaining to the pelvis. [EU] Penicillin: An antibiotic drug used to treat infection. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Pepsinogens: Proenzymes secreted by chief cells, mucous neck cells, and pyloric gland cells, which are converted into pepsin in the presence of gastric acid or pepsin itself. (Dorland, 28th ed) In humans there are 2 related pepsinogen systems: pepsinogen A (formerly pepsinogen I or pepsinogen) and pepsinogen C (formerly pepsinogen II or progastricsin). Pepsinogen B is the name of a pepsinogen from pigs. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Chain Elongation: The process whereby an amino acid is joined through a substituted amide linkage to a chain of peptides. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]

Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to

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the inside, the epineurium, the perineurium, and the endoneurium. [NIH] 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] Peripheral stem cells: Immature cells found circulating in the bloodstream. New blood cells develop from peripheral stem cells. [NIH] Peristalsis: The rippling motion of muscles in the intestine or other tubular organs characterized by the alternate contraction and relaxation of the muscles that propel the contents onward. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Pernicious: Tending to a fatal issue. [EU] Pernicious anemia: A type of anemia (low red blood cell count) caused by the body's inability to absorb vitamin B12. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Pharmacodynamic: Is concerned with the response of living tissues to chemical stimuli, that is, the action of drugs on the living organism in the absence of disease. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phosphates: Inorganic salts of phosphoric acid. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine

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(sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylating: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]

Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pirenzepine: An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as cimetidine and ranitidine. It is generally well tolerated by patients. [NIH] Plague: An acute infectious disease caused by Yersinia pestis that affects humans, wild rodents, and their ectoparasites. This condition persists due to its firm entrenchment in sylvatic rodent-flea ecosystems throughout the world. Bubonic plague is the most common form. [NIH] Plant Diseases: Diseases of plants. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to

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the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelet Factor 4: A high-molecular-weight proteoglycan-platelet factor complex which is released from blood platelets by thrombin. It acts as a mediator in the heparin-neutralizing capacity of the blood and plays a role in platelet aggregation. At high ionic strength (I=0.75), the complex dissociates into the active component (molecular weight 29,000) and the proteoglycan carrier (chondroitin 4-sulfate, molecular weight 350,000). The molecule exists in the form of a dimer consisting of 8 moles of platelet factor 4 and 2 moles of proteoglycan. [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]

Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] Poison Control Centers: Facilities which provide information concerning poisons and treatment of poisoning in emergencies. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Policy Making: The decision process by which individuals, groups or institutions establish policies pertaining to plans, programs or procedures. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH]

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Polyp: A growth that protrudes from a mucous membrane. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polyradiculoneuropathy: Diseases characterized by injury or dysfunction involving multiple peripheral nerves and nerve roots. The process may primarily affect myelin or nerve axons. Two of the more common demyelinating forms are acute inflammatory polyradiculopathy (Guillain-Barre syndrome) and polyradiculoneuropathy, chronic inflammatory demyelinating. Polyradiculoneuritis refers to inflammation of multiple peripheral nerves and spinal nerve roots. [NIH] Polyradiculopathy: Disease or injury involving multiple spinal nerve roots. Polyradiculitis refers to inflammation of multiple spinal nerve roots. [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Porphyria: A group of disorders characterized by the excessive production of porphyrins or their precursors that arises from abnormalities in the regulation of the porphyrin-heme pathway. The porphyrias are usually divided into three broad groups, erythropoietic, hepatic, and erythrohepatic, according to the major sites of abnormal porphyrin synthesis. [NIH]

Porphyrins: A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH]

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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] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Premalignant: A term used to describe a condition that may (or is likely to) become cancer. Also called precancerous. [NIH] Presumptive: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] 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] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Proglumide: 4-Benzamido-N,N-dipropylglutaramic acid. A drug that exerts an inhibitory effect on gastric secretion and reduces gastrointestinal motility. It is used clinically in the drug therapy of gastrointestinal ulcers. [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] Prolapse: The protrusion of an organ or part of an organ into a natural or artificial orifice. [NIH]

Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed

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over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteoglycan: A molecule that contains both protein and glycosaminoglycans, which are a type of polysaccharide. Proteoglycans are found in cartilage and other connective tissues. [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]

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Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Proton Pump: Integral membrane proteins that transport protons across a membrane against a concentration gradient. This transport is driven by hydrolysis of ATP by H(+)transporting ATP synthase. [NIH] Proton Pump Inhibitors: Medicines that stop the stomach's acid pump. Examples are omeprazole (oh-MEH-prah-zol) (Prilosec) and lansoprazole (lan-SOH-prah-zol) (Prevacid). [NIH]

Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Prune Belly Syndrome: A syndrome characterized by abdominal wall musculature deficiency, cryptorchism, and urinary tract abnormalities. The syndrome derives its name from its characteristic distended abdomen with wrinkled skin. [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychogenic: Produced or caused by psychic or mental factors rather than organic factors. [EU]

Psychophysiology: The study of the physiological basis of human and animal behavior. [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] Pulmonary Embolism: Embolism in the pulmonary artery or one of its branches. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of

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pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]

Purifying: Respiratory equipment whose function is to remove contaminants from otherwise wholesome air. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Putrescine: A toxic diamine formed by putrefaction from the decarboxylation of arginine and ornithine. [NIH] Pyelonephritis: Inflammation of the kidney and its pelvis, beginning in the interstitium and rapidly extending to involve the tubules, glomeruli, and blood vessels; due to bacterial infection. [EU] Pyogenic: Producing pus; pyopoietic (= liquid inflammation product made up of cells and a thin fluid called liquor puris). [EU] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [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] Rabies: A highly fatal viral infection of the nervous system which affects all warm-blooded animal species. It is one of the most important of the zoonoses because of the inevitably fatal outcome for the infected human. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Random Allocation: A process involving chance used in therapeutic trials or other research

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endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects. [NIH] Randomization: Also called random allocation. Is allocation of individuals to groups, e.g., for experimental and control regimens, by chance. Within the limits of chance variation, random allocation should make the control and experimental groups similar at the start of an investigation and ensure that personal judgment and prejudices of the investigator do not influence allocation. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Ranitidine: A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers. [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] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectal: By or having to do with the rectum. The rectum is the last 8 to 10 inches of the large intestine and ends at the anus. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflective: Capable of throwing back light, images, sound waves : reflecting. [EU] 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] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regional lymph node: In oncology, a lymph node that drains lymph from the region around a tumor. [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]

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Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal cell cancer: Cancer that develops in the lining of the renal tubules, which filter the blood and produce urine. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Resected: Surgical removal of part of an organ. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (granulomatous disease, chronic) often die as a result of recurrent bacterial infections. [NIH] Respiratory Paralysis: Complete or severe weakness of the muscles of respiration. This condition may be associated with motor neuron diseases; peripheral nerve disorders; neuromuscular junction diseases; spinal cord diseases; injury to the phrenic nerve; and other disorders. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH]

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Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rickets: A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rodentia: A mammalian order which consists of 29 families and many genera. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents. [NIH]

Rotavirus: A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. [NIH] Rubber: A high-molecular-weight polymeric elastomer derived from the milk juice (latex) of Hevea brasiliensis and other trees. It is a substance that can be stretched at room temperature to atleast twice its original length and after releasing the stress, retractrapidly, and recover its original dimensions fully. Synthetic rubber is made from many different chemicals, including styrene, acrylonitrile, ethylene, propylene, and isoprene. [NIH] Salicylate: Non-steroidal anti-inflammatory drugs. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Salivation: 1. The secretion of saliva. 2. Ptyalism (= excessive flow of saliva). [EU] Salmonella: A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that utilizes citrate as a sole carbon source. It is pathogenic for humans, causing enteric fevers, gastroenteritis, and bacteremia. Food poisoning is the most common clinical manifestation. Organisms within this genus are separated on the basis of antigenic characteristics, sugar fermentation patterns, and bacteriophage susceptibility. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to

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characterize schizophrenia. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Secretin: A hormone made in the duodenum. Causes the stomach to make pepsin, the liver to make bile, and the pancreas to make a digestive juice. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Seminal vesicles: Glands that help produce semen. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Sequence Analysis: A multistage process that includes the determination of a sequence (protein, carbohydrate, etc.), its fragmentation and analysis, and the interpretation of the resulting sequence information. [NIH] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serology: The study of serum, especially of antigen-antibody reactions in vitro. [NIH] Serotypes: A cause of haemorrhagic septicaemia (in cattle, sheep and pigs), fowl cholera of birds, pasteurellosis of rabbits, and gangrenous mastitis of ewes. It is also commonly found in atrophic rhinitis of pigs. [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] Sessile: Attached directly by the base, denoting a tumor without penduncle or stalk; in zoology, attached so that it is not possible to move about. [NIH] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Sexually Transmitted Diseases: Diseases due to or propagated by sexual contact. [NIH]

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Shedding: Release of infectious particles (e. g., bacteria, viruses) into the environment, for example by sneezing, by fecal excretion, or from an open lesion. [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]

Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Sinusitis: An inflammatory process of the mucous membranes of the paranasal sinuses that occurs in three stages: acute, subacute, and chronic. Sinusitis results from any condition causing ostial obstruction or from pathophysiologic changes in the mucociliary transport mechanism. [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] 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]

Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of

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the body. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatostatin: A polypeptide hormone produced in the hypothalamus, and other tissues and organs. It inhibits the release of human growth hormone, and also modulates important physiological functions of the kidney, pancreas, and gastrointestinal tract. Somatostatin receptors are widely expressed throughout the body. Somatostatin also acts as a neurotransmitter in the central and peripheral nervous systems. [NIH] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasmodic: Of the nature of a spasm. [EU] 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] Spectrometer: An apparatus for determining spectra; measures quantities such as wavelengths and relative amplitudes of components. [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] Spermidine: A polyamine formed from putrescine. It is found in almost all tissues in association with nucleic acids. It is found as a cation at all pH values, and is thought to help stabilize some membranes and nucleic acid structures. It is a precursor of spermine. [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] Spinal Nerve Roots: The paired bundles of nerve fibers entering and leaving the spinal cord at each segment. The dorsal and ventral nerve roots join to form the mixed segmental spinal nerves. The dorsal roots are generally afferent, formed by the central projections of the spinal (dorsal root) ganglia sensory cells, and the ventral roots efferent, comprising the axons of spinal motor and autonomic preganglionic neurons. There are, however, some exceptions to this afferent/efferent rule. [NIH]

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Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [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] Splenomegaly: Enlargement of the spleen. [NIH] Spondylitis: Inflammation of the vertebrae. [EU] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Spores: The reproductive elements of lower organisms, such as protozoa, fungi, and cryptogamic plants. [NIH] Sprue: A non febrile tropical disease of uncertain origin. [NIH] Standardize: To compare with or conform to a standard; to establish standards. [EU] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroids: Drugs used to relieve swelling and inflammation. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]

Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stomach Ulcer: An open sore in the lining of the stomach. Also called gastric ulcer. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Styrene: A colorless, toxic liquid with a strong aromatic odor. It is used to make rubbers, polymers and copolymers, and polystyrene plastics. [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]

