LISTERIA
MONOCYTOGENES A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Listeria monocytogenes: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-497-00666-9 1. Listeria monocytogenes-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on Listeria monocytogenes. 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 LISTERIA MONOCYTOGENES ..................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Listeria monocytogenes ................................................................. 5 E-Journals: PubMed Central ....................................................................................................... 61 The National Library of Medicine: PubMed ................................................................................ 90 CHAPTER 2. NUTRITION AND LISTERIA MONOCYTOGENES ......................................................... 137 Overview.................................................................................................................................... 137 Finding Nutrition Studies on Listeria monocytogenes.............................................................. 137 Federal Resources on Nutrition ................................................................................................. 142 Additional Web Resources ......................................................................................................... 142 CHAPTER 3. ALTERNATIVE MEDICINE AND LISTERIA MONOCYTOGENES ................................... 145 Overview.................................................................................................................................... 145 National Center for Complementary and Alternative Medicine................................................ 145 Additional Web Resources ......................................................................................................... 157 General References ..................................................................................................................... 158 CHAPTER 4. DISSERTATIONS ON LISTERIA MONOCYTOGENES ..................................................... 159 Overview.................................................................................................................................... 159 Dissertations on Listeria monocytogenes................................................................................... 159 Keeping Current ........................................................................................................................ 161 CHAPTER 5. PATENTS ON LISTERIA MONOCYTOGENES................................................................ 163 Overview.................................................................................................................................... 163 Patents on Listeria monocytogenes ............................................................................................ 163 Patent Applications on Listeria monocytogenes ........................................................................ 175 Keeping Current ........................................................................................................................ 180 CHAPTER 6. BOOKS ON LISTERIA MONOCYTOGENES ................................................................... 181 Overview.................................................................................................................................... 181 Book Summaries: Online Booksellers......................................................................................... 181 Chapters on Listeria monocytogenes.......................................................................................... 181 CHAPTER 7. PERIODICALS AND NEWS ON LISTERIA MONOCYTOGENES ..................................... 185 Overview.................................................................................................................................... 185 News Services and Press Releases.............................................................................................. 185 Academic Periodicals covering Listeria monocytogenes ............................................................ 187 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 191 Overview.................................................................................................................................... 191 NIH Guidelines.......................................................................................................................... 191 NIH Databases........................................................................................................................... 193 Other Commercial Databases..................................................................................................... 195 APPENDIX B. PATIENT RESOURCES ............................................................................................... 197 Overview.................................................................................................................................... 197 Patient Guideline Sources.......................................................................................................... 197 Finding Associations.................................................................................................................. 199 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 201 Overview.................................................................................................................................... 201 Preparation................................................................................................................................. 201 Finding a Local Medical Library................................................................................................ 201 Medical Libraries in the U.S. and Canada ................................................................................. 201 ONLINE GLOSSARIES................................................................................................................ 207 Online Dictionary Directories ................................................................................................... 207
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LISTERIA MONOCYTOGENES DICTIONARY .................................................................... 209 INDEX .............................................................................................................................................. 275
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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 Listeria monocytogenes 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 Listeria monocytogenes, 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 Listeria monocytogenes, 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 Listeria monocytogenes. 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 Listeria monocytogenes, 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 Listeria monocytogenes. The Editors
1
From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON LISTERIA MONOCYTOGENES Overview In this chapter, we will show you how to locate peer-reviewed references and studies on Listeria monocytogenes.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and Listeria monocytogenes, 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 “Listeria monocytogenes” (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: •
Safe at the Table Source: Digestive Health and Nutrition. p. 28-31. May-June 2000. Contact: Available from American Gastroenterological Association. 7910 Woodmont Avenue, 7th Floor, Bethesda, MD 20814. (877) DHN-4YOU or (301) 654-2055, ext. 650. Email:
[email protected]. Summary: Foodborne illness, more commonly referred to as 'food poisoning,' is a frequent but underrecognized cause of gastrointestinal distress that can lead to complications and even death. This article reviews foodborne illness and offers strategies for preventing food contamination. Quick diagnosis is essential to help prevent the sometimes lethal effects of a foodborne illness; however, diagnosis can be
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Listeria monocytogenes
difficult since food poisoning is often confused with stomach flu. Headache, vomiting, diarrhea, abdominal cramps, and fever can accompany either illness. And with the onset of food poisoning, symptoms occur sometimes as late as 36 hours after ingestion, so it is natural to first blame an intestinal bug rather than food ingested the day before yesterday. Children and infants are particularly threatened by foodborne bacterial infections, especially Escherichia coli, which can lead to the development of a secondary disorder called hemolytic uremic syndrome (HUS). Contamination of food by infected food handlers is probably the most common cause of foodborne illness; other common causes include eating shellfish harvested from sewage polluted waters, or improperly prepared chicken and other types of poultry. The article reviews the more common foodborne contaminants: Salmonella and Campylobacter, Perfringens, E. coli, Staphylococcus, and Listeria monocytogenes. The article concludes with a brief list of additional resources, including government agencies and websites. 2 tables. •
Treatment of Gastrointestinal Infections Source: Gastroenterology. 118(2, Supplement 1): S48-S67. February 1999. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 19106-3399. (800) 654-2452 or (407) 345-4000. Summary: Of all the treatment options available to gastroenterologists, therapies for enteric infections are the most complex because of the large number of antimicrobials, and the most changeable because of emerging infections and evolving drug resistance. This review article covers all common gastrointestinal infections and most uncommon ones. For infections encountered only rarely in a typical clinical setting, the authors provide recommendations in a table. The authors also indicate any recommendations that are controversial or for which acceptable alternatives are available. Conditions covered are infective esophagitis, including candidal esophagitis, herpes simplex virus esophagitis, and cytomegalovirus (CMV) esophagitis; protozoal infections, including Giardia lamblia, Cyclospora cayetanensis, Isospora belli, Cryptosporidium parvum, Microsporidia, Entameba histolytica, Balantidium coli, Trypanosoma cruzi, and Leishmania donovani; intestinal nematodes, cestodes, and trematodes; viral gastroenteritis, including viral diarrhea, and CMV colitis; bacterial food poisoning, including enterotoxin induced disease and Listeria monocytogenes; bacterial diarrhea, including Vibrio cholerae, Escherichia coli, Shigella, Salmonella, Campylobacter, Clostridium difficile, Yersinia enterocolitica, Aeromonas hydrophilia, Plesiomonas shigelloides, Mycobacterium avium complex, and Whipple's disease; bacterial overgrowth syndromes; and traveler's diarrhea, including preventive measures and treatment. 4 tables. 211 references.
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Microbes on the Menu: Recognizing Foodborne Illness Source: Patient Care for the Nurse Practitioner. 3(6): 33-34, 37-40, 43-45, 49-50, 53-54, 5657. June 2000. Contact: Available from Medical Economics Company. Subscriber Services Department, Patient Care for the Nurse Practitioner, P.O. Box 3000, Denville, NJ 07834-9662. (800) 432-4570. Summary: The possibilities for food contamination seem endless and the symptoms of foodborne illness are often vague. This article helps nurse practitioners reliably identify foodborne disease. The primary pathogens implicated in foodborne illness in the United States today are Campylobacter jejuni, Escherichia coli, Listeria monocytogenes, Norwalk and Norwalk like viruses, Salmonella species, Toxoplasma gondii, and Vibrio
Studies
5
vulnificus. Toxins such as heavy metals also can contaminate food and cause illness. The clinical picture associated with infection can range from a brief, mild illness for which medical attention is not sought to a severe, life threatening emergency. The very young, the very old, and the immunocompromised are at special risk if they become infected. A food history should be taken whenever foodborne illness is suspected. This should extend back several days because of varying latency periods for the different infections. Stool cultures are imperative for patients at risk, those who become severely ill, and during large outbreaks. Treatment is supportive, with fluids and acetaminophen if fever is present. Antibiotics are useful in some, but not all, foodborne illnesses and are most commonly used in the severely ill or immunocompromised patient. Washing of meat and produce, cooking implements, and the hands is of utmost importance in preventing foodborne illness. Thorough cooking of meat, especially hamburger and chicken, can prevent many types of potentially severe infection. The article includes a sidebar listing related resources on the web. 3 tables. 21 references. •
Emerging Issues in Microbiological Food Safety Source: Annual Review of Nutrition. Volume 17: p. 255-275. 1997. Contact: Available from Annual Reviews Inc. 4139 El Camino Way, P.O. Box 10139, Palo Alto, CA 94303-9910. (800) 523-8635 or (415) 493-4400, ext 1. Fax (415) 424-0910. E-mail:
[email protected]. PRICE: $60.00. Summary: This article reviews some emerging issues in microbiological food safety. Many microorganisms previously unrecognized as foodborne or harmful are emerging as human pathogens transmitted by food. This discovery is a result of recent acquisition of key virulence factors, detection by newly developed isolation procedures, or the astute detective-like laboratory skills of microbiologists. Six microbial pathogens, including Shiga toxin-producing Escherichia coli, Listeria monocytogenes, Arcobacter butzleri, Helicobacter pylori, Cryptosporidium parvum, and Cyclospora, have become recognized as significant causes of human illness. Although the ecology and epidemiology of illness caused by some of these pathogens have not been fully elucidated, it is clear that food has the potential of being an important vehicle in their dissemination. Control of foodborne disease is important at all levels, including food production, preparation, and delivery to consumers. Existing technologies and new approaches such as irradiation and hazard analysis critical control point (HACCP) programs are useful tools in the control of foodborne hazards. However, because of ever-changing products, processes, food handling practices, societal habits, and pathogens, emerging foodborne diseases will continue to be an important public health concern. 92 references. (AA-M).
Federally Funded Research on Listeria monocytogenes The U.S. Government supports a variety of research studies relating to Listeria monocytogenes. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. 2
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Listeria monocytogenes
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 Listeria monocytogenes. 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 Listeria monocytogenes. The following is typical of the type of information found when searching the CRISP database for Listeria monocytogenes: •
Project Title: A SAFE VACCINE STRAIN OF LISTERIA MONOCYTOGENES FOR HIV Principal Investigator & Institution: Frankel, Fred R.; Microbiology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 01-SEP-1998; Project End 28-FEB-2007 Summary: (Provided by Applicant) New HIV infections worldwide are occurring at alarming rates, and an HIV vaccine appears to be the only long-term solution. Listeria monocytogenes is a vector with potential for use as an oral vaccine against this disease. Listeria is an intracellular microorganism that is a paradigm for the induction of cell mediated immunity and is effective as a vaccine vector for model cancers, influenza, LCMV, and vaccinia virus infections. For use of this live vector against HIV in humans, the organism must be both safe and effective. We have constructed a highly attenuated, D-alanine-requiring strain of Listeria that can induce strong immunity when provided just sufficient D-alanine to initiate an infection, and have characterized the systemic and mucosal CD8 T cell response it generates in mice to HIV gag. Complete protection against mucosal challenge by recombinant vaccinia-gag virus is seen following either oral or systemic immunization. In this application, we propose to further explore the response to oral immunization in the following ways: 1) Examine the cellular and cytokine basis for mucosal protection in transgenic huEcad mice, a new mouse model for Listeria infection that is more appropriate for human comparisons than mouse strains used previously; 2) Examine new strategies to develop an attenuated strain of Listeria that is independent of investigator-supplied D-alanine; and 3) Examine the use of attenuated Listeria to deliver DNA vaccines. 4) We will also explore the response of human CD4 and CD8 T cells to Listeria using normal and HIV-infected human blood samples, and the cytokines induced in these cells. During this grant period we will place particular emphasis on the nature and role of the CD4 response to the attenuated Listeria, since CD4 cells appear to play a protective function in HIV. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ACELLULAR VACCINES AGAINST FRANCISELLA TULARENSIS Principal Investigator & Institution: Conlan, Wayne; Senior Research Officer; National Research Council of Canada Ottawa Kiaor6, Canada Ottawa, On Timing: Fiscal Year 2002; Project Start 15-JUN-2001; Project End 30-APR-2006 Summary: (Provided by Applicant): The facultative intracellular bacterial pathogen, Francisella tularensis, can cause severe pneumonia and death following the inhalation of very small numbers of infectious particles. For this reason, F. tularensis is considered a primary biological warfare agent. Acquired host immunity against this pathogen is predominantly T-cell-mediated rather than humoral. An attenuated strain of F.