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Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substrate: A substance upon which an enzyme acts. [EU] Sucralfate: A basic aluminum complex of sulfated sucrose. It is advocated in the therapy of peptic, duodenal, and prepyloric ulcers, gastritis, reflux esophagitis, and other gastrointestinal irritations. It acts primarily at the ulcer site, where it has cytoprotective, pepsinostatic, antacid, and bile acid-binding properties. The drug is only slightly absorbed by the digestive mucosa, which explains the absence of systemic effects and toxicity. [NIH] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Sunburn: An injury to the skin causing erythema, tenderness, and sometimes blistering and resulting from excessive exposure to the sun. The reaction is produced by the ultraviolet radiation in sunlight. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Suppressive: Tending to suppress : effecting suppression; specifically : serving to suppress activity, function, symptoms. [EU] 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]

Suspensions: Colloids with liquid continuous phase and solid dispersed phase; the term is used loosely also for solid-in-gas (aerosol) and other colloidal systems; water-insoluble drugs may be given as suspensions. [NIH] Symbiosis: The living together of organisms of different species. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Symptomatic treatment: Therapy that eases symptoms without addressing the cause of disease. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Systemic: Affecting the entire body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease

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marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] 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] Taurocholic Acid: The product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Tenesmus: Straining, especially ineffectual and painful straining at stool or in urination. [EU] Tetany: 1. Hyperexcitability of nerves and muscles due to decrease in concentration of extracellular ionized calcium, which may be associated with such conditions as parathyroid hypofunction, vitamin D deficiency, and alkalosis or result from ingestion of alkaline salts; it is characterized by carpopedal spasm, muscular twitching and cramps, laryngospasm with inspiratory stridor, hyperreflexia and choreiform movements. 2. Tetanus. [EU] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] 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] 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] Thymidine: A chemical compound found in DNA. Also used as treatment for mucositis. [NIH]

Thymidine Kinase: An enzyme that catalyzes the conversion of ATP and thymidine to ADP and thymidine 5'-phosphate. Deoxyuridine can also act as an acceptor and dGTP as a donor. (From Enzyme Nomenclature, 1992) EC 2.7.1.21. [NIH] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and

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multiply. The thymus is in the chest behind the breastbone. [NIH] 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] Thyroiditis: Inflammation of the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tocolysis: Any drug treatment modality designed to inhibit uterine contractions in pregnant women at risk for preterm labor. [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] 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] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxemia: A generalized intoxication produced by toxins and other substances elaborated by an infectious agent. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or

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animals. [NIH] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Tracheoesophageal Fistula: Abnormal communication between the esophagus and the trachea, acquired or congenital, often associated with esophageal atresia. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Translocate: The attachment of a fragment of one chromosome to a non-homologous chromosome. [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] Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Trichomoniasis: An infection with the protozoan parasite Trichomonas vaginalis. [NIH] Trophic: Of or pertaining to nutrition. [EU] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] Tumor infiltrating lymphocytes: White blood cells that have left the bloodstream and migrated into a tumor. [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

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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] Tumor-derived: Taken from an individual's own tumor tissue; may be used in the development of a vaccine that enhances the body's ability to build an immune response to the tumor. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Typhimurium: Microbial assay which measures his-his+ reversion by chemicals which cause base substitutions or frameshift mutations in the genome of this organism. [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] Ulcerogenic: Causing ulceration; leading to the production of ulcers. [EU] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [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] Urea Breath Test: A test used to detect Helicobacter pylori infection. The test measures breath samples for urease, an enzyme H. pylori makes. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Urethritis: Inflammation of the urethra. [EU] Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH] Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH]

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Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urogenital System: All the organs involved in reproduction and the formation and release of urine. It includes the kidneys, ureters, bladder, urethra, and the organs of reproduction ovaries, uterus, fallopian tubes, vagina, and clitoris in women and the testes, seminal vesicles, prostate, seminal ducts, and penis in men. [NIH] Uterine Contraction: Contraction of the uterine muscle. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Valerian: Valeriana officinale, an ancient, sedative herb of the large family Valerianaceae. The roots were formerly used to treat hysterias and other neurotic states and are presently used to treat sleep disorders. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [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] Vegetarianism: Dietary practice of consuming only vegetables, grains, and nuts. [NIH] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Venous Thrombosis: The formation or presence of a thrombus within a vein. [NIH] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertigo: An illusion of movement; a sensation as if the external world were revolving around the patient (objective vertigo) or as if he himself were revolving in space (subjective vertigo). The term is sometimes erroneously used to mean any form of dizziness. [EU] Vestibulocochlear Nerve: The 8th cranial nerve. The vestibulocochlear nerve has a cochlear part (cochlear nerve) which is concerned with hearing and a vestibular part (vestibular nerve) which mediates the sense of balance and head position. The fibers of the cochlear nerve originate from neurons of the spiral ganglion and project to the cochlear nuclei

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(cochlear nucleus). The fibers of the vestibular nerve arise from neurons of Scarpa's ganglion and project to the vestibular nuclei. [NIH] Vestibulocochlear Nerve Diseases: Diseases of the vestibular and/or cochlear (acoustic) nerves, which join to form the vestibulocochlear nerve. Vestibular neuritis, cochlear neuritis, and acoustic neuromas are relatively common conditions that affect these nerves. Clinical manifestations vary with which nerve is primarily affected, and include hearing loss, vertigo, and tinnitus. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Vibrio: A genus of Vibrionaceae, made up of short, slightly curved, motile, gram-negative rods. Various species produce cholera and other gastrointestinal disorders as well as abortion in sheep and cattle. [NIH] Vibrio cholerae: The etiologic agent of cholera. [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] Virulent: A virus or bacteriophage capable only of lytic growth, as opposed to temperate phages establishing the lysogenic response. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Vitamin D: The vitamin that mediates intestinal calcium absorption, bone calcium metabolism, and probably muscle activity. It usually acts as a hormone precursor, requiring 2 stages of metabolism before reaching actual hormonal form. It is isolated from fish liver oils and used in the treatment and prevention of rickets. [NIH] 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] Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide. [NIH] Warts: Benign epidermal proliferations or tumors; some are viral in origin. [NIH] Weight Gain: Increase in body weight over existing weight. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]

Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH]

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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] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zoonosis: Disease of animals, e. g. rabies, that can be transmitted to humans. A risk in major disasters; any disease and/or infection which is likely to be naturally transmitted from animals to man; disease caused by animal parasites. [NIH] Zoster: A virus infection of the Gasserian ganglion and its nerve branches, characterized by discrete areas of vesiculation of the epithelium of the forehead, the nose, the eyelids, and the cornea together with subepithelial infiltration. [NIH]

303

INDEX A Abdomen, 205, 219, 229, 230, 243, 246, 262, 265, 276, 279, 285, 293, 295 Abdominal Cramps, 168, 219 Abdominal Pain, 27, 168, 170, 171, 176, 219, 251, 263, 267, 298 Aberrant, 49, 64, 219 Ablation, 29, 219 Acatalasia, 219, 232 Acceptor, 219, 265, 275, 295 Acetaldehyde, 76, 219 Acetaminophen, 219, 250 Acetone, 13, 219, 263 Acetylcholine, 141, 219, 273 Achlorhydria, 11, 219 Acoustic, 219, 243, 300 Acrylonitrile, 219, 289 Actin, 14, 219, 269, 271 Acute leukemia, 107, 219 Acyl, 141, 219 Adaptability, 219, 232, 233 Adaptation, 30, 47, 220, 280 Adduct, 143, 220 Adenine, 220, 286 Adenocarcinoma, 14, 34, 39, 40, 42, 46, 47, 64, 70, 79, 132, 135, 140, 162, 168, 169, 220 Adenoma, 78, 220 Adenosine, 65, 91, 220, 231, 280 Adenosine Deaminase, 91, 220 Adherens Junctions, 57, 220 Adjustment, 220 Adjuvant, 38, 68, 220, 222, 252, 275 Adolescence, 220, 278 Adolescent Nutrition, 172, 220 Adoptive Transfer, 45, 59, 72, 220 Adsorption, 53, 220 Adsorptive, 220 Adverse Effect, 9, 175, 220, 291 Aerobic, 220, 269, 275 Aerosol, 220, 294 Affinity, 26, 56, 158, 221, 291 Agar, 221, 280 Agonist, 130, 147, 155, 221, 242, 272 Airway, 145, 221 Alertness, 221, 230 Algorithms, 171, 221, 229

Alimentary, 5, 6, 7, 8, 12, 65, 71, 74, 76, 77, 83, 98, 99, 103, 104, 105, 158, 221, 277, 278 Alkaline, 95, 143, 180, 221, 222, 231, 295 Alkalinization, 142, 221 Alkaloid, 221, 226, 235, 270 Alleles, 18, 31, 221 Allergen, 146, 163, 221 Allograft, 50, 221 Allylamine, 221, 222 Alpha Particles, 221, 286 Alternative medicine, 183, 221 Aluminum, 53, 122, 153, 222, 294 Aluminum Compounds, 53, 222 Aluminum Hydroxide, 53, 122, 153, 222 Amebiasis, 222, 269 Ameliorating, 142, 143, 149, 222 Amenorrhea, 222, 224 Amine, 160, 222, 256, 267 Amino Acid Sequence, 148, 222, 224, 252 Amino Acids, 185, 222, 246, 252, 267, 274, 278, 282, 284, 289, 290, 298 Amino Alcohols, 222, 267 Ammonia, 6, 56, 80, 139, 164, 179, 220, 222, 253, 267, 298 Ammonium Sulfate, 156, 222 Amoxicillin, 4, 7, 93, 101, 204, 222 Amphetamines, 222, 235 Ampicillin, 222 Amplification, 29, 222 Ampulla, 223, 244, 248 Anabolic, 185, 223 Anaemia, 71, 97, 223, 268 Anaerobic, 223, 246, 289 Anaesthesia, 223, 260 Anal, 168, 170, 172, 223, 259 Anal Fissure, 168, 170, 172, 223 Analgesic, 157, 219, 223, 270, 274 Analog, 77, 223 Analogous, 223, 297 Anaphylatoxins, 223, 236 Anatomical, 223, 230, 259, 290 Anemia, 16, 30, 50, 181, 198, 199, 216, 223, 249, 267, 279 Anergic, 54, 223 Anergy, 223 Anesthesia, 141, 160, 221, 223 Anesthetics, 145, 223, 246