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7
tularensis is an effective live vaccine against virulent strains of the pathogen. However, this strain retains its virulence for mice, and might cause disease if administered to immunocompromised individuals. Thus, for mass-vaccination purposes, a defined fastacting acellular vaccine would be preferable to the current live vaccine. Our institute has developed a novel vaccine delivery technology based on liposomes manufactured from the total polar lipids of various Archaebacteria. These liposomes termed, archaeosomes, generate robust cell-mediated immune responses to model antigens entrapped within them, without the aid of any additional immune stimulants. Recently, we showed that a short peptide antigen of another intracellular pathogen, Listeria monocytogenes, packaged in archaeosomes, provides a high level of protective immunity against this pathogen in a murine listeriosis model after only a single vaccination. Because multiple studies indicate that the same host defenses are needed to combat F. tularensis and L. monocytogenes, it is likely that appropriate antigens of the former pathogen encapsulated in archaeosomes will provide effective acellular vaccines. This proposal will explore this possibility. It is expected that the findings from the proposed studies will be applicable to the development of acellular vaccines against other intracellular respiratory pathogens such as Mycobacterium tuberculosis, and Chlamydia pneumoniae. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ADAPTIVE MACROMOLECULES
IMMUNOTHERAPY--LONG
CIRCULATING
Principal Investigator & Institution: Paterson, Yvonne; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002 Summary: (Applicant's Description) In this proposal we wish to explore the potential of Listeria monocytogenes, as a cancer therapeutic for NER-2/neu expressing breast tumors. We have shown using other tumor associated antigens that a recombinant L. monocytogenes that secretes a tumor specific antigen can not only protect against tumor challenge but cal also induce a regression of macroscopic established tumors after transplantation into normal syngeneic mice. This impressive anti-tumor response is probably due to the unusual ability of this facultative intracellular bacterium to escape the phagolysosome and live and grow in the cytoplasm cells. Antigens secreted by L monocytogenes, therefore, are very effectively targeted to both the class II and class I restricted pathways for antigen presentation resulting in strong cell mediated immunity. Thus this bacterium may be the ideal vaccine vector for boosting the TH1, CD4+ and CD8+ T cell response to tumor specific antigens as a cancer therapeutic. In order to determine how to optimize the use of L monocytogenes as a cancer vaccine in humans we will use the HER-2/neu transgenic mouse model of breast cancer to design and test the ability of L monocytogenes as a delivery system of HER-2/neu to overcome tolerance to spontaneously arising tumors. In specific aim 1 we will construct strains of L monocytogenes that deliver Her-2/neu to the immune system as secreted polypeptide products and as a DNA vaccine. The goal of specific aim 2 is to test the ability of the LmHer-2/neu recombinants to induce the regression of established tumors in a transplantable HER-2/neu expressing tumor model developed by Dr Elizabeth Jaffee in Her-2/neu transgenic mice where HER-2/neu is a self antigen. Effective vaccines in this less stringent model will then be tested both their ability to impact on naturally arising tumors in the HER-2/neu transgenic mouse. Finally, in specific aim 2, we will compare the efficacy of the Listeria vector approach with a wider range of therapeutic approaches developed in the other laboratories of this program project. Immune parameters will
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Listeria monocytogenes
also be measured for these vaccine approaches in order to select combination strategies that will enhance or compliment different arms of the immune system. The best of the vaccine strategies will be compared side by side at each site, i.e., JHUSM in the laboratories of Drs. Pardoll, Wu and Jaffee and U. Penn by Dr. Paterson, in order to control for differences in animal colonies etc. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ATTENUATED LISTERIA VECTORS AS AN AIDS VACCINE IN MACAQUES Principal Investigator & Institution: Ruprecht, Ruth M.; Professor of Medicine; Cbr Institute for Biomedical Research 800 Huntington Ave Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: We seek to develop recombinant Lmdd, a vector generated from Listeria monocytogenes (Lm) by deleting two genes essential for the biosynthesis of the unnatural D-alanine (D-ala), as an oral AIDS vaccine. Without exogenous D-ala, the resulting vector, termed Lmdd, is unable to form cell walls or replicate. The first vaccine candidate, Lmdd-gag, was generated by stably inserting HIV gag into the Lmdd chromosome. In mice, Lmdd-gag, co-administered with D-ala, elicited long-lived CD8+ T-cell responses. In rhesus monkeys, wild-type Lm closely mimics infection and pathogenesis in humans (stillbirths, sepsis), who get infected mostly via contaminated food. Because of this natural oral route of Lm infection, Lmdd vectors hold promise as oral AIDS vaccines, in a pilot study, we administered Lmdd-gag orally to two monkeys with short D-ala courses; one monkey was boosted orally and developed cytotoxic Tlymphocyte (CTL) responses against HIV Gag, indicating that this candidate vaccine is immunogenic after oral administration. The other monkey developed strong antibody responses after i.m. boosting. The Specific Aims are to: 1. Test the hypothesis that oral vaccination will generate T helper type 1 (Thl) responses, whereas oral priming/i.m, boosting will result in Th2 responses. 2. Test safety, immunogenicity, and efficacy of Lmdd encoding SHIV89.6P gag, tat, env or nef. Groups of monkeys will be vaccinated with Lmdd encoding individual viral genes or with a combination all four vectors and challenged mucosally with pathogenic SHIV89.6P. 3. Test safety, immunogenicity, and efficacy of Lmdd encoding genes of SHIV-1157ip, which contains env of a HIV clade C isolated from a maternally infected African infant. SHIV-1157ip has been adapted to rhesus monkeys and replicates to high levels. Vaccinees will be challenged mucosally or intravenously with SHIV-1157ip. 4. Test long-term safety, immunogenicity, and efficacy of Lmdd vaccines against SHIV-1157ip in pregnant macaques and monitor long-term safety in Lmdd vaccine-exposed offspring. 5. Test safety, immunogenicity and efficacy of the best anti-SHIV1157ip Lmdd vaccine in newborn monkeys. These primate studies represent crucial steps towards developing recombinant Lmdd vectors for clinical trials as oral AIDS vaccine candidates that could be administered easily, even in the developing world. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DETECTION
BACTERIAL
PATHOGEN
AMPLIFICATION
&
REAL-TIME
Principal Investigator & Institution: U'ren, Jack R.; Director of Research; Saigene Corporation 7126 180Th Ave Ne, Ste C-104 Redmond, Wa 980524971 Timing: Fiscal Year 2003; Project Start 01-MAY-2003; Project End 30-NOV-2003
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Summary: (provided by applicant): As we all know, bio-terrorism in America is a reality. However in addition to the Category A agents like anthrax, Yersinia pestis and smallpox, which are difficult to safely grow and disseminate, exist the Category B agents that could be used to infect our food or water supply. These organisms include bacterial pathogens, protozoa, and viruses. In addition to these natural pathogenic organisms they could also be genetically engineered to increase their virulence or to resist standard antibiotic treatments. Therefore new methods for rapid sensitive food and waterborne pathogen detection are greatly needed, especially if they can also be used to identify drug sensitivity within these organisms. Bio-terrorism using a food pathogen is not just a hypothetical threat to America. A religious cult in Dalles Oregon sickened at least 751 people by contaminating food in grocery stores and restaurants in the fall of 1984. The group simply grew cultures of the food pathogen Salmonella typhimurium that they obtained from their local scientific supply house and sprinkled the cultures on produce in the grocery stores and the restaurant salad bars. If the group had used a more deadly pathogen like Salmonella typhi that causes typhoid fever many people would certainly have died. The overall goal of this program is to develop an integrated isothermal DNA amplification and a probe array detection slide capable of rapidly identifying a variety of food and waterborne pathogens. All of the NIAID Biodefense Category B food and waterborne bacterial pathogens E. coli, Vibrio cholera, Shigella dysentery, Salmonella species, Listeria monocytogenes, Camphylobacter jejuni, and Yersinia enterocolitica will be detected in this program. A single integrated slide capable of isothermal amplifying and detecting all of these organisms in real-time in a closed sealed device is proposed. The program can also distinguish live organisms from dead organisms killed by the food or water sanitation process. Also, the test can be used to identify the antibiotic sensitivity of the pathogen to identify genetically altered organisms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CANCER IMMUNOTHERAPY FOR HEAD AND NECK TUMORS Principal Investigator & Institution: Sewell, Duane A.; Otorhinolaryngology Head & Neck Surgery; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 05-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): It is my long-term career goal to become a clinicianscientist in the field of head and neck cancer. Despite medical advances in other areas, treatment modalities for head and neck cancer have not changed over the past 30 years. Surgery, radiation, and chemotherapy are still the mainstays of treatment, and five-year survival rates for many tumors remain poor. New therapies are needed. Recent studies indicate that most oropharyngeal squamous cell carcinomas have undergone transformation by human papilloma virus (HPV). Two early transforming HPV proteins, E6 and E7, are expressed in these tumors and they provide attractive targets for cancer immunotherapy. Listeria monocytogenes-based vaccines have been developed that cause regression of HPV-associated tumors in animal models. In this proposal, we hope to develop new strategies that will make this type of therapy more effective and clinically applicable. In Specific Aim #1, we will test a unique strategy that targets both transforming proteins expressed in HPV-associated tumors. Heretofore, experiments and clinical trials have only targeted either E6 or E7. Several different live recombinant vaccines, including Listeria and Vaccinia constructs, will be used in order to determine which combination is the most efficacious. In Specific Aim #2, a novel Listeria construct will be engineered. This construct will include the Listeria protein ActA fused to the transforming proteins. The rationale behind creating this vaccine is the fact that ActA contains several PEST (P, proline; E, glutamic acid; S, serine; T,
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threonine) regions within its amino acid sequence. PEST regions have recently been shown to be critical for the efficacy of the Listeria constructs. In Specific Aim #3, we will develop transgenic mice that will express E6 and E7 under the control of the thyroglobulin promoter. These mice will spontaneously produce HPV-transformed thyroid tumors. Using this model, the vaccines targeting HPV-associated tumors will be tested in mice with head and neck tumors that may be tolerant to the transforming proteins. This model mimics the situation that is seen in human head and neck cancer patients. In order to achieve my goal of treating these patients with immunotherapy, I am applying for a period of mentored research in Dr. Yvonne Paterson's laboratory. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CD8+T MONOCYTOGENES
CELL
EFFECTOR
MECHANSISMS
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Principal Investigator & Institution: Harty, John T.; Carver College of Medicine Endowed Profe; Microbiology; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2003; Project Start 01-APR-1998; Project End 31-JAN-2008 Summary: (provided by applicant): CD8+ T cells are important mediators of adaptive immunity to Listeria monocytogenes (LM) in wild-type (WT) BALB/c (H-2d MHC) and B6 (H-2b MHC) mice. In the last grant period, we determined that that perforin, IFNgamma and TNF are not required CD8+ T cell effector molecules for resistance to LM infection. However, we also learned that perforin and IFN-gamma play key roles in regulating the normal expansion (perforin) and contraction (IFN-gamma) phases of antigen (Ag)-specific CD8+ T cell homeostasis after primary LM infection. Importantly, the absence of one or both molecules resulted in elevated levels of memory CD8+ T cells after vaccination, which may account for the observed protection. Thus, Aim 1 will determine if perforin and IFN-gamma are essential for optimal CD8+ T cell immunity to LM infection. We also demonstrated that vaccination of H-2b MHC TNF-deficient mice evoked high-level CD8+ T cell mediated antilisterial immunity. In H-2b mice, both MHC class Ia (classical) and MHC class Ib (non-classical) restricted CD8+ T cells participate in antilisterial immunity. Like IFN-gamma, TNF is a pleiotropic cytokine with the capacity to participate in the normal regulation of CD8+ T cell homeostasis. Consistent with this notion, we have evidence for altered homeostasis of MHC class Ia and class Ib restricted CD8+ T cells in TNF-deficient mice. Aim 2 will determine how TNF regulates CD8+ T cell homeostasis and whether common mechanisms are used in regulation of MHC class Ia and MHC class Ib restricted CD8+ T cells. Recently, we showed that contraction of both primary and secondary CD8+ T cell responses was programmed, and independent of the rate of pathogen clearance or Ag-display. Importantly, these experiments showed that contraction of the secondary CD8+ T cell responses was markedly prolonged compared to contraction of the primary response, even in the same host animal. Since prolonged contraction of secondary responses may impact the function of memory cells in protective immunity, Aim 3 will address the mechanistic basis for this observation. Our long-term goal is to understand how memory CD8+ T cells are generated and provide immunity to intracellular pathogens. We will continue our analysis of the relationship between CD8+ T cell effector molecules, protective immunity and regulation of Ag-specific CD8+ T cell homeostasis through the following specific aims. Aim-1. Determine the influence of perforin and/or IFN-gamma-deficiency on the protective capacity, repertoire and functional avidity of LM-specific memory CD8+ T cells. Aim-2. Define the impact of TNF-deficiency on the homeostasis of Ag-specific CD8+ T cell responses to LM infection. Aim-3. Investigate the
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mechanisms responsible for prolonged contraction of CD8+ T cells during the secondary response to infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CLASS IB GENES IN RESPONSE TO INFECTIONS Principal Investigator & Institution: Forman, James M.; Professor; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2002 Summary: Class IA molecules play a major role in the presentation of peptide epitopes from intracellular parasites to CD8 T cells. Class IB molecules are not as polymorphic as class IA and their function is less well understood. We plan to utilize H-2b mice that have their class IA (KbDb) genes deleted. Unlike previously described class I deficient animals (beta-2M-/- and Tap-1-/-) these mice have a complete absence of class IA molecules but retain class IB expression. They will be tested for their ability to respond to 3 intracellular pathogens, Listeria monocytogenes (LM), vaccinia virus, and vesicular stomatitis virus. CD8 cells are known to play a role in resistance to these pathogens and in the case of LM, it is known that CTL can be generated in vitro against this pathogen presented by 2 class IB molecules, M3 and Qa-1b. The role that class IB molecules play in these infections in providing immunity will be analyzed by assessing the role of various T cell subsets as well as NK cells in vivo. We will also analyze these responses in vitro and identify the epitopes presented by class IB molecules to antigen specific CD8 cells. Finally, since Kb-/-Db-/- mice cannot generate their CD8 repertoire on class IA molecules, we will determine whether these animals have a repertoire directed against both self H-2b class IA molecules as well as other class IA alloantigens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: COMPARTMENTALIZATION OF BACTERIAL ANTIGENS Principal Investigator & Institution: Shen, Hao; Associate Professor; Microbiology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 15-FEB-1999; Project End 31-JAN-2004 Summary: (Adapted from the Applicant's Abstract):The long term, goal of this study is to understand how various aspects of bacteria antigens influence the nature and magnitude of host defense, and how the resulting immune response modifies the course of infection. The Gram- positive bacterium, Listeria monocytogenes (LM), offers an excellent model to address these questions since both the pathogen and the murine host are amenable to experimental manipulation. The investigators have developed a genetic system for constructing recombinant LM (rLM) expressing foreign antigens, molecular tools for manipulating bacterial antigens and the pathogenic process, and a murine model for characterizing immune responses induced by the rLM strains. By manipulating antigen secretion, they have shown that both secreted and non-secreted bacterial proteins efficiently prime CD8 T cells. However, only secreted bacterial proteins serve as protective antigens for CTL- mediated immunity. Thus, antigen compartmentalization results in a striking dichotomy between CTL priming and protective immunity. The objective of this proposal is to understand the mechanism(s) that is responsible for this dichotomy. Specifically, they will: 1) examine the kinetics of activating naive and memory CD8 T cells by secreted vs. non-secreted bacterial antigens. These studies will directly test a long standing hypothesis that secreted proteins are recognized by the immune system before non-secreted ones, and thus are more relevant vaccine targets. 2) test a Quantitative Difference model which stipulates that CTL
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Listeria monocytogenes
responses to non-secreted bacterial antigens are too weak and/or too late to prevent the progression of LM infection. 3) test a Cell Tropism model which stipulates that nonsecreted antigens are presented only by a subset of infected cells. As a result, CTL specific to the non-secreted antigen are unable to recognize all infected cells and thus, cannot control infection. The results of these studies should unveil the mechanism(s) responsible for the dichotomy between CTL priming and protective immunity as a result of antigen compartmentalization. Elucidation of the underlying mechanisms will have important implications in our understanding of immune surveillance of intracellular bacteria, for designing effective vaccines that will induce a potent response, and for selecting candidate antigens that can serve as protective targets. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CONTAINING BIOTERROIST AND EMERGING INFECTIOUS DISEASES Principal Investigator & Institution: Longini, Ira M.; Biostatistics; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2004; Project Start 01-MAY-2004; Project End 30-APR-2009 Summary: (provided by applicant): The overall objective of this research is to develop, validate, and implement mathematical models for the transmission and within-host dynamics of bioterrorism agents or naturally occurring infectious diseases. These models will be used to assess the effectiveness and efficacy of various interventions to aid the distribution and allocation of resources in response to such outbreaks. Specific aim 1 is to develop epidemic simulation models for the transmission of infectious diseases in question: a. to develop stochastic epidemic simulation models for a typical American community; b. to use the epidemic simulation models to evaluate the effectiveness of interventions involving surveillance and containment, vaccination, antimicrobials, closing of key institutions, and other control strategies; c. to develop stochastic optimization methods to find the best intervention strategy, constrained by the resources available; d. to adapt the epidemic simulation models for smallpox, pandemic influenza, SARS, and other possible bioterrorism agents or naturally occurring infectious diseases; e. to use the epidemic simulation models to determine the important parameters for infection transmission and to use this information to design field studies and intervention studies; f. to use and develop statistical methods to estimate the important parameters and variables from data. Specific aim 2 is to develop models of the within-host dynamics of pathogens which cause acute infections in vertebrates: a. to construct exploratory models for the interplay between the pathogen and host immune response; b. to refine, to develop further and to test these models of pathogenesis including the use of existing data on lymphocytic choriomeningitis virus (LCMV) and listeria monocytogenes (LM) infections of mice; c. to use the experience from the specific aim 2.b. to extend the models in the specific aim 2.a. to examine the more challenging acute infections of humans including bioterrorism agents or naturally occurring infectious diseases; d. to model development of resistance under selective pressure by antimicrobial and antiviral treatment and prophylaxis by antimicrobials or vaccination; e. to combine the stochastic epidemic simulation models with models for within-host generation of resistance to examine spread of resistance within the host population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CONTROL OF SIGMA B ACTIVITY IN B SUBTILIS Principal Investigator & Institution: Haldenwang, William G.; Professor; Microbiology and Immunology; University of Texas Hlth Sci Ctr San Ant 7703 Floyd Curl Dr San Antonio, Tx 78229 Timing: Fiscal Year 2002; Project Start 30-SEP-1992; Project End 30-APR-2006 Summary: (provided by applicant): In response to environmental stress, sigma B, a transcriptional regulator of B. subtilis, is released from an inhibitory association with an anti-sigma B protein (RsbW) to activate expression of the bacterium's general stress regulon. The stress-generated signal that activates sigma B is unknown; however, recent evidence implicates the bacterium's ribosome and a small GTP binding protein (Obg) in this process. The proposal seeks to determine the roles of the ribosome and Obg in the stress induced activation of sigma B. Both Obg and the non-essential ribosome protein L11 are needed for environmental stress to activate sigma B. We will perform directed and random alterations of the coding sequences for each of these proteins to identify regions or activities that modify the inducibility of sigma B and determine how these changes influence each of these proteins' other known functions. The analyses should identify regions of Obg and L11 that are important for their biochemical activities and suggest which of these properties are required for sigma B induction. Several components of the stress activation cascade (RsbR, S and T) have been observed to cofractionate with ribosomes. This putative association will be examined, using velocity centrifugation and gel filtration analyses under conditions that are likely to cause partial or total dissociations. The specific ribosome fraction components and Rsb proteins that are involved in the associations will be identified. The types of complexes found and the identities of proteins directly involved could give clues as to the role of the association in stress signaling and sigma B induction. Finally, a detailed mutational analysis will be undertaken of rsbT, the most upstream positive regulator in the sigma B stress induction pathway and the gene whose product is the most likely to be directly influenced by stress signaling. It is anticipated that the changes in rsbT and their resulting phenotypes will provide a test of RsbT's proposed activities as well as identify sites where stress directed signals alter RsbT activity. This work will not only explore the fundamental biological question of how cells recognize and react to hostile environments, but, given the presence of sigma B and its principal regulators in the human pathogens Staphylococcus aureus, Listeria monocytogenes and Mycobacterium tuberculosis, it may have practical applications, identifying weaknesses in these pathogens' stress adaptation responses to host defenses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CRYSTAL STRUCTURES OF BACTERIAL PATHOGEN PROTEINS Principal Investigator & Institution: Ghosh, Partho; Chemistry and Biochemistry; University of California San Diego La Jolla, Ca 920930934 Timing: Fiscal Year 2002; Project Start 01-MAY-2000; Project End 30-APR-2005 Summary: (Verbatim from the applicant's abstract) The broad, long-term objectives of this proposal are to understand the structural steps required for bacterial pathogens to invade mammalian host cells. Host cell invasion is a critical step in the life cycle of intracellular pathogens and parasites, which are major causes of human morbidity and mortality. The mechanism of cell invasion is being investigated in the pathogen Listeria monocytogenes, a cause of recent outbreaks of human illness and death. A protein attached to the cell wall of L. monocytogenes, internalin B (67 kD), is solely responsible for triggering the uptake of the bacterium into several nonphagocytic mammalian cell
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Listeria monocytogenes
types. Included among these are hepatocytes, which are the major locus of bacterial proliferation in vivo. Internalin B acts by binding to a mammalian receptor, gClq receptor (gClq-R), and activating host phosphoinositide (PI) 3-kinase, leading to induction of phagocytosis. A 25 kD mammalian cell effector domain of internalin B is necessary and sufficient to activate PI-3 kinase, whereas the intact molecule is required for bacterial uptake. How internalin B activates host signaling pathways and causes uptake is not understood structurally. The specific aims of the proposal are to: (1) Determine the structure of the 25 kD effector domain of internalin B. Crystals of the 25 kD effector domain that diffract x-rays to 1.5 A resolution have been grown and heavyatom phasing has been achieved, allowing an interpretable electron density map to be calculated. (2) Determine the structure of intact internalin B. Crystals of intact internalin B that diffract x-rays to 3.15 A resolution have been grown and phasing information is being sought. (3) Co-crystallize and determine the structure of internalin B bound to gCIq-R. For these studies, a number of internalin B constructs are available in milligram quantities, as is gCIq-R in a form that crystallizes. The proposed structures are important to revealing the stereochemical basis by which internalin B induces phagocytosis and causes host cell invasion. This knowledge will be generally applicable to devising strategies to combat L. monocytogenes and other intracellular pathogens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CYTOTOXIC RESPONSE TO HISTOCOMPATIBILITY ANTIGENS Principal Investigator & Institution: Bevan, Michael J.; Professor; Immunology; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2003; Project Start 01-JUN-1990; Project End 31-DEC-2007 Summary: provided by applicant): Our goal is to investigate the CD4 and CD8 T cell response to pathogenic infectious agents to uncover basic principles of T cell biology in controlling these infections. Two contrasting models of intracellular bacterial pathogens are chosen to ask fundamental questions about how the immune system perceives, responds, contains and eliminates these pathogens. One model to be studied is virulent Mycobacterium tuberculosis delivered via aerosol to the lungs of mice. This organism can survive inside vacuoles within macrophages and set up a chronic infection which can be contained, but not eliminated, by adaptive CD4+T cell immunity. The role of CD8+ T cells in controlling tuberculosis is controversial. Recombinant organisms producing a model antigen containing well-studied epitopes for CD4 and CD8 T cells will allow a study of the tempo of the T cell response, and provide new information on protection against what has been called the world's most successful pathogen. M. tuberculosis may infect one third of the world's population. The second intracellular pathogen we plan to use is a common food-borne pathogen, Listeria monocytogenes. Excellent mouse models exist already for the study of this Gram positive pathogen, where it appears that adaptive CD8+ T cell immunity is the critical force in eliminating the infection. L. monocytogenes is a candidate vaccine vector for the induction of CD8 immunity, for example, against tumor antigens. The massive response of CD8+ T cells to acute infection with Listeria and the generation of long-lived protective immunity may also require CD4+ T cell help. The proposed studies are aimed at a greater understanding of the development of long-lived, protective immunity induced by this pathogen. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DISCOVERY OF NOVEL TLR LIGANDS WITH ADJUVANT PROPERTIES Principal Investigator & Institution: Powell, Thomas J.; Senior Director; Vaxinnate Corporation 300 George St, Ste 311 New Haven, Ct 06511 Timing: Fiscal Year 2004; Project Start 20-MAY-2004; Project End 30-APR-2006 Summary: (provided by applicant): The interactions of Toll-like receptors (TLR) with their cognate ligands, Pathogen-Associated Molecular Patterns (PAMPs), trigger the immediate response of the innate immune system and set off a cascade of events that influence the adaptive immune response. PAMP:antigen fusion protein vaccines target the antigen to the appropriate accessory cell population and trigger both antigenspecific and critical costimulatory signals in the same cell. At the present time, only a handful of polypeptide PAMPs has been identified. We propose to discover and develop novel polypeptide TLR ligands that are highly specific for individual TLRs and incorporate these ligands into vaccines for use against infectious diseases that pose a public health and national defense threat. The phage display technology will be used to screen a large number (>10[9]) of random or biased peptides for binding to cells overexpressing the TLR of interest. Biased peptide libraries will be based on sequences of known polypeptide TLR ligands, such as bacterial flagellin (TLR5 ligand) or measles virus HA protein (TLR2 ligand). Phages displaying TLR-binding peptides will be enriched by 3 to 6 rounds of panning on mammalian cells expressing the TLR of interest. Relevant biological activity of the enriched phage will be confirmed in NF-kappaBdependent luciferase reporter assays in a panel of mammalian cell lines expressing different TLRs. Novel TLR-binding peptides will be expressed as histidine-tagged fusion proteins with model antigens (e.g., LLO and p60 from Listeria monocytogenes) and purified by state of the art biochemical techniques. Purified recombinant proteins will be formulated in phosphate-buffered saline for administration to mice without conventional adjuvants. Immunized mice will be challenged with the appropriate infectious agent (such as L. monocytogenes). Analysis of cytotoxic T-lymphocyte responses, antibody responses, and cytokine profiles induced by triggering different TLRs will help elucidate the mechanisms of action of different TLR ligands. The goal of the program is to identify, characterize, and express polypeptide ligands for known TLR, and use the ligands as tools to develop a better understanding of the immunological sequelae associated with triggering each TLR. Such studies could lead to the generation of very efficacious and cost-effective vaccines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ENGINEERED LISTERIA MONOCYTOGENES AS AN AIDS VACCINE Principal Investigator & Institution: Lieberman, Judy; Associate Professor; Cbr Institute for Biomedical Research 800 Huntington Ave Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JAN-2008 Summary: (provided by applicant): Listeria monocytogenes (Lm) is an attractive bacterial vector to elicit T cell immunity to HIV because it specifically infects key antigen presenting cells (APCs) and because natural infection originates at the mucosa. Immunization with recombinant Lm protects mice from LCMV, influenza and tumor inoculation. Lm expressing HIV gag elicits sustained high levels of gag-specific CTL in mice. Since Lm can cause serious disease in immuno-compromised hosts, a more highly attenuated strain that requires D-Ala for viability and is attenuated at least 105 fold in mice was produced. The hyper-attenuated bacteria expressing HIV-1 gag (Lmdd-gag)
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Listeria monocytogenes
are efficient as wild-type recombinants at stimulating gag-specific murine CTL in vivo when administered with D-Ala. Oral or systemic immunization with Lmdd-gag protects mice in a vaccinia challenge model and induces mucosal CTL in mouse gut-associated lymphoid tissues, even after systemic immunization. Immunization of newborn mice protects against heterologous mucosal or systemic challenge as adults. Preliminary studies in 2 macaques suggest that Lmdd-gag is safe and stimulates HIV-specific immune responses, even when administered orally. Attenuated nef and gag constructs boost human CTL responses in vitro. Because Lmdd is an attractive candidate vaccine vector to induce T cell immunity to HIV in humans, this program will perform preclinical studies in rhesus macaques to establish the proof of principle that Lmddvectored vaccines encoding SHIV antigens are immunogenic and provide protection from SHIV challenge in rhesus macaques. The focus of the program will be on developing Lmdd vectors as oral vaccines to optimize mucosal immunity at the predominant sites of HIV transmission. Lmdd vectors will be constructed expressing SHIV genes for macaque challenge experiments and expressing consensus HIV clad B, B' and C genes suitable for later-human studies. Mouse experiments will lay the groundwork for optimizing the immunization route, dose and boosting schedule. Recombinant Lmdd stably expressing SHIV89.6P and clade C R5-using SHIV11578ip gag, nef, env and tat genes will be tested for safety, immunogenicity and protection from challenge in adult rhesus macaques. A pregnant mother/neonatal transfer model in macaques will also be used to test for safety and immunogenicity in an animal model that utilizes the animals most vulnerable to Listeria toxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENZYMOLOGY OF ANTIBIOTIC RESISTANCE Principal Investigator & Institution: Armstrong, Richard N.; Professor; Biochemistry; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2003; Project Start 01-FEB-1998; Project End 31-DEC-2007 Summary: (provided by applicant): In the last two decades it has become increasingly clear that the efficacy of antibiotics for the treatment of infectious diseases is in jeopardy due to the common appearance of drug resistant strains of microorganisms. Understanding the mechanisms of antimicrobial resistance is crucial for effective patient care in the clinic and essential for developing strategies to enhance biodefense against intentionally disseminated of pathogens. Fosfomycin is a potent, broad-spectrum antibiotic effective against both Gram-positive and Gram-negative microorganisms. A decade after its introduction plasmid-mediated resistance to fosfomycin was observed in the clinic. Investigations supported by this project have established that the resistance is due to a metalloenzyme (FosA) that catalyzes the addition of glutathione to the antibiotic, rendering it inactive. Similar resistance elements have now been shown to exist in the genomes of several pathogenic microorganisms including, Pseudomonas aeruginosa, Staphylococcus aureus, Bacillus anthrasis, Brucella melitensis, Listeria monocytogenes and Clostridium botulinum. Genomic and biochemical analysis from this project suggest that there are three distinct subgroups of metalloenzymes, termed FosA, FosB and FosX, that confer resistance through somewhat different chemical mechanisms. The objectives of this research project are to identify plasmid and genomically encoded proteins involved in microbial resistance to fosfomycin and to elucidate the underlying structural and mechanistic enzymology of resistance. These objectives will be accomplished by integrating enzymological, biophysical and genomic analyses of the resistance problem. The three-dimensional structures of the FosA from Pseudomonas aeruginosa and its relatives FosB and FosX will be determined by X-ray
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crystallography. The chemical mechanisms of catalysis will be elucidated by: (i) examination of the inner coordination sphere of Mn 2+ in FosA and FosX by EPR and ENDOR spectroscopy; (ii) a steady state kinetic analysis of the thiol selectivity of FosA and FosB, and (iii) a mechanistic study of the unique hydration reaction catalyzed by FosX. Potential transition state inhibitors will investigated by structural, spectroscopic and kinetic techniques. The thermodynamics of the interaction of substrates and inhibitors with the enzymes will be examined by isothermal titration calorimetry Particular emphasis will be placed on the enzymes from the pathogens Pseudomonas aeruginosa, Staphylococcus aureus, Listeria monocytogenes and Clostridium botulinum. The intent of this investigation is to establish the mechanistic and structural bases for the design of drugs to counter both plasmid borne and genomically encoded resistance to fosfomycin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ESCAPE OF BACILLUS ANTHRACIS FROM THE PHAGOSOME Principal Investigator & Institution: Goldfine, Howard; Professor; Microbiology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): In the pulmonary form of anthrax caused by the pathogen Bacillus anthracis (Ba), spores in the lung are ingested by macrophages. Once phagocytosed, the spores are transported to regional lymph nodes and germinate inside macrophages. In order for the disease to progress, Ba must resist killing by the macrophage and further disseminate into the blood for vegetative growth. The exact means by which Ba survives and escapes the macrophage are unknown. Recent work has shown that newly vegetative bacilli escape from the phagocytic vesicles of macrophages and replicate in the cytosol, a process that was first described and best studied in another human pathogen Listeria monocytogenes (Lm). Lm escapes from the primary phagocytic vacuole of a macrophage using listeriolysin O (LLO) and a phosphatidylinositol-specific phospholipase C (PI-PLC). Genes orthologous to LLO and PI-PLC have recently been discovered in Ba by the genome sequencing project. In order to investigate the functions of the Ba orthologs of LLO and PI-PLC, Lm will be used as a heterologous host to express these proteins and to analyze their role in mediating bacterial escape from phagocytic vesicles and release from the host cell. For safety reasons a strain of Lm that has been developed as a potential vaccine vector and is unable to grow in cells without a D-alanine supplement will be used. The first aim is to determine if the LLO ortholog permits escape of Lm from the macrophage phagosome. Its potential for signaling through a recently discovered protein kinase C signaling pathway, thought to be needed for escape from the phagosome, will also be explored. Since the Ba PI-PLC ortholog is 94% identical in amino acid sequence to the PI-PLC from Bacillus cereus, it almost certainly has that enzymatic activity, but there are potential structural differences between the Bacillus enzymes and the Lm enzyme that would affect their activity both outside and inside the host. The effects of these structural differences will be examined in the second aim, in which the role of Ba PI-PLC in escape from the phagosome and host cell signaling is explored. Lastly, studies on inhibitors of PI-PLC will test their efficacy in blocking the biological role of this enzyme and may lead to eventual high throughput screening for drugs to combat anthrax infections. The results of this study will provide evidence on the potential role of the LLO and PI-PLC orthologs of Ba in mediating its survival, growth and escape from the macrophage, essential elements in its ability to cause a devastating disease with high mortality in humans.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ETHANOL-FED, CPG-TREATED MICE: LISTERIA SUSCEPTIBILITY Principal Investigator & Institution: Ray, Nancy B.; Biochemistry; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2006 Summary: (provided by applicant): Chronic ethanol consumption causes immunosuppression, particularly related to Th1 cytokine expression, and causes increased susceptibility to infection including infection with the intracellular bacterial human pathogen, Listeria monocytogenes. CpG DNA induces innate Thl-like responses and reduced susceptibility to Listeria monocytogenes detected by decreased replication of L. monocytogenes in murine spleens and livers. CpG immunostimulatory DNA will be used to stimulate innate systemic and mucosal immune responses in ethanol- fed and water-fed control mice. Induction of cytokine expression in vitro and in vivo in spleen and Peyer's patch cells from CpG-treated, ethanol-fed and water-fed control mice will be detected by enzyme-linked immunosorbant assay (ELISA), and specific Thl cytokine expressing cells will be identified by magnetic cell sorting (MACS) and intracellular cytokine staining. CpG DNA treatment and immunostimulation will be used to overcome ethanol-induced immunosuppression, which will be detected by reduced replication of L. monocytogenes in spleens and livers by a colony forming (CFU) assay. Various routes and doses of CpG treatment and challenge with L. monocytogenes including intraperitoneal (IP), intravenous (IV), and oral will be used to elicit both systemic and mucosal immunity and to determine the limits of protection induced by CpG DNA. Reduced replication of L. monocytogenes will be correlated with cytokine expression detected by ELISA and the mechanism of CpG-induced reduction in replication will be determined by identifying by flow cytometry and intracellular cytokine staining whether specific cells may be suppressed or depleted by chronic ethanol consumption and stimulated by CpG treatment. Because defects in killing Mycobacterium avium, an intracellular bacteria similar to L. monocytogenes and to the organism that causes tuberculosis, have been demonstrated for macrophages following exposure to alcohol, intracellular killing of L. monocytogenes by peritoneal macrophages will be examined to determine whether ethanol-fed mice are deficient in killing L. monocytogenes and whether CpG DNA stimulation may enhance killing. These studies could lead to treatments for protecting alcoholic patients from intracellular bacterial infections such as those caused by L. monocytogenes or Mycobacterium tuberculosis (TB). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FUNCTION & REGULATION OF THE HUMAN ARP2/3 COMPLEX Principal Investigator & Institution: Welch, Matthew D.; Assistant Professor; Molecular and Cell Biology; University of California Berkeley Berkeley, Ca 947205940 Timing: Fiscal Year 2002; Project Start 01-SEP-1999; Project End 31-AUG-2004 Summary: Cell locomotion is essential for embryonic development, wound healing, and immune system function. Moreover, it is critical factor in the pathogenesis of cancer and of cardiovascular disease. One subprocess of overall cell locomotion, the protrusion of the leading lamellipodia of locomoting cells, is thought to be driven by actin polymerization. The long term goal of this project is to elucidate the molecular mechanisms that control actin polymerization in cells and to determine how polymerization contributes to the forces that drive this aspect of cell locomotion. We