304 Gastritis

Angiogenesis, 223, 267 Animal model, 22, 26, 33, 38, 49, 55, 99, 223 Anions, 223, 262 Annealing, 224, 281 Anorexia, 161, 170, 172, 222, 224, 251, 298 Anorexia Nervosa, 170, 172, 224 Antagonism, 141, 224, 231 Anthelmintics, 160, 224 Antibacterial, 25, 43, 77, 151, 157, 158, 160, 224, 292 Antibiotic, 5, 6, 9, 10, 25, 55, 133, 143, 149, 156, 163, 222, 224, 230, 235, 246, 278, 292 Anticholinergics, 153, 224 Anticoagulant, 224, 284, 300 Antidiarrheals, 157, 224 Antigen-Antibody Complex, 224, 236 Antigen-presenting cell, 224, 240 Antihypertensive, 157, 224 Anti-infective, 9, 224, 257 Anti-inflammatory, 55, 65, 146, 148, 153, 155, 163, 171, 219, 224, 226, 253, 260, 283, 289 Anti-Inflammatory Agents, 146, 153, 163, 225, 226 Antimicrobial, 38, 91, 133, 145, 149, 225 Antioxidant, 47, 66, 225, 226, 275 Antiseptic, 219, 225 Anti-Ulcer Agents, 149, 225 Antiviral, 160, 225, 261 Anuria, 225, 263 Anus, 223, 225, 226, 230, 249, 287 Anxiety, 141, 225, 276 Anxiety Disorders, 225, 276 Aplastic anemia, 64, 75, 225 Apolipoproteins, 225, 265 Apoptosis, 22, 32, 34, 39, 41, 42, 46, 51, 54, 66, 87, 94, 225 Appendicitis, 146, 163, 164, 171, 172, 225 Approximate, 34, 225 Aptitude, 156, 225 Aqueous, 225, 228, 239, 257, 267 Arachidonic Acid, 225, 264, 284 Arginase, 31, 36, 225 Arginine, 31, 122, 223, 225, 273, 275, 286 Aromatic, 225, 279, 293 Arterial, 221, 225, 234, 258, 284, 295 Arteries, 225, 229, 238, 266, 269, 271 Arteriography, 225, 262 Arthrography, 226, 262 Ascites, 171, 226 Ascorbic Acid, 71, 84, 226

Aspergillus, 96, 226 Aspirin, 122, 188, 205, 226 Assay, 19, 21, 24, 80, 226, 298 Asthenia, 223, 226 Astrovirus, 44, 226 Asymptomatic, 19, 30, 47, 52, 54, 56, 135, 140, 175, 180, 184, 219, 222, 226, 276 Ataxia, 199, 226, 295 Atelectasis, 144, 145, 226 Atresia, 177, 226 Atrial, 226, 300 Atrial Fibrillation, 226, 300 Atrophy, 5, 6, 8, 9, 11, 12, 32, 34, 43, 63, 66, 70, 87, 184, 199, 226, 251, 265 Atropine, 153, 226, 228 Attenuated, 34, 53, 226 Atypical, 226, 260 Autacoids, 226, 260 Autoantibodies, 92, 101, 185, 227 Autoantigens, 227 Autodigestion, 138, 227, 276 Autoimmune disease, 37, 53, 55, 227, 270 Autoimmune Hepatitis, 63, 227 Autoimmunity, 54, 61, 68, 86, 98, 227 Autonomic, 219, 227, 228, 278, 279, 292 Autonomic Nervous System, 227, 228, 279 Axonal, 26, 227 Axons, 26, 227, 278, 282, 292 B Bacillus, 149, 227 Bacteremia, 227, 289 Bacterial Infections, 54, 136, 156, 227, 254, 288 Bacterial Physiology, 56, 220, 227 Bacterial Proteins, 30, 227 Bactericidal, 9, 227 Bacteriophage, 227, 280, 289, 297, 300 Basal Ganglia, 226, 227, 228, 250 Basal Ganglia Diseases, 226, 228 Base, 46, 220, 228, 240, 247, 250, 252, 263, 264, 267, 290, 298 Basement Membrane, 49, 228, 248, 264 Basophils, 228, 254, 264 Belladonna, 226, 228 Benign, 84, 169, 220, 228, 231, 250, 254, 272, 286, 300 Beta carotene, 23, 228 Beta-Defensins, 91, 228 Beta-Thromboglobulin, 228, 262 Bezoar, 176, 228 Bile Acids, 228, 251, 295 Bile Acids and Salts, 228

Index 305

Bile Ducts, 228, 250, 283 Bile Pigments, 228, 263 Bile Reflux, 95, 120, 176, 205, 228 Biliary, 89, 111, 169, 171, 176, 228, 229, 231, 241, 276 Biliary Tract, 171, 229, 231, 276 Bilirubin, 228, 229, 250, 257 Bioassay, 26, 229 Bioavailability, 117, 229 Biochemical, 26, 119, 221, 229, 249, 252, 264 Biological response modifier, 229, 261 Biomarkers, 43, 99, 229 Biopsy, 50, 51, 57, 87, 106, 116, 161, 162, 176, 205, 217, 229, 278 Biopsy specimen, 161, 162, 229 Biosynthesis, 14, 35, 43, 56, 225, 229, 275, 290 Biotechnology, 58, 62, 174, 183, 195, 198, 199, 200, 229 Bismuth, 56, 110, 112, 133, 189, 204, 229 Bladder, 145, 168, 229, 259, 270, 284, 298, 299 Blast phase, 229, 234 Bloating, 229, 251, 260, 263, 267, 273 Blood Cell Count, 229, 279 Blood Coagulation, 229, 231 Blood Glucose, 229, 255, 258, 261 Blood pressure, 157, 160, 224, 229, 231, 258, 270, 291 Blood Volume, 230, 231 Blot, 38, 230 Body Fluids, 229, 230, 242, 274, 291, 297 Body Mass Index, 230, 275 Body Regions, 230, 235 Bone Marrow, 107, 219, 225, 229, 230, 234, 239, 246, 254, 258, 266, 270 Bone Marrow Transplantation, 107, 230 Bowel, 12, 16, 48, 150, 168, 170, 217, 219, 223, 230, 241, 245, 251, 260, 262, 264, 279, 293, 298 Bowel Movement, 170, 230, 241, 293 Brachytherapy, 230, 262, 263, 286, 301 Bradykinin, 230, 273 Branch, 213, 230, 243, 244, 266, 277, 292, 295 Breakdown, 55, 230, 241, 250 Broad-spectrum, 222, 230 Bronchial, 230, 256 Buccal, 230, 266 Bulimia, 161, 170, 230

C Cadherins, 220, 230 Caffeine, 172, 188, 230, 286 Calcium, 11, 146, 163, 230, 231, 236, 267, 275, 277, 291, 295, 300 Calcium Oxalate, 231, 275 Calculi, 231, 253 Capsules, 118, 231, 252 Carbohydrate, 158, 231, 253, 282, 290 Carbon Dioxide, 139, 164, 231, 240, 288 Carcinogen, 22, 30, 33, 42, 220, 231, 269 Carcinogenesis, 4, 18, 22, 34, 42, 231 Carcinogenic, 30, 39, 42, 76, 231, 261, 274, 283 Carcinoid, 11, 64, 67, 70, 79, 92, 231 Carcinoma, 27, 33, 36, 47, 58, 59, 63, 71, 73, 77, 84, 86, 87, 92, 98, 131, 133, 152, 175, 231, 246 Cardia, 68, 231 Cardiac, 19, 27, 221, 226, 230, 231, 238, 246, 247, 251, 271, 288 Cardiovascular, 130, 147, 148, 151, 161, 231, 241, 265, 280 Cardiovascular Agents, 130, 147, 151, 231 Cardiovascular disease, 148, 161, 231 Carotene, 116, 117, 122, 228, 231 Carotenoids, 228, 231 Carrier State, 40, 222, 232 Case report, 75, 77, 78, 79, 92, 111, 118, 232 Catalase, 30, 219, 232 Catheterization, 232, 262 Catheters, 145, 232, 259, 262 Cations, 232, 262 Causal, 26, 134, 163, 232 Causality, 69, 232 Cause of Death, 4, 36, 232 Caustic, 171, 232 Celiac Disease, 12, 70, 110, 170, 172, 185, 232 Cell Adhesion, 27, 230, 232, 261 Cell Cycle, 22, 232 Cell Death, 42, 46, 225, 232, 252, 272 Cell Differentiation, 49, 232, 291 Cell Division, 199, 227, 232, 233, 268, 269, 280, 283, 290 Cell membrane, 220, 232, 241, 247, 280 Cell motility, 232, 256 Cell proliferation, 27, 34, 55, 68, 84, 87, 232, 262, 291 Cell Respiration, 233, 269, 275, 288 Cell Size, 233, 249 Cell Survival, 49, 53, 233

306 Gastritis

Cellulose, 233, 280 Central Nervous System, 219, 222, 227, 230, 233, 235, 250, 253, 255, 265, 270, 280 Cerebellar, 226, 233, 287 Cerebral, 226, 227, 233, 246, 247, 267, 277, 292 Cerebrovascular, 228, 231, 233, 295 Cerebrum, 233, 297 Character, 233, 240, 253 Chemokines, 52, 58, 70, 72, 233 Chemoprevention, 18, 22, 74, 233 Chemotactic Factors, 233, 236, 273 Chemotaxis, 17, 233 Chemotherapy, 149, 233 Chest Pain, 19, 27, 233 Chlorine, 151, 164, 233, 258 Chlorophyll, 233, 245 Cholangitis, 146, 163, 171, 172, 177, 233 Cholecystectomy, 95, 171, 233 Cholecystitis, 171, 172, 177, 234 Cholelithiasis, 168, 234 Cholera, 44, 59, 234, 290, 300 Cholesterol, 121, 170, 172, 228, 234, 238, 250, 257, 265, 266 Cholesterol Esters, 234, 265 Cholic Acid, 234, 295 Chromatin, 225, 234, 246 Chromosomal, 222, 234, 252 Chromosome, 33, 234, 237, 254, 265, 290, 297 Chronic Disease, 15, 170, 234 Chronic lymphocytic leukemia, 234 Chronic myelogenous leukemia, 229, 234 Chronic phase, 205, 234 Chronic renal, 156, 234, 281, 298 Chylomicrons, 234, 265 Cimetidine, 141, 153, 234, 280 Circulatory system, 150, 234, 244 CIS, 33, 234 Citrus, 226, 234 Clarithromycin, 4, 7, 9, 93, 163, 188, 235 Clathrin, 235, 244 Clinical Medicine, 235, 283 Clinical trial, 9, 13, 19, 195, 235, 238, 239, 270, 278, 285, 287 Cloning, 44, 139, 229, 235, 261 Coagulation, 229, 235, 255, 295, 300 Coated Vesicles, 235, 244 Coca, 235 Cocaine, 176, 235 Cochlear, 235, 296, 299, 300 Cochlear Diseases, 235, 296

Codons, 235, 252, 274 Coenzyme, 133, 226, 235 Cofactor, 42, 134, 135, 139, 140, 235, 273, 284 Colic, 136, 168, 235 Colitis, 16, 41, 49, 52, 59, 136, 168, 170, 173, 177, 235, 263 Collagen, 228, 235, 248, 252, 267, 281 Collapse, 230, 236 Colloidal, 112, 236, 243, 294 Colonic Polyps, 156, 170, 236 Colorectal, 44, 170, 236 Colorectal Cancer, 44, 170, 236 Commensal, 49, 236 Complement, 12, 26, 223, 236, 237, 252, 261 Complement Activation, 12, 223, 236 Complementary and alternative medicine, 115, 124, 236 Complementary medicine, 115, 237 Complete remission, 237, 288 Computational Biology, 195, 198, 237 Conception, 237, 248, 293 Concomitant, 71, 92, 162, 237 Confounding, 73, 237 Confusion, 237, 242, 298 Congestion, 27, 237, 246 Conjugated, 228, 234, 237, 239 Conjugation, 237, 295 Conjunctiva, 237, 260 Connective Tissue, 226, 230, 236, 237, 248, 250, 252, 266, 271, 278, 284, 288, 294 Consciousness, 223, 237, 240, 242, 256, 288 Constipation, 162, 168, 170, 171, 172, 185, 237, 263 Constriction, 237, 263 Consultation, 19, 237, 247 Consumption, 15, 81, 111, 118, 237, 241, 251, 274, 288 Contamination, 204, 237, 289 Contraindications, ii, 168, 238 Controlled study, 10, 50, 238 Conventional therapy, 238 Conventional treatment, 132, 148, 238 Coordination, 25, 238, 270 Cornea, 238, 301 Coronary, 149, 231, 238, 269, 271 Coronary Disease, 149, 238 Coronary heart disease, 231, 238 Coronary Thrombosis, 238, 269, 271 Coronary Vessels, 238

Index 307

Corpus, 5, 8, 9, 58, 61, 66, 67, 69, 71, 74, 99, 102, 105, 182, 238, 278 Cortex, 226, 238, 247, 275, 287 Corticosteroids, 50, 238, 253, 283 Cortisone, 238, 283 Cranial, 238, 254, 262, 276, 278, 279, 299 Craniocerebral Trauma, 228, 238, 255, 295, 296 Crossing-over, 238, 287 Crowding, 135, 140, 238 Curative, 134, 239, 289, 295 Cutaneous, 169, 239, 263, 266 Cyanosis, 239, 247 Cyclic, 184, 231, 239, 254, 273, 282, 284 Cyclosporine, 50, 239 Cysteine, 124, 233, 239 Cytochrome, 30, 234, 239, 288 Cytochrome b, 239, 288 Cytokine, 17, 21, 27, 31, 32, 33, 36, 37, 39, 40, 45, 48, 52, 80, 87, 88, 96, 239, 262 Cytomegalovirus, 72, 96, 175, 239 Cytoplasm, 48, 225, 228, 232, 239, 243, 246, 254, 270, 289 Cytoprotection, 177, 239 Cytoskeleton, 14, 28, 44, 220, 239, 261 Cytotoxic, 63, 81, 131, 140, 239, 259, 286, 291 Cytotoxicity, 131, 221, 239 Cytotoxins, 179, 239 D Dairy Products, 184, 239 Data Collection, 240, 249 Databases, Bibliographic, 195, 240 Deamination, 240, 298 Decarboxylation, 13, 240, 256, 275, 286 Defense Mechanisms, 21, 47, 240, 261 Degenerative, 16, 27, 149, 240, 256 Dehydration, 168, 184, 234, 240 Deletion, 51, 225, 240 Dementia, 69, 110, 240 Denaturation, 240, 281 Dendrites, 240, 273 Dendritic, 12, 27, 240, 268 Dendritic cell, 12, 27, 240 Density, 9, 71, 230, 240, 249, 265, 274, 292 Dental Caries, 240, 249 Dental Plaque, 7, 10, 72, 240 Dentifrices, 222, 240 Depersonalization, 240, 276, 289 Depolarization, 241, 291 Derealization, 241, 276 Dermatitis, 121, 146, 163, 164, 241

Detoxification, 30, 139, 241 Deuterium, 241, 257 Developed Countries, 4, 5, 134, 135, 140, 184, 241 Developing Countries, 15, 36, 39, 43, 132, 134, 135, 139, 140, 145, 163, 175, 184, 241 Diagnostic procedure, 129, 183, 241 Dialysate, 185, 241 Dialyzer, 185, 241, 255 Diaphragm, 241, 256 Diarrhoea, 148, 160, 161, 241, 251 Diastolic, 241, 258 Dicyclomine, 224, 241 Dietitian, 185, 241 Diffusion, 241, 260, 273 Digestive system, 172, 241, 251, 270 Digestive tract, 26, 148, 153, 170, 228, 242, 247, 291 Dilatation, 242, 283 Diploid, 242, 280 Direct, iii, 26, 34, 36, 41, 42, 53, 55, 59, 106, 131, 137, 182, 187, 235, 242, 252, 266, 277, 287 Disorientation, 184, 237, 242 Dissociation, 221, 242 Distal, 14, 34, 145, 150, 227, 242, 251, 285 Diuresis, 230, 242 Diuretic, 157, 242 Diverticula, 242 Diverticulitis, 170, 172, 177, 242 Diverticulum, 242 Dizziness, 242, 276, 299 Dopamine, 235, 242, 279 Drive, ii, vi, 4, 7, 10, 109, 161, 170, 171, 172, 175, 176, 204, 242, 265 Drug Interactions, 189, 242 Drug Tolerance, 242, 296 Duct, 142, 223, 232, 233, 242, 244, 247, 256, 289 Duodenitis, 94, 139, 175, 185, 243 Duodenogastric Reflux, 81, 243 Duodenum, 138, 144, 145, 150, 163, 169, 170, 175, 228, 242, 243, 244, 250, 251, 276, 290, 293 Dura mater, 243, 268, 275 Dysentery, 168, 222, 243 Dyspepsia, 5, 15, 19, 25, 46, 59, 82, 88, 102, 156, 167, 169, 185, 243, 260 Dysplasia, 23, 35, 67, 70, 86, 103, 112, 119, 138, 199, 243 Dyspnea, 243, 247, 276 Dystrophy, 199, 243

308 Gastritis

E Eating Disorders, 171, 243 Echography, 62, 243 Effector, 37, 219, 236, 243 Efficacy, 3, 11, 12, 25, 28, 50, 55, 243 Egg Yolk, 137, 154, 156, 243 Electrolyte, 175, 243, 264, 274, 291, 298 Electrons, 225, 228, 243, 262, 275, 286 Electrophoresis, 96, 243 Electrophysiological, 26, 243 Emboli, 243, 244, 300 Embolism, 243, 285, 300 Embolization, 244, 300 Embolus, 244, 260 Embryo, 232, 243, 244, 260 Emergency Medicine, 170, 244 Emergency Treatment, 244 Empiric, 46, 244 Encephalitis, 146, 163, 164, 244 Encephalitis, Viral, 244 Endemic, 22, 39, 234, 244, 267, 293 Endocrine System, 244 Endocrinology, 169, 244 Endocytosis, 142, 244 Endoscope, 244, 247 Endoscopic, 4, 19, 57, 59, 63, 69, 71, 76, 78, 86, 90, 93, 94, 103, 145, 171, 244, 251 Endoscopic retrograde cholangiopancreatography, 171, 244 Endosomes, 38, 244 Endothelial cell, 27, 57, 244, 262 Endothelium, 27, 57, 245, 273 Endothelium, Lymphatic, 245 Endothelium, Vascular, 245 Endothelium-derived, 245, 273 Endotoxin, 43, 62, 145, 245, 298 End-stage renal, 234, 245, 281 Energy Intake, 185, 245 Enhancers, 153, 245 Enteric bacteria, 41, 52, 245 Enteric Nervous System, 27, 245 Enteritis, 146, 153, 155, 158, 163, 164, 168, 245 Enterochromaffin-like Cells, 96, 245 Enterocolitis, 245 Environmental Exposure, 245, 274 Environmental Health, 194, 196, 245 Enzymatic, 134, 231, 236, 240, 245, 256, 269, 281 Eosinophilic, 69, 76, 111, 175, 176, 245 Eosinophilic Gastroenteritis, 69, 176, 245 Eosinophils, 27, 245, 246, 254, 264

Epidemiologic Factors, 180, 246 Epidemiological, 21, 28, 42, 246 Epidermal, 32, 76, 138, 146, 163, 246, 263, 268, 300 Epidermis, 246, 263 Epigastric, 145, 246, 276 Epinephrine, 242, 246, 298 Epithelium, 14, 19, 20, 38, 46, 48, 66, 79, 102, 228, 245, 246, 251, 276, 301 Epitopes, 68, 246 Epstein, 90, 101, 152, 246, 260 Epstein-Barr virus, 90, 152, 246, 260 Erythema, 216, 246, 294 Erythrocytes, 223, 229, 230, 246 Erythromycin, 235, 246 Erythropoietin, 185, 246 Escherichia, 13, 59, 157, 246, 251 Escherichia coli, 13, 59, 157, 246, 251 Esophageal, 15, 44, 171, 247, 251, 297 Esophageal Atresia, 171, 247, 297 Esophageal Motility Disorders, 171, 247 Esophagitis, 61, 66, 68, 99, 103, 141, 170, 182, 185, 247, 251, 294 Esophagogastroduodenoscopy, 9, 217, 247 Esophagus, 9, 44, 78, 104, 168, 177, 226, 241, 242, 247, 251, 255, 266, 274, 279, 287, 293, 297 Essential Tremor, 199, 247 Ethnic Groups, 30, 247 Eukaryotic Cells, 247, 259, 274, 275 Evacuation, 237, 247, 250, 264 Evoke, 247, 293 Excipients, 156, 247 Excitability, 27, 247 Excitation, 222, 247, 249 Excrete, 225, 247, 263 Exhaustion, 224, 247, 267 Exocrine, 63, 247, 276 Exocytosis, 142, 247 Exogenous, 220, 247 Exotoxin, 145, 247 Expert Systems, 247, 258 Extensor, 247, 285 External-beam radiation, 247, 263, 286, 301 Extracellular, 49, 220, 237, 244, 248, 261, 267, 291, 295 Extracellular Matrix, 49, 237, 248, 261, 267 Extracellular Matrix Proteins, 248, 267 Extracellular Space, 248 Extraction, 25, 248

Index 309

F Faecal, 241, 248 Failure to Thrive, 171, 248 Fallopian Tubes, 248, 299 Family Planning, 195, 248 Famotidine, 153, 248 Fat, 172, 225, 228, 230, 231, 234, 238, 243, 244, 248, 263, 265, 269, 270, 275, 282, 288, 291, 294 Fatty acids, 248, 265, 284 Feasibility Studies, 27, 248 Febrile, 248, 267, 293 Feces, 16, 21, 158, 237, 248, 293 Fermentation, 248, 289 Ferrets, 162, 248 Fetus, 58, 142, 246, 248, 299 Fibroblasts, 28, 248, 262 Fibrosis, 17, 40, 49, 142, 171, 177, 198, 199, 221, 248, 289, 290 Filtration, 50, 249, 263 Fistula, 249, 251 Flaccid, 26, 249 Flagellin, 131, 249 Flatulence, 168, 249 Flatus, 249, 250 Flow Cytometry, 79, 249, 259 Fluorescence, 14, 44, 249 Fluorescent Dyes, 249 Fluorine, 151, 249 Focus Groups, 15, 249 Folate, 69, 249 Fold, 21, 30, 64, 249 Folic Acid, 249 Follicles, 67, 249 Foramen, 249, 279 Forearm, 229, 249 Fractionation, 222, 249 Frameshift, 250, 298 Frameshift Mutation, 250, 298 Fructose, 177, 250 Fructose Intolerance, 177, 250 Fulminant Hepatic Failure, 171, 250 Fungi, 150, 176, 237, 250, 262, 269, 293, 301 G Galactosemia, 177, 250 Gallbladder, 170, 171, 219, 228, 229, 233, 234, 241, 244, 250, 251 Gallstones, 168, 170, 171, 172, 228, 234, 250 Ganglia, 219, 228, 245, 250, 272, 279, 292 Ganglion, 250, 299, 301 Ganglioside, 26, 250