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have explored this issue by examining the actin-polymerization driven motility of the pathogenic bacterium Listeria monocytogenes, which represent a model for understanding the protrusion of the plasma membrane at the leading edge of motile cells. We purified a protein complex from platelets, the Arp2/3 complex. That nucleates actin assembly at the surface of L. monocytogenes and mediates bacterial motility. The Arp2/3 complex is localized to lamellipodia in locomoting fibroblast cells, suggesting that it also plays a role in nucleating actin polymerization during lamellipodial protrusion. Therefore the complex is likely to represent a central component of the cellular actin polymerization machinery. Moreover, it may also be a key target of signaling pathways that regulate cell motility in response to extracellular cues. The complex has seen polypeptide subunits that are conserved in sequence among diverse eukaryotes, suggesting that its structure and function have been conserved through eukaryotic evolution. However, we do not yet understand how the other proteins in L. monocytogenes motility and lamellipodial protrusion. We will take a biochemical approach to understand the mechanism of Arp2/3 complex nucleates actin assembly, what factors regulate its activity in cells, and how it functions with other proteins in L. monocytogenes motility and lamellipodial protrusion. We will take a biochemical approach to understand the mechanism of Arp2/3 complex function and its interaction with other cytoskeletal and regulatory proteins in the context of L. monocytogenes propulsion and cell locomotion. The aims are to: (1) Examine the requires for the formation of the Arp2/3 complex, (2) Determine the function of ARP2/3 complex subunits in actin nucleation, (3) Dissect the mechanism by which Arp2/3 complex nucleating activating is stimulated by the L. monocytogenes ActA protein, (4) Identify cellular factors that enhance L. monocytogenes motility and (5) identify cellular factors that activate Arp2/3 complex nucleating activity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FUNCTION AND MECHANISMS OF THE N-END RULE PATHWAY Principal Investigator & Institution: Kwon, Yong T.; Assistant Professor; Center for Pharmacogenetics; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): The ubiquitin-dependent N-end rule pathway relates the in vivo half-life of a protein to the identity of its N-terminal residue. As an effort to understand the physiological functions and the underlying molecular mechanisms of the N-end rule pathway, we began the biochemical and genetic dissection of this pathway in mice. We have shown the functions of N-terminal asparagine-specific deamidation in socially conditioned behavior, of N-terminal arginylation in cardiovascular development, and of N-terminal cysteine oxidation as an oxygen sensor. Mammalian UBR1/E3calpha is the first identified ubiquitin ligase (E3) of the ubiquitin system, and has been known as the only E3 that recognizes type 1 and type 2 N-terminal destabilizing residues of proteins. For the last two decades, the in vitro biochemical studies have suggested numerous biological functions of UBR1, including neuronal cell differentiation, amphibian limb regeneration, apoptosis, muscle wasting, and the degradation of various proteins (Sindbis virus RNA polymerase, HIV integrase, the Listeria monocytogenes p60, RGS4 and RGS16, and the encephalomyocarditis virus 3C protease). Surprisingly, however, mice lacking UBR1 were apparently normal except for the subtle defects in muscle protein degradation and fat metabolism. We hypothesize that the substrate recognition in the mammalian N-end rule pathway is mediated by the cooperative activity of a set of distinct E3s. Indeed we identified novel UBRl-like E3s
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Listeria monocytogenes
termed UBR2 and UBR3, and further hypothesize that UBR2 and/or UBR3 are the E3(s) that may cooperatively function with UBRI. As a preliminary effort to address these issues, we have constructed UBR2 -/-, UBR3 -/-, and UBR1-/-UBR2 -/- and UBR1-/UBR3 -/- mice, and found that UBR2-1oss caused male-specific infertility and femalespecific lethality. Thus, we hypothesize that UBR2 is essential for spermatogenesis. This proposal focuses on the following aims: (1) To characterize the biochemical properties of UBR2 and UBR3 as candidate E3s that may function cooperatively with UBR1 in the Nend rule pathway, (2) To characterize UBR2 -/- mice to assess the in vivo function of UBR2 in spermatogenesis, (3) To identify the UBR2-interacting proteins or UBR2dependent molecular circuits underlying the UBR2- dependent spermatogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENE EXPRESSION LEVELS ACROSS DIVERSE GENOMES Principal Investigator & Institution: Karlin, Samuel; Robt. Grimmett Prof. of Mathematics; Mathematics; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2003; Project Start 01-JAN-1979; Project End 30-APR-2007 Summary: (provided by applicant): Prokaryotic and eukaryotic whole genome sequence data is accumulating at an unprecedented pace. The next phase will be increasingly dominated by efforts to characterize, categorize, and analyze these data with the goal of understanding molecular sequence information and its significance in biological systems. Much current biological and medical research centers on DNA microarrays. The main focus of our research is to evaluate gene expression levels based on codon usage. Our sequence methods are complementary to the experimental procedures of 2Dgel electrophoresis in assessing gene expression levels. We have introduced a theoretical computational method for characterizing gene expression levels based on codon usage differences between gene classes. The method has been applied to a variety of genomes including fast-growing bacteria, the cyanobacterium of Synechocystis PCC6803, and the radiation resistant Deinococcus radiodurans (see Progress Report). We can predict highly expressed genes in each bacterial genome, which correlate very well with 2D-gel protein abundances. We propose to apply the methods to all complete genomes and illustrate here pilot studies for two groups of bacterial genomes: the first group consists of all available low G+C Gram-positive genomes including the pathogens Listeria monocytogenes, Staphylococcus aureus, Streptococcus pyogenes, and the nonpathogenic dairy fermentation bacterium Lactococcus lactis. The second group consists of all available high G+C a-proteobacteria. The latter genomes are important for understanding nitrogen fixation. A second aspect of our research will be to investigate the status of genes in several metabolic pathways and of several protein families among archaeal and bacterial species contrasting presence, absence, and expression levels of genes. A third major objective of our research will be to extend our codon usage methods for predicting gene expression levels to eukaryotic genomes, including yeast, D. melanogaster, C. elegans, and human. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HORMONAL REPRODUCTION
REGULATION
AND
ROLES
OF
CSF-1
IN
Principal Investigator & Institution: Pollard, Jeffrey W.; Professor; Developmtl & Molecular Biology; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2002; Project Start 01-AUG-1994; Project End 31-MAY-2003
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Summary: The last few years have documented the expression of many different cytokines/growth factors in the female reproductive tract. In many cases their synthesis is regulated by the polypeptide and sex steroid hormones known to exert overall control of reproduction, suggesting that these growth factors are the local mediators of hormone action. This has been confirmed using null mutants in the cytokine/growth factor genes. Amongst the first growth factors to be studied was the mononuclear phagocytic growth factor, colony stimulating factor-1 (CSF-1), whose expression pattern, together with that of its receptor, in the ovary and uterus suggested roles in reproduction, in addition to those in regulating mononuclear phagocytic function. Our analysis of the CSF-1 nullizygous mice has confirmed these roles for CSF-1 in reproduction with major effects being on neuroendocrine function, ovulation and mammary gland development. Because in all null mouse mutants the gene product is ablated from conception, the effects of its absence in one cell type can have pleiotropic effects on other cell types. An important challenge therefore, is to identify unequivocally the effector cells for each individual phenotype. In this application we will use transgenic technology to spatially and temporally restore, or ablate, CSF-1 signaling to fully define the cell type specific mechanisms of CSF-1 action in female reproduction. Many of the growth factors/cytokines found in the female reproductive tract were originally characterized as hematopoietic cytokines. CSF-1 is one of these, being originally isolated as a macrophage growth factor. A significant gap in immunological knowledge is how infection is controlled at the utero-placental interface, while at the same time an immune reaction is not mounted against the allogenic fetus. The CSF-1 receptor is not only expressed in macrophages but also in trophoblast. Based upon our observations of acute susceptibility of CSF-1 nullizygous mice to placental infection with Listeria monocytogenes, we hypothesize that CSF-1 has an important immunological role during reproduction through the regulation of immune cytokine synthesis by the trophoblast. Our studies aim to identify the important cytokines and to restore CSF-1 signaling in trophoblast independently of other cell types and examine the effect of this on the immune response to L. monocytogenes in order to test this hypothesis. Furthermore, we will identify CSF-1 regulated cytokines in the placenta and use genetic means to ablate them to confirm their importance in controlling this infection. Since L. monocytogenes causes significant fetal morbidity and mortality during pregnancy in humans, such studies might also point to areas for therapeutic intervention in this infection during pregnancy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HOST DEFENSE TO NEONATAL INRACELLULAR PATHOGENS Principal Investigator & Institution: Wilson, Christopher B.; Professor and Chair; Pediatrics; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2004; Project Start 01-APR-1990; Project End 28-FEB-2009 Summary: (provided by applicant): Control of infection with intracellular pathogens depends on the ability of the innate immune response to limit microbial replication and injury in the initial days of infection and then to efficiently facilitate the development of adaptive (antigen-specific) immunity. The innate immune system has an inherent ability to discriminate between microbial pathogens and self, a function fulfilled in part by tolllike receptors (TLRs). In addition to their important role in activating innate defenses, TLRs are thought to play an essential role in the activation of dendritic cells (DCs), which link innate and adaptive immunity, influencing the quality and magnitude of the antigen-specific immune response and the outcome of the infection. Interferon-gamma (IFN-gamma)-producing Th1 CD4+T cells and cytotoxic CD8+T cells are key
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Listeria monocytogenes
components of protective antigen-specific immunity to intracellular pathogens. This proposal addresses the role of TLRs in innate immunity and in the activation of DCs leading to the induction of antigen-specific immunity to the intracellular bacterial pathogen, Listeria monocytogenes (Lm), and the mechanisms by which IFN-gamma is regulated in the context of this infection. Lm is a food-borne pathogen that causes severe disease in the fetus and newborn infant, and the murine model of Lm infection provides a robust system in which to address mechanisms linking innate and adaptive immunity in adults and neonates. Aim 1. Determine which TLRs contribute and the cumulative role of TLRs in the innate immune response to Lm. Aim 2. Determine the cumulative role of TLRs and MyD88 in activating DCs and in linking innate to adaptive immunity to Lm. Aim 3. Determine whether deficits in TLR/Myd88-dependent or -independent mechanisms impair the development of T cell-mediated immunity to and protection from Lm in the neonate. Aim 4. Determine the importance of conserved non-coding sequences (CSE1/2) in proper expression of IFN-gamma in the context of the immune response to Lm. These studies will provide insights into mechanisms for host defense against Lm and for the greater susceptibility of the neonate to this and related intracellular bacterial pathogens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HOST REGULATION OF SECRETED, BACTERIAL VIRULENCE FACTORS Principal Investigator & Institution: Decatur, Amy L.; Assistant Professor; Molecular and Cell Biology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-MAR-2008 Summary: (provided by applicant): The long-term goal of this study is to understand how an intracellular pathogen interacts with its host to establish a protected niche in which the pathogen can replicate. For the bacterial pathogen Listeria monocytogenes establishing and maintaining its intracellular niche, the host cytosol, requires precise spatial regulation of an essential virulence factor, listeriolysin O (LLO). LLO is a secreted pore-forming protein that mediates bacterial escape from the host vacuole to the host cytosol. Despite being continuously secreted by the bacterium, LLO is active only in the host vacuole. We have identified a cis-acting sequence in the amino terminus of LLO that is necessary to restrict the activity of LLO to the vacuole. Mutants that lack this sequence fail to correctly compartmentalize LLO activity, permeabilize the host plasma membrane in addition to the vacuolar membrane, and consequently destroy their intracellular niche. Importantly, these mutants are avirulent in vivo. The above sequence is rich in the amino acids proline (P), glutamate (E), serine (S), and threonine (T) and thus resembles eukaryotic PEST sequences. PEST sequences can target eukaryotic proteins for phosphorylation and/or degradation. We have shown that a mutant LLO lacking the PEST region accumulates to higher intracellular levels than the wild type protein suggesting that this region may influence intracellular stability of LLO. In addition, we have shown that LLO is phosphorylated in the host cytosol and that mutants lacking potential phospho-acceptor sites located within the PEST sequence also permeabilize the host plasma membrane and have decreased virulence. The specific goal of this proposal is to understand the mechanism by which LLO's PEST sequence regulates the protein's activity in the host cytosol. In Aim 1, we will identify specific residues within LLO's PEST sequence that are important for its function and which may represent contact sites for interacting host molecules. In Aim 2, we will define the pathway of LLO degradation and determine whether the PEST sequence affects this pathway. Lastly, in Aim 3, we will define the role of intracellular phosphorylation of