Gas, 78, 168, 170, 222, 231, 233, 241, 249, 250, 257, 260, 263, 267, 273, 294 Gastric Acid, 8, 11, 21, 65, 134, 137, 141, 143, 145, 153, 157, 161, 164, 169, 222, 234, 247, 250, 273, 278 Gastric atrophy, 33, 39, 85, 86, 106, 131, 250 Gastric Emptying, 250, 251 Gastric Juices, 251, 278 Gastric Outlet Obstruction, 76, 171, 251 Gastrin, 11, 21, 32, 93, 100, 111, 141, 153, 174, 234, 245, 251, 257 Gastrinoma, 176, 251 Gastritis, Atrophic, 34, 251 Gastroduodenal, 6, 36, 45, 48, 52, 76, 84, 133, 164, 176, 251 Gastroenteritis, 118, 168, 170, 172, 226, 251, 289 Gastroenterologist, 185, 251 Gastroesophageal Reflux, 19, 69, 167, 171, 177, 251 Gastroesophageal Reflux Disease, 19, 69, 167, 251 Gastrointestinal Transit, 27, 251 Gastroparesis, 185, 205, 251 Gastroscopy, 145, 217, 251 Gastrostomy, 144, 145, 252 Gelatin, 252, 253, 295 Gene Expression, 17, 27, 29, 35, 43, 48, 49, 58, 71, 89, 200, 252 Gene Pool, 30, 252 Genetic Code, 252, 274 Genetic Engineering, 229, 235, 252 Genetic Techniques, 56, 252 Genetic testing, 252, 281 Genetics, 30, 86, 184, 220, 237, 252 Genital, 252, 299 Genitourinary, 252, 299 Genomics, 35, 252 Genotype, 10, 19, 28, 46, 52, 252, 279 Geriatric, 69, 204, 252 Germ-free, 29, 41, 252 Giant Cells, 252, 289 Giardiasis, 252, 269 Gland, 238, 252, 266, 276, 277, 278, 284, 290, 293, 296 Glomerular, 50, 252, 253, 263 Glomeruli, 253, 286 Glomerulonephritis, 57, 253 Glomerulus, 252, 253, 272 Glucocorticoid, 253, 283 Gluconeogenesis, 250, 253

310 Gastritis

Glucose, 13, 199, 226, 229, 233, 250, 253, 255, 261 Glucuronic Acid, 253, 255 Glutamate, 56, 253 Glutamic Acid, 249, 253 Glutamine, 56, 123, 253 Glutathione Peroxidase, 30, 253 Gluten, 170, 185, 232, 253 Glycine, 32, 228, 234, 253, 290 Glycoprotein, 246, 252, 253, 264, 298 Glycosaminoglycans, 248, 253, 284 Goats, 239, 253 Gout, 168, 172, 253 Governing Board, 253, 282 Government Agencies, 177, 254, 282 Grade, 7, 74, 76, 82, 102, 254 Grading, 71, 81, 97, 104, 254 Graft, 50, 53, 175, 176, 254, 257, 259, 271 Graft Rejection, 254, 259 Graft Survival, 50, 254 Graft-versus-host disease, 53, 176, 254, 271 Gram-negative, 14, 43, 56, 134, 137, 149, 154, 156, 161, 162, 246, 254, 255, 289, 300 Gram-positive, 254, 264 Granule, 17, 254, 289 Granulocytes, 254, 291, 300 Granulomatous Disease, Chronic, 254, 288 Guanylate Cyclase, 254, 273 H Habitat, 254, 273 Habitual, 51, 233, 254 Haploid, 254, 280 Haptens, 221, 254 Headache, 231, 254, 260 Health Services, iv, 12, 19, 197, 255 Heart attack, 231, 255 Heartburn, 53, 136, 167, 170, 172, 185, 255, 256, 260 Helminthiasis, 168, 224, 255 Heme, 229, 239, 255, 282 Hemochromatosis, 171, 255 Hemodialysis, 75, 185, 241, 255, 263, 264 Hemoglobin, 223, 229, 239, 246, 255, 264, 282 Hemoglobinuria, 199, 255 Hemorrhage, 3, 4, 11, 19, 168, 238, 255, 293 Hemorrhoids, 168, 172, 255 Hemostasis, 255, 261 Heparin, 32, 255, 281 Hepatic, 6, 171, 244, 250, 256, 282 Hepatic Duct, Common, 244, 256

Hepatic Encephalopathy, 6, 171, 256 Hepatitis, 15, 44, 146, 148, 163, 164, 168, 171, 177, 250, 256, 260, 300 Hepatocyte, 28, 256 Hepatocyte Growth Factor, 28, 256 Hepatomegaly, 256, 260 Hereditary, 253, 256, 288 Heredity, 252, 256 Herpes, 28, 256 Herpes Zoster, 256 Heterodimers, 256, 261 Heterogeneity, 60, 221, 256 Heterotrophic, 250, 256 Hiatal Hernia, 170, 172, 176, 256 Histamine, 117, 141, 144, 146, 149, 163, 223, 234, 245, 248, 256, 273, 287 Histidine, 56, 256 Histology, 6, 8, 9, 73, 85, 86, 87, 91, 93, 139, 256 Homeobox, 89, 256 Homeopathic remedies, 170, 256 Homeostasis, 53, 133, 256 Homologous, 221, 238, 256, 290, 294, 297 Hormonal, 19, 134, 185, 226, 257, 300 Host, 12, 16, 21, 24, 28, 29, 31, 32, 33, 34, 36, 39, 40, 43, 44, 45, 46, 47, 48, 52, 60, 61, 62, 91, 133, 146, 150, 152, 158, 163, 169, 175, 184, 227, 232, 236, 254, 257, 258, 259, 264, 299, 300 Human growth hormone, 55, 257, 292 Human papillomavirus, 152, 257 Humoral, 12, 36, 45, 254, 257 Humour, 257 Hybrid, 63, 257 Hybridization, 14, 31, 257 Hydrochloric Acid, 136, 219, 245, 257, 277 Hydrogen Peroxide, 232, 253, 257, 265 Hydrolysis, 56, 220, 225, 257, 279, 282, 284, 285 Hydrophobic, 257, 265 Hydroxides, 53, 257 Hyperbilirubinemia, 257, 263 Hypercholesterolemia, 168, 257 Hyperglycemia, 181, 257 Hyperplasia, 8, 9, 32, 60, 70, 71, 101, 257 Hypersecretion, 11, 176, 257 Hypersensitivity, 36, 60, 221, 257, 265, 288 Hypertension, 171, 231, 258, 262, 298 Hypertrophy, 32, 257, 258 Hyperuricemia, 253, 258 Hypochlorous Acid, 164, 258 Hypoglycemia, 250, 258

Index 311

Hypoglycemic, 151, 153, 258 Hypoglycemic Agents, 153, 258 Hypothalamus, 227, 258, 292 I Ice Cream, 155, 156, 258 Id, 113, 120, 206, 212, 214, 258 Idiopathic, 16, 118, 258, 289 Image Cytometry, 87, 258 Imidazole, 256, 258, 287 Immune function, 37, 258, 259 Immune Sera, 38, 258 Immunity, 12, 20, 27, 38, 40, 44, 49, 53, 70, 71, 72, 73, 98, 99, 239, 258, 297 Immunity, Mucosal, 49, 258 Immunization, 45, 49, 55, 59, 132, 155, 220, 258, 259 Immunocompromised, 162, 259 Immunodeficiency, 199, 259 Immunoglobulin, 60, 66, 71, 224, 259, 270 Immunohistochemistry, 21, 26, 36, 259 Immunologic, 12, 22, 28, 38, 220, 233, 258, 259, 275, 286 Immunophenotyping, 21, 259 Immunosuppressive, 50, 253, 259 Immunosuppressive Agents, 50, 259 Immunosuppressive therapy, 50, 259 Immunotherapy, 20, 220, 259 Impairment, 50, 226, 259 Imperforate Anus, 177, 259 Implant radiation, 259, 262, 263, 286, 301 Impotence, 52, 259 In situ, 23, 36, 87, 259 In Situ Hybridization, 36, 259 In vitro, 14, 21, 22, 23, 25, 26, 27, 33, 34, 35, 37, 38, 49, 51, 52, 88, 131, 259, 281, 290, 296 In vivo, 21, 22, 25, 27, 29, 31, 33, 34, 35, 37, 38, 40, 42, 49, 51, 143, 256, 259 Incision, 144, 145, 259, 262 Incompetence, 251, 259 Incontinence, 148, 160, 161, 170, 171, 241, 259 Incubated, 34, 259 Indicative, 173, 260, 277, 299 Indigestion, 168, 170, 172, 185, 216, 260, 264 Indolent, 48, 260 Indomethacin, 93, 111, 260 Induction, 12, 14, 27, 34, 40, 41, 46, 49, 59, 60, 61, 141, 260 Infancy, 172, 260, 289 Infantile, 260, 265

Infarction, 75, 260 Infectious Mononucleosis, 101, 260 Infertility, 142, 260 Infiltration, 35, 48, 253, 260, 301 Inflammatory bowel disease, 12, 16, 17, 19, 40, 44, 51, 103, 138, 146, 163, 164, 171, 260 Influenza, 172, 260 Information Centers, 168, 260 Informed Consent, 10, 260 Infusion, 32, 261 Ingestion, 9, 16, 171, 250, 261, 281, 295 Inhalation, 220, 261, 281 Initiation, 29, 261, 297 Inoculum, 21, 261 Inorganic, 222, 257, 261, 267, 270, 279 Insecticides, 261, 279 Insertional, 14, 261 Insight, 16, 38, 49, 261 Insulator, 261, 270 Insulin, 185, 261, 263 Insulin-dependent diabetes mellitus, 261 Integrins, 17, 73, 261 Interferon, 48, 261 Interferon-alpha, 261 Interleukin-8, 17, 40, 58, 61, 70, 164, 262 Interleukins, 259, 262 Internal Medicine, 5, 17, 20, 46, 86, 110, 244, 251, 262 Internal radiation, 262, 263, 286, 301 Interstitial, 49, 57, 230, 248, 262, 263, 272, 301 Intestinal, 5, 6, 8, 9, 16, 21, 30, 32, 39, 41, 42, 49, 64, 66, 67, 68, 69, 70, 74, 83, 86, 92, 95, 98, 135, 136, 143, 145, 158, 162, 168, 170, 184, 231, 232, 245, 255, 262, 264, 267, 300 Intestinal Flora, 135, 262 Intestinal Polyps, 32, 262 Intestine, 44, 143, 224, 228, 230, 236, 245, 246, 251, 262, 264, 279 Intoxication, 262, 296, 301 Intracellular, 14, 30, 146, 163, 231, 235, 252, 260, 261, 262, 268, 273, 284, 291 Intracellular Membranes, 262, 268 Intracranial Hypertension, 255, 262, 296 Intraepithelial, 91, 262 Intramuscular, 262, 277 Intravenous, 261, 262, 277 Intrinsic, 221, 228, 262 Intubation, 144, 232, 262