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LLO. Controlling when and where a virulence factor acts is critical for an intracellular pathogen to orchestrate a productive infection and cause disease. By defining the mechanism by which LLO activity is compartmentalized within a host cell, we will learn more about how intracellular pathogens can take advantage of host cell machinery to regulate the activity of key virulence factors that function within the host cytosol. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DROSOPHILA
HOST-PATHOGEN
GENETICS
USING
LISTERIA
AND
Principal Investigator & Institution: Freitag, Nancy E.; Assistant Professor; Seattle Biomedical Research Institute 307 Westlake Ave N, Suite 500 Seattle, Wa 98109 Timing: Fiscal Year 2004; Project Start 01-JUL-2004; Project End 30-JUN-2009 Summary: (provided by applicant): Listeria monocytogenes is a facultative intracellular bacterial pathogen that is an important agent of serious human food-borne infections. L. monocytogenes has served for decades as an outstanding model system for elucidating cellular and molecular interactions that take place during host infection. This proposal seeks to combine the power of bacterial genetics with the use of a genetically tractable model host system to isolate host mutants with altered resistance to L. monocytogenes infection. The fruit fly Drosophila melanogaster has been intensely studied as a model genetic system for decades, and it offers several advantages as a model host including the striking conservation of its innate immune recognition pathways with those of vertebrate animals. Studies have demonstrated the conservation of pathogenic mechanisms used by infectious agents within flies and vertebrates, and the feasibility of screening thousands of flies to isolate mutants with altered responses to infection provides a powerful means of identifying host factors that contribute to host survival. Recent work has demonstrated that D. melanogaster serves as a suitable host for L. monocytogenes infection, thus this proposal seeks to exploit the use of these genetically tractable organisms to functionally identify critical factors of both pathogen and host that contribute to the establishment of microbe infection. In Aim 1, experiments will examine the cellular course of L. monocytogenes infection within insect tissue culture cells, larvae, and adult flies. These studies will provide a foundation for the functional analysis of pathogen and host gene products identified for their potential roles in influencing the outcome of microbial infection. Aim 2 will functionally characterize L. monocytogenes mutants that are attenuated for virulence in flies. Bacterial gene products required for insect infection will be analyzed for potential roles in mammalian infection. Aim 3 will isolate and identify Drosophila mutants with altered susceptibility to Listeria infection. These studies will help identify the host factors that contribute to immune responses directed against intracellular pathogens. The ultimate goal of the experiments described will be the functional characterization of bacterial factors that support survival within the host, and the elucidation of host mechanisms that serve to counter bacterial survival strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HUMAN STUDIES OF LISTERIA MONOCYTOGENES VECTORS Principal Investigator & Institution: Hohmann, Elizabeth L.; Associate Professor; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2002; Project Start 15-JUN-2002; Project End 31-MAY-2007 Summary: (Provided by Applicant) Listeria monocytogenes are Gram-positive intracellular bacteria which stimulate cellular immune responses, those necessary for
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Listeria monocytogenes
elimination of viruses. Engineered L. monocytogenes are effective vaccine vectors for delivery of both viral and tumor antigens in animals. Both therapeutic and prophylactic approaches are successful in animals. Listeria spp. Are present in foods, enter the body through the intestine and may disseminate to cause serious infection with a tropism for the central nervous system and placenta. Safety is therefore a major consideration in use of L. monocytogenes as a vector in humans. We have initiated (to our knowledge) the first safety study of a live attenuated L. monocytogenes vector organism in human volunteers. A highly attenuated derivative of L. monocytogenes 10403S deleted for the virulence elements actA and plcB is being studied. There have been no serious adverse events to date in 18 volunteers who received single oral escalating doses of this attenuated strain (10E5 to 10E9 colony forming units). This proposal sets forth a plan for ongoing evaluation of Listeria bacteria as vaccine vectors in humans. Attenuated L. monocytogenes will be engineered to express defined influenza A and HIV Gag epitopes as secreted fusion proteins of listeriolysin. Strains constructed will be evaluated bacteriologically, in mice and in tissue culture systems. Promising strains will be carried on for evaluation in small inpatient clinical studies designed to evaluate safety, shedding and human immunogenicity. Contemporary immunological studies using tetramer, FACS and ELISPOT technologies will be used to determine whether discrete human cellular immune responses to vectored viral antigens can be detected in humans after these investigational immunizations. These studies will provide important data on the feasibility and utility of using Listeria monocytogenes vectors in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IDENTIFICATION OF FACTORS REQUIRED FOR LISTERIA MOTILITY Principal Investigator & Institution: Jeng, Robert L.; Molecular and Cell Biology; University of California Berkeley Berkeley, Ca 947205940 Timing: Fiscal Year 2002; Project Start 01-FEB-2002 Summary: (provided by applicant): The actin cytoskeleton participates in a range of cellular behaviors involving motility. A number of bacterial pathogens hijack the host cell cytoskeleton as part of their infectious cycle. Listeria monocytogenes, for example, polymerizes actin to form comet-like tails that propels it through the cytoplasm. Because these pathogens bypass many of the normal cytoskeletal controls and because their movement has been recapitulated in cell-free extracts, they have been used as model systems to study actin polymerization. Here, we describe the use of Listeria to identify novel factors involved in actin dynamics and force generation. We have found that Listeria move at different rates in different cells extracts. Listeria move at high rates in human platelet and frog egg extracts, but at low rates in mouse or bovine brain extracts. Addition of high-motility extracts to the brain extracts confers fast movement to brain extract. We propose to use this activity to purify components present in platelet and egg extracts that are involved in fast bacterial motility. Specifically, we plan to: (1) further characterize Listeria motility in different cell extracts, (2) fractionate extracts and follow high-motility activity to purify factors that enhance bacterial movement, and (3) identify and characterize the purified proteins. We believe this approach will isolate novel factors involved in actin dynamics and force generation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: IDENTIFICATION OF TLR SIGNALING NETWORK Principal Investigator & Institution: Makarov, Sergei S.; Attagene, Inc. 125 Ironwoods Dr Chapel Hill, Nc 27516
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25
Timing: Fiscal Year 2004; Project Start 15-JUL-2004; Project End 30-JUN-2009 Summary: (provided by applicant): Toll-like receptors play a critical role in the initiation of the innate and adaptive immune responses. Members of the TLR family recognize conserved microbial structures and activate signaling pathways that result in immune responses against microbial infections. All TLRs activate common pathways to induce a core set of stereotyped responses, such as inflammation. However, individual TLRs can also induce immune responses that are tailored to a given microbial infection. The mechanisms and components of these varied responses are poorly understood. Given the importance of TLRs in host defense, dissection of these pathways is key to the rational design of immunomodulators and adjuvants. To address the complexity of the TLR signaling network, it is imperative to put in place technologies enabling systematic examination of the signal transduction. ATTAGENE Inc. has developed a reversible genetic approach that affords screening expression libraries of tens of thousands of cDNAs to identify signaling intermediates. We used this methodology to identify a number of novel components of the pathways that mediate interleukin-1-inducible activation of the transcription factor NF-kB. Our studies indicate that the reversible genetic approach offers a highly versatile tool for a systematic, genome-wide identification of signal transduction. This comprehensive approach does not rely on preconceived notions and it has built-in procedures that eliminate false-positive background. In this study, we will adapt the reversible genetic approach to systematic identification of components of the TLR signaling network. Our objectives are (1) to identify the components of signal transduction that link individual members of the TLR family with activation of the transcription factor NF-kB; (2) to annotate those components as positive/negative and differential/common intermediates; (3) to examine biological functions of the identified mediators in innate immune responses in vitro; and (4) to create knock-out animal models in order to assess the identified mediators as potential targets to modulate the innate and adaptive immune responses to different pathogens, including Listeria monocytogenes and Salmonella typhimurium. Successful implementation of the proposed plan should provide comprehensive knowledge of molecular mechanisms controlling immune responses to pathogens, thus greatly facilitating the development of highly specific immunomodulators and adjuvants. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IMMUNE TOLERANCE AND IMMUNE DEVIATION PROTECT AGAINST A* Principal Investigator & Institution: Dekruyff, Rosemarie H.; Senior Research Scientist; Pediatrics; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-JUL-2005 Summary: (provided by applicant): The long-term goals of this project are to understand the immunobiology of asthma and allergic diseases. While our knowledge of the role of Th2 responses in the pathogenesis of asthma has improved over the past 10 years, our understanding of the mechanisms that dampen Th2 biased inflammation and that protect against the development of asthma remains rudimentary. Th1 cells may have a role in protection against asthma, however, our recent studies indicate that multiple additional mechanisms play more critical roles in regulating asthma and allergy. In this proposal we will identify and examine in detail these additional immune mechanisms that down-modulate Th2 responses, and determine the cell types and molecules that participate in the protection against Th2-biased inflammation and asthma. In Specific Aim 1 (Hypothesis 1), we will determine the mechanisms by which immunological
26
Listeria monocytogenes
tolerance protects against asthma and allergic disease. We will define the cellular and molecular events by which pulmonary dendritic cells mediate T cell tolerance induced by the respiratory exposure to allergen, and determine the characteristics of the regulatory cells induced by these pulmonary dendritic cells. In Specific Aim 2 (Hypothesis 2), we will determine the mechanisms by which immune deviation, involving IL-10, TGF- CD8 cells and toll-like receptor signaling, regulates asthma and allergic disease. These molecules, cytokines and cell types are activated by immunization with the adjuvant heat killed Listeria monocytogenes (HKL), a very effective stimulator of the innate immune system. We will examine the characteristics of immune responses induced with HKL, which potently down regulate airway inflammation and protect against the development of airway hyperreactivity. Finally, in Specific Aim 3 (Hypothesis 3) we will identify novel pathways involved in protection against asthma, by studying a unique congenic BALB/c mouse strain (HBA), that produces low levels of IL-4 and resists the development of airway hyperreactivity. In collaboration with Dr. Patrick Brown at Stanford, we will use gene expression profiling with cDNA microarrays to compare the specific genes and molecular pathways in BALB/c versus HBA mice, thereby developing a distinctive molecular portrait of the biology of protective immunity. These studies will greatly extend our knowledge of immune responses that protect against asthma and the Th2 biased immune responses that are pathologic for asthma and allergy. These studies therefore, are likely to lead to greatly improved therapies that protect against and potentially cure asthma and allergic diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INDUCTION OF GAMMA/DELTA T CELLS BY MICROBIAL PRODUCTS Principal Investigator & Institution: Ziegler, Kirk H.; Professor; Microbiology and Immunology; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2002; Project Start 01-SEP-1994; Project End 31-DEC-2005 Summary: (Verbatim from Applicant's Abstract): While T lymphocytes that express the gamma delta (gamma/delta) T cell receptor represent a small subset of T cells present in lymphoid organs, gamma/delta T cells appear to predominate in epithelial tissue. This tissue localization may indicate their involvement in "front line" defense mechanisms by recognition of microbial or induced antigens present at these sites. The ability to rapidly respond to pro-inflammatory cytokines may provide an important sentinel function for gamma/delta T cells. In addition to their defensive role in infectious disease, it is also becoming clear that gamma/delta T cells can play a significant regulatory role in tolerance, allergy, autoimmunity, and inflammatory disease. It has become clear that gamma/delta T cells recognize and respond to antigens and cytokines in a manner markedly different than the other major T cell, the alpha beta (alpha/beta) T cell. While a clear consensus remains to emerge, it appears that gamma/delta T cells do not generally recognize peptide epitopes in association with the MHC. Unlike alpha/beta T cells, the gamma/delta cell receptor may function more like immunoglobulin and recognize antigens directly. Another interesting feature of gamma/delta T cells is their ability to respond rapidly to cytokines produced early in the immune response. They constitutively express receptors for cytokines that are only inducible on other cell types such as alpha/beta T cells. In the proposed studies we will attempt to understand the mechanism of gamma/delta T cell function in resistance to infectious disease in a welldefined mouse mode. Mice lacking gamma/delta T cells (delta knockout mice) will be utilized in hopes of understanding cytokine production and response patterns of