312 Gastritis

Invasive, 20, 24, 32, 39, 46, 52, 56, 93, 258, 262 Involuntary, 228, 247, 262, 271, 291 Iohexol, 50, 262 Ions, 56, 159, 228, 242, 243, 257, 262 Irradiation, 172, 262, 301 Irritable Bowel Syndrome, 19, 27, 170, 172, 177, 185, 263 Irritants, 243, 263 Ischemia, 176, 226, 250, 263 Islet, 251, 263 Isothiocyanates, 162, 263 J Jaundice, 168, 171, 185, 257, 263 Joint, 226, 263, 294, 295 K Kb, 194, 263 Keratinocytes, 262, 263 Ketone Bodies, 13, 219, 263 Kidney Disease, 194, 199, 263 Kidney Failure, 53, 245, 263, 264 Kidney Failure, Acute, 263 Kidney Failure, Chronic, 263, 264 Kidney stone, 264, 275, 298 Kinetic, 53, 58, 72, 264 L Labile, 236, 264 Lactates, 158, 264 Lactobacillus, 9, 41, 135, 137, 154, 157, 158, 264 Lactose Intolerance, 170, 172, 264 Laminin, 73, 228, 248, 264 Large Intestine, 236, 241, 242, 245, 262, 264, 287, 291 Latent, 152, 264, 283 Laxative, 221, 264, 267 Lectin, 29, 158, 264, 268 Lesion, 39, 42, 49, 264, 265, 291, 298 Lethal, 227, 264 Leucine, 264, 278 Leukemia, 199, 234, 264 Leukocytes, 17, 23, 44, 46, 57, 228, 229, 230, 233, 246, 254, 260, 261, 262, 264, 270, 298 Leukopenia, 50, 264 Leukotrienes, 146, 163, 225, 264 Libido, 161, 265 Library Services, 212, 265 Life cycle, 250, 265 Ligament, 265, 284 Ligands, 91, 147, 261, 265 Ligation, 54, 265

Linkages, 253, 255, 265, 278 Lipid, 43, 158, 225, 261, 265, 270, 275 Lipid Peroxidation, 265, 275 Lipodystrophy, 177, 265 Lipopolysaccharide, 43, 254, 265 Lipoprotein, 56, 254, 265, 266 Lipoxygenase, 264, 265 Liver, 13, 15, 44, 50, 78, 87, 90, 96, 98, 100, 152, 162, 168, 169, 170, 171, 172, 176, 178, 219, 225, 227, 228, 234, 239, 241, 246, 248, 249, 250, 251, 253, 255, 256, 265, 283, 289, 290, 298, 300 Liver cancer, 15, 152, 265 Liver Transplantation, 171, 265 Lobe, 257, 265 Localization, 26, 27, 77, 259, 265 Localized, 55, 240, 260, 264, 265, 275, 280, 298 Locomotion, 266, 280 Loop, 32, 266 Low-density lipoprotein, 265, 266 Lower Esophageal Sphincter, 185, 247, 251, 266 Lucida, 264, 266 Lumen, 138, 142, 143, 150, 245, 247, 262, 266 Luminol, 30, 266 Lupus, 170, 266, 295 Lymph, 28, 218, 234, 244, 245, 257, 260, 266, 287, 289 Lymph node, 28, 266, 287, 289 Lymphadenopathy, 260, 266 Lymphatic, 71, 245, 260, 266, 293, 295 Lymphatic system, 266, 293, 295 Lymphocyte, 55, 57, 224, 266, 268 Lymphocytic, 66, 69, 70, 82, 90, 105, 110, 176, 266 Lymphoid, 33, 59, 60, 67, 82, 101, 149, 152, 153, 162, 224, 238, 266, 267 Lymphoma, 13, 33, 47, 82, 144, 149, 150, 162, 168, 175, 199, 246, 266, 267 Lymphoproliferative, 50, 266 Lymphoproliferative Disorders, 50, 266 Lytic, 266, 300 M Macrophage, 31, 266 Magnesium Hydroxide, 267 Magnesium Oxide, 153, 267 Maintenance therapy, 83, 144, 267 Malabsorption, 16, 66, 171, 172, 185, 199, 232, 267 Malabsorption syndrome, 171, 267

Index 313

Malaria, 168, 267 Malaria, Falciparum, 267 Malaria, Vivax, 267 Malignancy, 20, 28, 33, 35, 152, 267, 276 Malignant, 17, 22, 34, 36, 43, 84, 144, 162, 169, 199, 220, 258, 265, 267, 272, 286 Malnutrition, 172, 185, 226, 267, 271 MALT lymphoma, 33, 71, 85, 267 Manifest, 27, 227, 267 Mannich Bases, 161, 267 Maple Syrup Urine Disease, 177, 267 Matrix metalloproteinase, 40, 267 Meat, 184, 268 Mediate, 27, 37, 40, 56, 242, 268, 287 Mediator, 17, 268, 281 Medicament, 136, 145, 159, 268 MEDLINE, 195, 198, 199, 268 Megaloblastic, 16, 198, 249, 268 Meiosis, 268, 294 Melanin, 268, 279, 298 Melanocytes, 268 Melanoma, 27, 199, 268 Membrane Proteins, 35, 268, 285 Memory, 184, 224, 240, 268 Meninges, 233, 238, 243, 268 Meningitis, 146, 163, 164, 268 Mercury, 12, 249, 268 Metabolic disorder, 185, 253, 268 Metabolite, 162, 268 Metastasis, 152, 267, 269 Methylmalonic Acid, 69, 269 Metronidazole, 24, 60, 188, 204, 269 MI, 75, 94, 218, 269 Microbe, 34, 269, 296 Microbiological, 10, 269 Microfilaments, 220, 269 Microorganism, 157, 158, 235, 269, 277, 300 Micro-organism, 150, 240, 255, 269 Microscopy, 30, 44, 66, 90, 228, 269, 274 Migration, 17, 164, 269 Mitochondria, 30, 269, 275 Mitochondrial Swelling, 269, 272 Mitosis, 225, 269 Mitosporic Fungi, 226, 269 Mobility, 48, 131, 137, 154, 269 Modeling, 19, 269 Modification, 43, 252, 270, 286 Modulator, 62, 270 Monitor, 33, 71, 77, 90, 91, 270, 274 Monoclonal, 26, 263, 270, 286, 301 Monocytes, 27, 262, 264, 270

Mononuclear, 21, 260, 270, 298 Morphine, 162, 270, 272, 274 Morphological, 27, 174, 244, 268, 270 Morphology, 28, 40, 161, 270 Motility, 19, 27, 145, 260, 270, 280, 283 Motion Sickness, 270, 272 Mucins, 240, 270, 289 Mucociliary, 270, 291 Mucosal Ulceration, 176, 270 Mucositis, 270, 295 Mucus, 14, 39, 135, 140, 149, 153, 156, 158, 176, 228, 243, 270, 298 Multicenter study, 67, 270 Multiple sclerosis, 88, 270 Muscle Contraction, 185, 271 Muscle Fibers, 271 Muscular Atrophy, 199, 271 Muscular Dystrophies, 243, 271 Musculature, 271, 285 Musculoskeletal Diseases, 51, 271 Mutagenesis, 14, 28, 47, 271 Mutagens, 250, 271 Myalgia, 260, 271 Mycophenolate mofetil, 50, 271 Myelin, 270, 271, 282 Myelography, 262, 271 Myocardial infarction, 228, 238, 269, 271, 300 Myocardial Ischemia, 238, 271 Myocarditis, 146, 163, 164, 271 Myocardium, 269, 271 Myosin, 271 Myositis, 146, 163, 164, 271 Myotonic Dystrophy, 199, 271 N Naive, 26, 37, 271 Naloxone, 272 Naltrexone, 54, 272 Narcolepsy, 160, 161, 272 Narcotic, 219, 270, 272 Nasal Mucosa, 260, 272 Nausea, 168, 185, 205, 216, 251, 260, 272, 273, 276, 298 NCI, 1, 193, 234, 272 Necrosis, 61, 99, 225, 260, 269, 271, 272, 289 Neonatal, 37, 68, 93, 111, 272 Neoplasia, 34, 39, 91, 133, 199, 251, 272 Neoplasm, 141, 272, 298 Neoplastic, 22, 32, 49, 266, 272 Nephritis, 57, 146, 163, 164, 272 Nephropathy, 263, 272

314 Gastritis

Nephrotoxic, 50, 272 Networks, 35, 258, 272 Neural, 257, 258, 272 Neurologic, 184, 272 Neuromuscular, 219, 272, 273, 288, 298 Neuromuscular Junction, 219, 273, 288 Neuronal, 27, 273, 278 Neurons, 27, 235, 240, 250, 273, 292, 294, 299 Neuropathy, 26, 273 Neurotic, 273, 299 Neutralization, 53, 177, 273 Neutrons, 221, 262, 273, 286 Neutrophil, 5, 17, 40, 47, 273 Neutrophil Activation, 40, 273 Neutrophil Infiltration, 17, 273 Niche, 56, 273 Nickel, 56, 139, 273 Nitric Oxide, 31, 40, 51, 88, 273 Nitrogen, 31, 164, 221, 222, 248, 253, 264, 273, 276 Nizatidine, 153, 273 Nonulcer Dyspepsia, 27, 46, 168, 273 Nosocomial, 171, 273 Nuclear, 227, 237, 243, 247, 250, 272, 274 Nucleic acid, 134, 252, 257, 259, 271, 273, 274, 286, 292 Nucleic Acid Hybridization, 257, 274 Nucleolus, 274, 289 Nucleus, 225, 227, 228, 234, 239, 241, 246, 247, 268, 270, 273, 274, 283, 285, 293, 295, 300 Nutritional Status, 185, 274 Nutritional Support, 252, 274 O Ocular, 274, 280 Oesophagitis, 71, 78, 148, 274 Oliguria, 263, 274 Oncogene, 152, 199, 256, 274 Oncogenic, 261, 274 Opacity, 240, 274 Open Reading Frames, 59, 73, 274 Operon, 13, 35, 274, 288 Opium, 270, 274 Opportunistic Infections, 50, 274 Organ Culture, 274, 296 Organelles, 235, 239, 268, 270, 274 Ornithine, 31, 116, 275, 286 Ornithine Decarboxylase, 116, 275 Osmolality, 262, 275 Osteomyelitis, 146, 163, 164, 275 Osteoporosis, 172, 275