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gamma/delta T cells during infection with Listeria monocytogenes. The regulatory role of gamma/delta T cells in the production of pro-inflammatory cytokines will be studied. An attempt will be made to determine the function, receptor specificity, and activation requirements of gamma/delta T cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INFLAMMATION AND T CELL IMMUNITY TO LISTERIA Principal Investigator & Institution: Pamer, Eric G.; Professor/ Chief, Infectious Diseases; Sloan-Kettering Institute for Cancer Res New York, Ny 100216007 Timing: Fiscal Year 2002; Project Start 01-JUL-1996; Project End 28-FEB-2007 Summary: (provided by applicant): The murine immune response to Listeria monocytogenes infection is rapid, robust and highly effective at providing long term protective immunity. We have characterized the expansion of L. monocytogenes specific CD8 T cells during in vivo infection and find that the duration of T cell proliferation is not influenced by the duration or severity of infection. The experiments described in this grant application will test the hypothesis that CD8 T cells and the immune environment are programmed during the first 24 to 48 hours of infection by the innate inflammatory response, and that subsequent expansion and memory formation occurs independently of in vivo antigen presentation or infection induced inflammation. Our first aim is to test this hypothesis by transferring antigen specific T cells from infected mice into recipients that are uninfected, infected with antigen deficient strains of L. monocytogenes or infected for different durations with wild type bacteria. These studies will characterize the in vivo impact of inflammation and antigen presentation on antigen specific T lymphocytes expansion and memory formation. Our second aim is to characterize the CD8 T cell response to immunization with heat killed L. monocytogenes (HKLM). Our preliminary studies demonstrate that immunization with HKLM induces antigen specific CD8 T cell proliferation, but the duration and extent of proliferation is attenuated compared to that induced by live infection. We have designed experiments to determine the role of CD40 and IL-12 in the programming of CD8 T cell expansion. The third aim is to determine the role of innate inflammation induced by TLR signaling and by inflammatory chemokines on CD8 T cell expansion and memory formation. We will use mice deficient in TLR-2, TLR-4, MyD88, MIP-1a, CCR2 and CCR5 for these studies. Understanding the mechanisms that drive in vivo T cell expansion and memory information is important, since potent vaccines should be designed to elicit robust, long lasting T cell responses. Our studies will shed light on the important interactions between innate immunity and adaptive T cell responses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INHIBITION OF T CELL RESPONSES BY BACTERIA Principal Investigator & Institution: Starnbach, Michael N.; Associate Professor; Microbiol & Molecular Genetics; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 15-JUN-2003; Project End 30-NOV-2007 Summary: (provided by applicant): We have initiated studies to characterize the role of CD8+ T cells in immunity to the intracellular bacterium, Shigella flexneri. During infection, S. flexneri enters cells and escapes into the host cell cytosol. We expected that proteins excreted from Shigella would be proteolytically degraded into peptides by the MHC-I processing pathway, and that the resulting cell-surface peptide:MHC-I complexes would stimulateCD8 + T-cells. During infection with Listeria
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Listeria monocytogenes
monocytogenes, another cytosolic bacterial pathogen, Listeria-derived peptides, in complex with host MHC-I, are recognized by CD8+ T cells and contribute to the generation of protective immunity. However, we have found that CD8+ T cells do not appear to play a role in protective immunity to S. flexneri. Even when the Shigella have been engineered to constitutively secrete heterologous epitopes known to stimulate potent CD8 + T cell responses, those responses were not detected. We also found that when cultured cells were infected with these epitope-tagged S. flexneri strains, the cells were not recognized by established T-cell clones specific for the epitope tag. These findings have suggested to us that a step (or steps) in the normal MHC-I processing pathway is inhibited in cells infected with S. flexneri. The experiments in this proposal seek to identify and characterize the defect in MHC-I processing and/or presentation that occurs during S. flexneri infection. Specifically: 1) using biochemical assays, we will analyze the MHC-I pathway during Shigella infection to determine if there is inhibition of specific activities; and 2) we will use two parallel genetic screens to identify S. flexneri gene product(s) responsible for the inhibition. Through these experiments, we expect to identify and describe the activity of a bacterial inhibitor of MHC-I processing and presentation. Such an inhibitor might represent a novel class of virulence determinants specifically able to inhibit pathogen recognition by the adaptive immune system of the host. Understanding how this inhibition affects bacterial virulence and acquired immunity will further our understanding of the complex interaction of this bacterial pathogen and its mammalian host. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: L. MONOCYTOGENES CLONAL GROUPS: ECOLOGY AND TRANSMISSION Principal Investigator & Institution: Wiedmann, Martin; Food Science; Cornell University Ithaca Office of Sponsored Programs Ithaca, Ny 14853 Timing: Fiscal Year 2002; Project Start 01-MAR-2001; Project End 28-FEB-2005 Summary: This project will combine the efforts of research groups at Cornell, the Technical University of Munich, and at the Wadsworth Center to quantify and statistically model associations between clonal Listeria monocytogenes groups and different environments and hosts. An independently funded parallel study in China will allow us to evaluate whether patterns and associations in the US are broadly applicable. Preliminary results show (i) that clonal L. monocytogenes groups differ in their likelihood to cause human and animal disease and (ii) that L. monocytogenes virulence genes appear to also be functionally important outside mammalian hosts (e.g., for interactions with protozoan cells). Laboratory studies will characterize phenotypes of clonal subgroups associated with specific environments or host species to determine the biological relevance of associations among clonal L. monocytogenes groups and different habitats. Laboratory studies will also define specific habitats (including nonmammalian host species) that may provide selective pressures for maintenance of virulence genes and the emergence of new L. monocytogenes strains. The outcome of this project will be a model of transmission dynamics of Listeria clonal groups and of environmental, host, and agent factors affecting transmission dynamics. Our studies will define environments likely to significantly and directly affect Listeria transmission dynamics when influenced by anthropogenic changes. The specific objectives of our study are: 1. Determine the distribution of clonal L. monocytogenes groups among (i) human hosts; (ii) non-primate mammalian hosts; and (iii) non-host related environments using culturing techniques and molecular and phenotypic approaches for characterization of isolates. 2. In parallel to Objective 1, use non-culturing-based
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techniques to determine the distribution of L. monocytogenes clonal groups in different environments using molecular approaches to avoid culturing bias. 3. Determine associations between L. monocytogenes clonal groups and different environments and host species and develop a transmission model for different clonal groups. 4. Determine the phenotypes of L. monocytogenes clonal groups associated with specific environments and hosts and determine the genetic basis for phenotypes associated with a preference for specific habitats. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LISTERIA AND SHIGELLA USE HOST CELL ACTIN Principal Investigator & Institution: Southwick, Frederick S.; Professor; Medicine; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2002; Project Start 01-JUL-1993; Project End 31-MAY-2007 Summary: (provided by applicant): The gram-positive bacillus Listeria monocytogenes predominantly infects immunocompromised patients, causing bacteremia and meningitis while the gram-negative bacillus Shigella flexneri infects normal hosts causing severe diarrhea and dehydration. The pathogenesis of Listeriosis and Shigellosis absolutely requires these intracellular bacteria to usurp the host cell's contractile system. Listeria and Shigella induce host cell actin to assemble into rocket tails that rapidly propel the bacteria through the cytoplasm, allowing their cell-to-cell spread and avoidance of the humoral immune system. Actin assembly occurs in a discrete polymerization zone directly behind the motile bacteria. This region blocks the host cell actin-regulatory proteins, gelsolin, CapZ and CapG, that normally cap the fast growing ends of actin filaments. This blocking activity allows actin filaments to rapidly assemble in this discrete zone. Two of these proteins, gelsolin and CapG, require micromolar calcium to function. We will: Aim I - Elucidate how Listeria blocks barbed end-capping proteins in the polymerization zone. Pyrenyl actin and right angle light scattering will be used to examine how profilin combined PIP2 and VASP or N-WASP effects actin filament capping by CapG, CapZ and gelsolin. Capping inhibition by Listeria will be investigated in brain cell free extracts before and after depletion of profilin and VASP. Localization of PIP2 (well known to block capping activity) in Listeria and Shigella infected cells will be studied using a GFP labeled probe. The effects of blocking PIP2 production using the PI kinase inhibitors Wortmannin and quercetin, infecting cells with Listeria ActA mutants lacking PIP2 binding sites, and ActA mutants lacking VASP binding sites will be examined. Aim II - Study the Calcium-Dependence of Listeria and Shigella actin-based motility. Calcium is a critical signal for turning on and off actin regulatory proteins, and we have found that the chelator BAPTAM blocks Shigella actinbased motility and slows the disassembly of Listeria rocket tails. The Ca2+-sensitivity of N-WASP and vinculin, cell proteins unique to Shigella-induced actin assembly, as well as gelsolin will be studied. These investigations should clarify key regulatory pathways required for Listeria- and Shigella-induced actin assembly and may identify new therapeutic targets for treating Listeriosis and Shigellosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LISTERIA HEMOLYSIN AND ESCAPE FROM A VACUOLE Principal Investigator & Institution: Portnoy, Daniel A.; Professor; Div/Biochem/Molecualr Biology; University of California Berkeley Berkeley, Ca 947205940 Timing: Fiscal Year 2002; Project Start 15-JUN-1988; Project End 31-MAY-2003
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Listeria monocytogenes
Summary: (Adapted from the applicant's abstract): Listeria monocytogenes is a model facultative intracellular pathogen which primarily infects pregnant women and immunocompromised individuals. A primary determinant of L. monocytogenes pathogenesis is a secreted pore-forming protein referred to as listeriolysin O (LLO). LLO is largely responsible for rupture of the host vacuole which results from phagocytosis. Perfringolysin O (PFO) is a related pore-forming protein which is involved in the pathogenesis of infections by an extracellular pathogen. When expressed by L. monocytogenes, PFO mediates escape from the phagocytic vacuole, but is toxic to the cell. Normally, LLO is continually expressed during infection, but in contrast to PFO, it is proteolytically degraded in the cytosol and presented on the cell surface in association with MHC class I molecules. It is hypothesized that pH optimum and cytosolic processing are essential LLO-encoded determinants which distinguish it from PFO. The focus of the current proposal is to define the precise structural and mechanistic features of LLO which differentiate it from other members of the family of thiol-activated cytolysins, facilitate its intravacuolar activity, and direct its fate in the cytosol. In Aim I, protein sequences responsible for LLO's acidic pH optimum and processing in the host cytosol will be identified. This will be accomplished by domain and sub-domain swapping between LLO and PFO, and modified charged-to-alanine scanning mutagenesis. The LLO/PFO chimeras will be purified from E. coli and characterized biochemically. Next, the chimeras will be introduced into L. monocytogenes and characterized in tissue culture models of infection., In Aim II, the pathway of LLO processing in the host cytosol will be fully evaluated. LLO will be identified by metabolic labeling of L. monocytogenes within infected host cells, followed by immunoprecipitation. Precursor/product relationships will be determined by pulsechase experiments. Specific inhibitors will be used to evaluate the role of the proteosome and other proteases in degradation. The role of LLO phosphorylation will be evaluated biochemically and genetically. In Aim III, the precise nature of the L. monocytogenes phagosome will be characterized with regard to pH, time of perforation, and markers of the endosome/lysosome pathway of maturation. The role of pH optimum and the L. monocytogenes phospholipases will be evaluated by using mutant and chimeric strains. In Aim IV, the investigators will evaluate the feasibility of using E. coli K12 expressing LLO and a recombinant protein as a novel system to introduce foreign proteins into the mammalian cytosol for antigen presentation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LISTERIA MONOCYTOGENES AND PHAGOSOME MEMBRANE TRAFFIC Principal Investigator & Institution: Stahl, Philip D.; Professor; Cell Biology and Physiology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002; Project Start 01-MAY-1994; Project End 30-JUN-2004 Summary: A wide variety of human pathogens including Listeria monocytogenes (LM) take up residence and thrive within host cells by interfering with membrane trafficking events. LM is internalized into phagosomes where it actively inhibits maturation of the phagosome. Virulent LM escapes to the cytoplasm. Listeria mutants (LMhly-) that lack listeriolysin fail to access the cytoplasm but retain the ability block phagosome maturation. Newly formed phagosomes mature by dynamic remodeling via a series of sequential membrane fusion events followed by phagosome-lysosome fusion. Each fusion event appears to be regulated by a RabGTPase. Rab5a is required for phagosomeendosome fusion. Live LMhly- blocks phagosome maturation by interfering with Rab5a function. Thus, analysis of Rab5a provides an attractive opportunity to examine the