Otitis, 144, 145, 275 Ovaries, 248, 275, 299 Overdosage, 168, 275 Overdose, 250, 275 Overexpress, 32, 275 Overweight, 112, 160, 161, 275 Oxalate, 170, 275 Oxazolone, 52, 275 Oxidation, 219, 225, 239, 253, 265, 266, 275 Oxidative metabolism, 264, 275 Oxidative Stress, 46, 47, 275 P Pachymeningitis, 268, 275 Palliative, 276, 295 Pancreas, 142, 169, 170, 171, 176, 219, 228, 229, 241, 251, 255, 261, 263, 276, 290, 292, 297 Pancreatic, 44, 63, 94, 142, 152, 170, 171, 199, 244, 251, 276 Pancreatic cancer, 170, 199, 276 Pancreatic Ducts, 142, 244, 276 Pancreatic Fistula, 171, 276 Pancreatic Insufficiency, 63, 142, 276 Pancreatic Juice, 142, 251, 276 Pancreatitis, 15, 44, 77, 142, 146, 163, 164, 170, 171, 185, 276 Panic, 141, 276 Panic Disorder, 141, 276 Papilla, 244, 276 Papillomavirus, 276 Paralysis, 26, 276, 292 Paranasal Sinuses, 276, 291 Parasite, 276, 297 Parasitic, 171, 224, 243, 255, 276 Parasitic Diseases, 171, 276 Parathyroid, 185, 277, 289, 295 Parathyroid Glands, 277, 289 Parathyroid hormone, 185, 277 Parenteral, 38, 171, 245, 277 Parenteral Nutrition, 171, 277 Paresthesias, 276, 277 Parietal, 14, 29, 32, 37, 48, 55, 62, 97, 99, 117, 164, 245, 277, 279 Parietal Cells, 29, 32, 37, 48, 55, 97, 117, 277 Parietal Lobe, 277 Parotid, 277, 289 Paroxysmal, 199, 277 Partial remission, 277, 288 Particle, 277, 292, 297 Pathogen, 13, 16, 21, 33, 36, 38, 44, 47, 48, 51, 139, 150, 255, 261, 277

Index 315

Pathologic, 43, 49, 106, 132, 225, 229, 238, 257, 277, 285 Pathologic Processes, 225, 277 Pathologies, 31, 277 Pathophysiology, 49, 167, 175, 176, 277 Patient Compliance, 25, 38, 277 Patient Education, 185, 204, 205, 210, 212, 218, 277 Patient Selection, 8, 169, 177, 180, 277 Pediatrics, 38, 45, 52, 56, 93, 97, 103, 111, 278 Peer Review, 23, 109, 278 Pelvic, 146, 163, 164, 278, 284 Penicillin, 222, 224, 278 Penis, 278, 299 Pepsin, 141, 153, 158, 159, 234, 278, 290 Pepsin A, 141, 234, 278 Pepsinogens, 107, 278 Peptide, 18, 27, 91, 235, 245, 278, 282, 284 Peptide Chain Elongation, 235, 278 Percutaneous, 144, 145, 278 Perforation, 171, 249, 278 Pericardium, 278, 295 Periodontal disease, 40, 278 Peripheral blood, 21, 36, 261, 278 Peripheral Nerves, 278, 282, 293 Peripheral Nervous System, 27, 279, 292, 294 Peripheral stem cells, 254, 279 Peristalsis, 157, 279 Peritoneal, 150, 176, 226, 241, 279 Peritoneal Cavity, 150, 226, 279 Peritoneal Dialysis, 241, 279 Peritoneum, 279 Pernicious, 16, 37, 156, 205, 268, 279 Pernicious anemia, 16, 37, 156, 205, 279 Pesticides, 172, 261, 279 Phagocytosis, 164, 279 Pharmacodynamic, 248, 279 Pharmacologic, 26, 223, 226, 279, 296 Pharynx, 145, 251, 260, 279 Phenotype, 20, 39, 45, 49, 52, 58, 83, 279 Phenyl, 148, 151, 157, 161, 279 Phenylalanine, 17, 278, 279, 298 Phosphates, 44, 279 Phospholipases, 279, 291 Phospholipids, 248, 265, 279 Phosphorus, 53, 231, 277, 280 Phosphorylated, 28, 235, 280 Phosphorylating, 42, 280 Phosphorylation, 17, 28, 42, 44, 95, 146, 163, 280

Physiologic, 17, 19, 175, 221, 229, 280, 284, 287 Physiology, 10, 13, 19, 21, 26, 87, 117, 171, 175, 176, 243, 244, 251, 280 Pigment, 156, 229, 268, 280 Pilot study, 112, 280 Pirenzepine, 112, 141, 153, 280 Plague, 170, 280 Plant Diseases, 245, 280 Plants, 168, 221, 226, 228, 231, 234, 235, 239, 253, 264, 270, 280, 282, 293, 296, 297 Plaque, 7, 10, 280 Plasma, 100, 116, 142, 152, 220, 224, 228, 230, 232, 234, 245, 252, 255, 263, 280, 290 Plasma cells, 224, 280 Plasticity, 59, 73, 280 Platelet Activation, 280, 291 Platelet Aggregation, 223, 273, 281 Platelet Factor 4, 262, 281 Platelets, 228, 273, 280, 281, 295 Platinum, 266, 281 Pneumonitis, 146, 163, 164, 281 Poison Control Centers, 168, 281 Poisoning, 121, 155, 170, 172, 204, 251, 262, 268, 272, 281, 289 Policy Making, 254, 281 Polycystic, 75, 199, 281 Polymerase, 158, 281, 288 Polymerase Chain Reaction, 158, 281 Polymers, 136, 281, 284, 293 Polymorphic, 16, 281 Polymorphism, 16, 66, 94, 281 Polyp, 79, 282 Polypeptide, 222, 235, 257, 278, 282, 284, 292 Polyposis, 19, 177, 236, 262, 282 Polyradiculoneuropathy, 26, 282 Polyradiculopathy, 282 Polysaccharide, 224, 233, 282, 284 Polyunsaturated fat, 75, 117, 282 Porphyria, 177, 282 Porphyrins, 282 Posterior, 223, 226, 276, 282 Postmenopausal, 275, 282 Postsynaptic, 282, 291 Potentiates, 280, 282 Potentiation, 282, 291 Practicability, 248, 282 Practice Guidelines, 197, 282 Precancerous, 5, 23, 70, 86, 106, 139, 282, 283 Precipitating Factors, 232, 283

316 Gastritis

Precursor, 21, 30, 42, 49, 225, 228, 242, 243, 245, 279, 283, 292, 298, 300 Predisposition, 152, 283 Prednisolone, 283 Prednisone, 50, 283 Premalignant, 18, 39, 66, 91, 117, 282, 283 Presumptive, 4, 50, 283 Prevalence, 4, 5, 7, 10, 18, 36, 52, 56, 61, 63, 90, 95, 99, 104, 105, 118, 175, 176, 184, 283 Primary Biliary Cirrhosis, 67, 185, 283 Probe, 19, 26, 57, 283 Proglumide, 153, 283 Progression, 18, 21, 23, 29, 30, 33, 36, 39, 42, 49, 96, 103, 223, 283 Progressive, 16, 29, 39, 50, 232, 234, 240, 242, 254, 264, 271, 272, 280, 283, 298 Projection, 240, 283, 287 Prolapse, 176, 283 Promoter, 14, 33, 283 Prone, 158, 185, 283 Prophase, 283, 294 Prophylaxis, 50, 135, 137, 139, 143, 144, 160, 283, 299, 300 Prospective study, 83, 110, 283 Prostaglandin, 34, 40, 157, 284 Prostaglandins A, 260, 284 Prostate, 199, 229, 284, 297, 299 Protein C, 61, 222, 225, 227, 235, 265, 284, 298 Protein Conformation, 222, 284 Protein Kinases, 14, 284 Protein S, 132, 158, 159, 174, 199, 200, 229, 235, 246, 252, 257, 284, 289 Proteoglycan, 49, 281, 284 Proteolytic, 38, 145, 236, 284 Protocol, 28, 285 Proton Pump, 5, 11, 14, 62, 68, 74, 81, 96, 105, 124, 138, 144, 149, 153, 285 Proton Pump Inhibitors, 96, 124, 138, 153, 285 Protons, 221, 257, 285, 286 Protozoa, 237, 243, 269, 285, 293 Proximal, 12, 74, 142, 242, 285 Prune Belly Syndrome, 177, 285 Psoriasis, 146, 163, 285 Psychiatric, 130, 147, 151, 285 Psychiatry, 54, 110, 285 Psychic, 265, 285, 290 Psychogenic, 145, 285 Psychophysiology, 19, 285 Public Policy, 195, 285

Publishing, 7, 10, 58, 168, 177, 285 Pulmonary, 120, 142, 144, 145, 229, 233, 237, 245, 263, 265, 285, 294, 300 Pulmonary Artery, 229, 285 Pulmonary Edema, 233, 263, 285 Pulmonary Embolism, 285, 300 Pulse, 270, 285 Purifying, 13, 286 Purines, 286, 290 Putrescine, 275, 286, 292 Pyelonephritis, 57, 286 Pyogenic, 246, 275, 286 Pyridoxal, 275, 286 Q Quality of Life, 15, 19, 144, 286 R Rabies, 286, 301 Race, 269, 286 Radiation, 150, 176, 245, 247, 249, 262, 269, 286, 294, 301 Radiation therapy, 247, 249, 262, 263, 286, 301 Radioactive, 16, 19, 257, 259, 262, 263, 274, 286, 301 Radiolabeled, 263, 286, 301 Radiological, 278, 286 Radiology, 75, 80, 97, 171, 286 Radiotherapy, 230, 263, 286, 301 Random Allocation, 286, 287 Randomization, 50, 287 Randomized, 9, 10, 18, 43, 50, 56, 65, 93, 95, 243, 287 Ranitidine, 153, 189, 280, 287 Reactive Oxygen Species, 22, 30, 42, 46, 66, 287 Reagent, 233, 257, 287 Recombinant, 27, 31, 45, 55, 59, 132, 287, 299 Recombination, 30, 237, 287 Rectal, 168, 170, 287 Rectum, 225, 230, 236, 241, 242, 249, 250, 259, 260, 264, 284, 287 Recurrence, 12, 88, 138, 144, 149, 180, 233, 280, 287 Red Nucleus, 226, 287 Refer, 1, 178, 230, 236, 242, 250, 256, 265, 266, 271, 273, 287 Reflective, 142, 287 Refraction, 287, 292 Regimen, 24, 50, 132, 204, 243, 277, 287 Regional lymph node, 251, 287 Regurgitation, 247, 251, 255, 287

Index 317

Relapse, 83, 141, 144, 288 Remission, 54, 267, 287, 288 Renal cell cancer, 27, 288 Repressor, 274, 288 Resected, 91, 288 Respiration, 231, 270, 275, 288 Respiratory Burst, 17, 288 Respiratory Paralysis, 219, 288 Restoration, 288, 301 Resuscitation, 175, 244, 288 Retina, 288, 289 Retinoblastoma, 199, 288 Retrograde, 288 Reversion, 48, 288, 298 Rheumatism, 288 Rheumatoid, 142, 288 Rheumatoid arthritis, 142, 288 Ribose, 220, 288 Ribosome, 161, 289 Rickets, 289, 300 Rigidity, 280, 289 Risk factor, 7, 11, 21, 28, 30, 34, 52, 98, 163, 169, 172, 232, 283, 289 Rod, 137, 154, 161, 227, 246, 264, 289 Rodentia, 52, 289 Rodenticides, 279, 289 Rotavirus, 44, 289 Rubber, 145, 219, 289 S Salicylate, 110, 289 Saliva, 7, 21, 152, 185, 289 Salivary, 239, 240, 241, 276, 280, 289 Salivary glands, 239, 240, 241, 289 Salivation, 247, 289 Salmonella, 44, 155, 251, 289 Sarcoidosis, 176, 177, 289 Schizoid, 289, 301 Schizophrenia, 160, 289, 290, 301 Schizotypal Personality Disorder, 241, 289, 301 Sclerosis, 199, 270, 290 Screening, 42, 99, 106, 235, 290 Secretin, 11, 141, 153, 290 Secretory, 19, 27, 60, 111, 141, 142, 160, 182, 245, 258, 290 Sedative, 290, 299 Segregation, 287, 290 Seizures, 277, 290 Semen, 284, 290 Seminal vesicles, 290, 299 Semisynthetic, 222, 235, 290 Senile, 275, 290

Sepsis, 43, 290 Sequence Analysis, 96, 290 Sequencing, 44, 158, 255, 281, 290 Serine, 42, 290 Serology, 57, 61, 87, 99, 290 Serotypes, 226, 290 Serous, 245, 290 Sessile, 236, 262, 290 Sex Determination, 199, 290 Sexually Transmitted Diseases, 172, 290 Shedding, 21, 291 Shock, 33, 100, 135, 140, 161, 291, 297 Side effect, 50, 55, 141, 144, 152, 153, 168, 187, 205, 220, 258, 291, 296 Signal Transduction, 17, 36, 291 Signs and Symptoms, 56, 172, 288, 291, 298 Sinusitis, 146, 164, 291 Skeleton, 219, 263, 284, 291 Small intestine, 170, 228, 234, 242, 243, 244, 245, 251, 252, 257, 262, 291 Smooth muscle, 221, 222, 223, 226, 230, 256, 270, 291, 294 Sneezing, 291 Social Environment, 286, 291 Sodium, 53, 148, 153, 253, 291, 295 Sodium Bicarbonate, 153, 291 Soft tissue, 230, 291 Solvent, 219, 275, 292 Somatic, 101, 220, 257, 268, 269, 279, 292 Somatostatin, 77, 102, 292 Sound wave, 287, 292 Soybean Oil, 282, 292 Spasmodic, 219, 292 Spastic, 263, 292 Specialist, 206, 292 Specificity, 11, 57, 221, 230, 292 Spectrometer, 53, 292 Spectrum, 11, 30, 103, 292 Sperm, 234, 292 Spermidine, 275, 292 Sphincters, 247, 292 Spinal cord, 26, 233, 234, 243, 245, 250, 268, 271, 272, 273, 275, 278, 279, 288, 292, 293 Spinal Nerve Roots, 282, 292 Spinal Nerves, 278, 279, 292, 293 Spleen, 110, 116, 239, 251, 266, 289, 293 Splenomegaly, 260, 293 Spondylitis, 16, 293 Sporadic, 288, 293 Spores, 261, 293

318 Gastritis

Sprue, 57, 169, 177, 293 Standardize, 25, 293 Stem Cells, 246, 279, 293 Sterile, 16, 277, 293 Sterility, 260, 293 Steroids, 238, 253, 293 Stimulant, 188, 230, 256, 293 Stimulus, 17, 242, 247, 262, 277, 293, 295 Stomach, 3, 4, 5, 6, 7, 8, 9, 10, 13, 15, 21, 30, 32, 33, 47, 48, 55, 68, 72, 74, 76, 78, 85, 86, 88, 91, 92, 96, 105, 106, 110, 111, 116, 117, 118, 121, 131, 132, 133, 134, 136, 138, 139, 140, 144, 145, 149, 150, 152, 160, 161, 162, 164, 168, 169, 170, 175, 176, 183, 184, 185, 204, 205, 219, 226, 227, 228, 231, 241, 242, 243, 245, 247, 250, 251, 252, 256, 257, 266, 272, 277, 278, 279, 285, 287, 290, 291, 293 Stomach Ulcer, 133, 170, 293 Stool, 19, 57, 82, 97, 217, 259, 263, 264, 293, 295 Strand, 281, 293 Stress, 14, 46, 47, 136, 153, 171, 175, 176, 216, 227, 251, 263, 272, 275, 283, 288, 289, 293 Stroke, 194, 231, 293 Styrene, 289, 293 Subacute, 260, 291, 293 Subclinical, 22, 260, 290, 293 Subcutaneous, 265, 277, 293 Subspecies, 292, 294 Substance P, 246, 268, 290, 294 Substrate, 143, 294 Sucralfate, 95, 153, 174, 189, 294 Suction, 249, 294 Sunburn, 146, 163, 294 Superoxide, 288, 294 Supplementation, 116, 117, 294 Support group, 54, 294 Suppression, 21, 46, 53, 68, 119, 294 Suppressive, 9, 12, 74, 119, 294 Surfactant, 136, 142, 294 Suspensions, 136, 294 Symbiosis, 158, 294 Symphysis, 284, 294 Symptomatic, 11, 52, 57, 92, 136, 224, 276, 294 Symptomatic treatment, 136, 224, 294 Synapsis, 294 Synaptic, 27, 291, 294 Systemic lupus erythematosus, 79, 294 Systolic, 258, 295

T Taurine, 228, 234, 295 Taurocholic Acid, 118, 295 Telangiectasia, 199, 295 Tenesmus, 243, 295 Tetany, 277, 295 Thalamic, 226, 295 Thalamic Diseases, 226, 295 Therapeutics, 5, 6, 7, 8, 12, 65, 71, 74, 76, 77, 83, 98, 99, 103, 104, 105, 189, 295 Thermal, 242, 273, 281, 295 Thorax, 219, 295 Threonine, 290, 295 Threshold, 34, 247, 258, 295 Thrombosis, 228, 261, 284, 293, 295 Thrombus, 238, 260, 271, 281, 295, 299 Thymidine, 28, 295 Thymidine Kinase, 28, 295 Thymus, 258, 266, 295 Thyroid, 277, 296, 298 Thyroid Gland, 277, 296 Thyroiditis, 63, 111, 296 Thyroxine, 279, 296 Tin, 184, 281, 296 Tinnitus, 160, 275, 296, 300 Tissue Culture, 31, 296 Tocolysis, 93, 111, 296 Tolerance, 37, 49, 53, 55, 86, 144, 162, 219, 296 Tonic, 247, 296 Tooth Preparation, 220, 296 Topical, 84, 118, 143, 257, 291, 296 Torsion, 260, 296 Toxemia, 136, 296 Toxic, iv, 137, 139, 144, 154, 226, 237, 239, 245, 247, 258, 272, 273, 286, 293, 296 Toxicity, 27, 55, 242, 262, 268, 273, 294, 296 Toxicology, 196, 296 Toxins, 224, 244, 253, 260, 296, 299 Trace element, 249, 273, 296, 297 Trachea, 279, 296, 297 Tracheoesophageal Fistula, 247, 297 Transcriptase, 35, 297 Transcription Factors, 22, 46, 48, 297 Transduction, 36, 291, 297 Transfection, 54, 57, 229, 297 Transfer Factor, 258, 297 Translocate, 48, 297 Translocation, 14, 235, 246, 297 Transmitter, 219, 242, 268, 297 Transplantation, 53, 171, 234, 258, 264, 297 Trauma, 218, 247, 272, 276, 297

Index 319

Trees, 289, 297 Trichomoniasis, 170, 269, 297 Trophic, 67, 297 Tropism, 29, 297 Tuberculosis, 237, 266, 297 Tuberous Sclerosis, 199, 297 Tumor infiltrating lymphocytes, 28, 297 Tumor marker, 229, 297 Tumor Necrosis Factor, 61, 99, 298 Tumor-derived, 152, 298 Tumour, 152, 250, 298 Typhimurium, 155, 298 Tyrosine, 17, 28, 146, 163, 242, 298 U Ulceration, 12, 20, 27, 40, 46, 47, 55, 56, 57, 133, 138, 139, 149, 171, 173, 270, 298 Ulcerative colitis, 16, 19, 49, 57, 78, 112, 119, 142, 150, 172, 260, 298 Ulcerogenic, 175, 298 Unconscious, 223, 240, 258, 298 Uraemia, 276, 298 Urea, 21, 31, 56, 57, 97, 139, 154, 164, 189, 225, 264, 275, 298 Urea Breath Test, 21, 57, 97, 298 Uremia, 6, 263, 298 Ureters, 264, 298, 299 Urethra, 278, 284, 298, 299 Urethritis, 146, 163, 164, 298 Uric, 88, 253, 258, 286, 298 Urinary, 148, 150, 160, 161, 231, 241, 252, 259, 274, 280, 285, 298, 299 Urinary tract, 150, 241, 285, 299 Urine, 16, 60, 145, 225, 229, 231, 242, 255, 259, 263, 264, 267, 274, 275, 288, 298, 299 Urogenital, 150, 252, 299 Urogenital System, 150, 299 Uterine Contraction, 157, 296, 299 Uterus, 238, 248, 275, 299 V Vaccination, 27, 36, 38, 39, 59, 60, 299 Vaccine, 27, 36, 45, 132, 134, 139, 140, 148, 149, 177, 182, 220, 285, 298, 299 Vacuoles, 18, 140, 244, 275, 299 Vagina, 264, 299 Valerian, 168, 299 Vascular, 16, 27, 57, 221, 245, 260, 273, 295, 296, 299 Vasculitis, 276, 299

Vasodilator, 230, 242, 256, 299 Vector, 261, 277, 297, 299 Vegetarianism, 172, 299 Venoms, 239, 299 Venous, 228, 229, 255, 284, 299, 300 Venous Thrombosis, 228, 299, 300 Ventral, 145, 258, 292, 293, 299 Vertebrae, 292, 293, 299 Vertigo, 275, 299, 300 Vestibulocochlear Nerve, 296, 299, 300 Vestibulocochlear Nerve Diseases, 296, 300 Veterinary Medicine, 195, 300 Vibrio, 234, 300 Vibrio cholerae, 234, 300 Villous, 232, 300 Viral, 15, 44, 54, 101, 152, 171, 244, 252, 260, 274, 286, 297, 300 Viral Hepatitis, 44, 171, 300 Virulence, 18, 20, 24, 28, 31, 35, 39, 40, 47, 48, 52, 56, 59, 73, 140, 175, 184, 226, 296, 300 Virulent, 23, 52, 131, 300 Virus, 15, 98, 152, 227, 245, 246, 252, 257, 261, 280, 297, 300, 301 Visceral, 19, 227, 279, 300 Vitamin D, 183, 289, 300 Vitro, 26, 32, 34, 51, 53, 256, 300 Vivo, 22, 25, 34, 37, 49, 53, 300 W Warfarin, 15, 104, 112, 300 Warts, 257, 300 Weight Gain, 248, 300 White blood cell, 205, 224, 229, 234, 245, 259, 260, 264, 266, 270, 273, 280, 297, 300 Windpipe, 279, 296, 300 Withdrawal, 50, 301 Wound Healing, 261, 267, 301 X Xenograft, 223, 301 X-ray, 145, 205, 217, 225, 244, 249, 262, 271, 274, 286, 301 X-ray therapy, 263, 301 Y Yeasts, 161, 250, 262, 279, 301 Z Zoonosis, 118, 301 Zoster, 107, 301

320 Gastritis

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