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regulation of phagosome maturation and the mechanism by which LM interferes with the process. Our central hypothesis is that the GTP/GDP cycle of Rab5a is tightly coupled to phagosome maturation and the activation of downstream GTPases required for efficient phagosome-lysosome fusion. Interferon gamma enhances intracellular killing of LM by selectively inducing Rab5a synthesis. Our goal is to determine how LM and Rab5a function in phagosome maturation, to define the role of interferon gamma in facilitating the process and to delineate the role of GTPases operating down-stream including Rab7 and Rab11. The Specific Aims include identifying the signal transduction mechanisms that control the guanine nucleotide status Rab5a during phagocytosis of LM. We will also delineate the role of protein kinase B/akt, a known regulator of Rab5. The second specific aim focuses on the mechanism by which IFNgamma stimulates phagosome maturation and killing. Interferon gamma selectively induces Rab5a synthesis and processing. We will investigate the mechanism by which IFNgamma elevates the prenylation of Rab5a. We will use phagosome-lysosome fusion assays to determine whether IFNgamma treatment enhances coupling of Rab5a to downstream Rab GTPases, Rab7 and Rab11. We will use knock out mice lacking the IFNgamma receptor to confirm the role played by this receptor. Since IFNgamma treatment selectively induces Rab5a but not Rab5b or Rab5c and since live LM causes Rab5a to accumulate on phagosomes, we will explore the possib ility that the endocytic apparatus is composed of sub-compartments marked by different rab5 isoforms. Rab5a may specifically connect the endocytic apparatus to the developing phagosomes whereas other Rab5 isoforms may have different functions. Using epitope tagged Rabs coupled with both light and electron microscopy and using GFP-Rab5 isoforms in living cells, we will identify a subset of endosomes that function in phagosome-endosome fusion. We will use GFP-Rab5 to observe in real time the docking and fusion of GFPRab5 isoform-marked endosomes to newly formed phagosomes harboring live or dead Listeria monocytogenes. We will determine the effects of IFNgamma treatment on vesicular traffic into and out of LM phagosomes using GFP-Rab5, GFP-Rab7 and GFPRab11. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LISTERIA PHOSPHOLIPASE ACTIVATION & CELL-TO-CELL SPREAD Principal Investigator & Institution: Marquis, Helene; Microbiology and Immunology; Cornell University Ithaca Office of Sponsored Programs Ithaca, Ny 14853 Timing: Fiscal Year 2002; Project Start 01-APR-1998; Project End 31-MAR-2003 Summary: Listeria monocytogenes is a facultative intracellular bacterial pathogen that causes serious illness in pregnant women, neonates, elderly, and immunocompromised individuals. Listeriosis is among the leading causes of death from contaminated food products in US. In the last decade, L.monocytogenes has served as an excellent model system for exploring the interactions that take place between an intracellular parasite and its host. The overall goal of this proposal is to define the mechanisms by which L.monocytogenes is capable of spreading from cell to cell without exposure to the extracellular environment. In previous studies, a broad-range bacterial phospholipase C (PC-PLC) was shown to be necessary for efficient bacterial cell-to-cell spread. PC-PLC is secreted as an inactive precursor (proPC-PLC), and proteolytic cleavage at its Nterminus generates the active form of the enzyme. Recently, we obtained genetic and biochemical evidence that the intracellular activation of pro PC-PLC is mediated by a bacterial metalloprotease (Mpl), which is also active in broth culture, and a cysteine protease, whose activity can only be detected during intracellular infection. The activity
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of PC-PLC generated by either protease is essentially the same, although there is a small shift in substrate preference. Furthermore, proPC-PLC activation by either pathway is dependent on bacterial localization to a vacuole, and on vacuolar acidification. These observations support a model of bacterial escape from double membrane vacuoles formed during cell-to-cell spread that is dependent on host and bacterial determinants. In this proposal, a multidisciplinary approach will be used to test this model of bacterial cell-to-cell spread. Intravacuolar activation of proPC-PLC will serve as a probe to define the host and bacterial requirements for efficient and rapid lysis of double membrane vacuoles. More specifically, this proposal will define (I) the vacuolar compartment in which proPC-PLC activation occurs, (II) the influence of other bacterial virulence determinants on vacuolar maturation and proPC-PLC activation, (III) the origin and identity of the intracellular-specific proPC-PLC activating cysteine protease, and (IV) the relative importance of the two activating proteases. The long term objective of this research is to define the mechanism by which L.monocytogenes spreads from cell to cell. This may provide a novel target for development of drugs to treat or prevent intracellular microbial infections in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LISTERIA-BASED VACCINES FOR OVARIAN CANCER THERAPY Principal Investigator & Institution: Dubensky, Thomas W.; Vice President of Research; Cerus Corporation 2411 Stanwell Dr Concord, Ca 945204810 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 01-OCT-2003 Summary: (provided by the applicant): Ovarian cancer causes the highest mortality rate among women with gynecologic malignancy, approximately 14,000 cancer deaths per year. Women with late-stage disease have a 2-year relapse rate of more than 50%, and a 5-year survival rate of less than 50%. The goal of this proposal is to identify the optimal configuration of a Listeria monocytogenes-based cancer vaccine encoding the tumor antigen mesothelin, for application as a targeted immunotherapy for ovarian cancer. Listeria is an intracellular bacterium that primes robust CD4+/CD8+ T-cell mediated responses, has striking potency in animal models of both infectious disease and cancer, and has been tested in healthy human volunteers. Mesothelin is a differentiation antigen that is expressed in 95% of ovarian cancers and lower levels in other cancers, but other than mesothelial cells, is not detected in diverse normal tissues, including normal ovaries. A panel of recombinant Listeria that express mesothelin fused to elements that augment antigen presentation will be derived, and tested for therapeutic efficacy in a newly-developed syngeneic mouse model that expresses mesothelin and recapitulates human ovarian cancer. Accomplishing these goals will set the stage in a Phase II SBIR for moving the project toward a clinical trial in women with advanced ovarian cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LISTERIA-CEA VACCINE-INFECTED DC FOR CANCER THERAPY Principal Investigator & Institution: Brockstedt, Dirk G.; Senior Scientist; Cerus Corporation 2411 Stanwell Dr Concord, Ca 945204810 Timing: Fiscal Year 2004; Project Start 01-APR-2004; Project End 30-SEP-2004 Summary: (provided by applicant): Dendritic cell (DC)-based immunotherapy has yielded encouraging evidence of providing clinical benefit for the treatment of a broad range of malignancies. Several strategies are being developed to isolate autologous DC, and load them with antigen or peptides ex vivo. Advances in the understanding of immune mechanisms have, in addition to efficient antigen loading, highlighted the
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importance of the activation and maturation state of DC used for vaccination. Whereas immature DC are more effective in the uptake and processing of antigen, activated/mature DC lose this capacity, and efficiently present antigen to naive T lymphocytes in the context of MHC molecules. Mature DC have been found to be potent antigen presenting cells (APC) to induce primary T lymphocyte responses, overcoming peripheral T cell tolerance and enhance anti-tumor immunity. There are not standard efficient and cost effective methods for combining antigen loading with DC activation and maturation. We propose to develop a novel potent and cost effective approach utilizing proprietary attenuated strains of the intracellular bacterium Listeria monocytogenes (Listeria), engineered to express defined tumor antigens. Listeria is rapidly phagocytosed by DC and transported into the phagolysosomal compartment. This encounter results in the phenotypic maturation of DC and subsequent secretion of a broad profile of immunostimulatory cytokines, including IFN-gamma, IL-12, and TNFalpha. We have demonstrated that infection of immature DC with recombinant Listeria results in rapid DC activation/maturation, together with MHC class I-restricted presentation of an encoded heterologous antigen. We have also engineered Listeria to be exquisitely sensitive to inactivation by psoralens, a group of compounds that form irreversible cross-links in the genomes of bacteria after illumination with ultraviolet A (UVA) light, so that the applicants are non-viable. The psoralen S-59 is one of a number of Cerus-proprietary compounds known as Helinx. Helinx is approved for sale in the EU as part of the INTERCEPT pathogen inactivation system for platelets. This technology will enable us to generate a safe vaccine for malignant colon cancer based on DC infected with Listeria-CEA vaccines that are genetically inactivated, yet retain the capacity to efficiently program CEA presentation as well as initiating the activation/maturation of the infected DC. The inability of the Listeria vaccine strain to propagate and cause disease ensures the safety of this proprietary immunotherapeutic platform. We believe that this represents a major technological breakthrough for the Listeria vaccine platform that will dramatically facilitate its advancement into clinical trials through eventual approval by regulatory agencies. We propose to generate S59/UVA inactivated CEA-expressing attenuated Listeria strains. Listeria-CEA vaccines will be used to identify optimal conditions for antigen loading and inducing activation/maturation of human DC. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MANIPULATION OF PHAGOCYTOSIS IN MACROPHAGES Principal Investigator & Institution: Swanson, Joel A.; Professor; Microbiology and Immunology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-MAY-1994; Project End 31-JAN-2004 Summary: Description (Adapted from the Applicant's Abstract): Phagotosis by macrophages is an essential component of innate immunity. Although post-phagocytic delivery of microbes into macrophage lysosomes typically leads to their degradation, some pathogenic microorganisms survive phagocytosis and evade macrophage defense mechanisms. Listeria monocytogenes is an intracellular pathogen that survives by passing from phagosomes into cytoplasm. Activation of macrophages with interferon-g plus LPS or TNFa increases resistance to many pathogens, including L. monocytogenes. The long-term objective of these studies is to identify those features of macrophage endocytic compartments that counteract intracellular pathogens. The hypothesis to be investigated in this proposal is that increased resistance to pathogens in activated macrophages results from altered phagosome progression to lysosomes, plus localized
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delivery of toxic compounds into acidic, late endosome-like phagosomes. To test this, quantitative fluorometric methods will be used to measure endocytic compartment dynamics and physiology in activated and non-activated macrphages. The first specific aim is to measure rates of phagosome maturation, fusion and lysosomes, and fluidphase solute recycling. In the second aim, biochemical and fluorescence microscopic methods will be used to measure intravacuolar pH and intracellular nitric oxide levels. Sites of peroxynitrite generation will be localized in the cytopolasm and in individual phagosomes. The third specific aim is to identify host and bacterial factors that influence escape of L. monocytogenes from phagosomes. L. monocytogenes secretes a hemolytic protein, listeriolysin O ( LLO ), which mediates bacterial passage from phagosomes to cytoplasm. Fluorescence microscopy will be used to identify the compartment permeabilized by L. monocytogenes , and to determine how this compartment is altered in activated macrophages. Features of LLO that mediate escape from phagosomes will be identified using bacteria expressing mutant and wild-type LLO. For each mutant, the compartment of escape, the efficiency of perforation and escape, and the pH of perforation will be determined. Both listericidal and nonlistericidal macrophages will be compared, as well as macrophages from mice with induced deletions for components of the nitric oxide or superoxide biosynthetic pathways. Because these studies will provide direct measurements of conditions inside the vacuolar compartments of activated macrophages, the results should improve understanding of host defense mechanism related to infecton by L. monocytogenes as well as other intracellular pathogens. Response to The Previous Summary Statement This is a revised application to continue studies on identifying features of the macrophage vacuolar compartments that counteract intracellular pathogens with particular emphasis on Listeria monocytogenes. Several serious criticisms were directed at the earlier proposal. Most importantly, it was felt that the research plan was underdeveloped in that it contained too limited a range of experimental approaches. Additional criticisms were that the specificity of the probes for nitric oxide ( NO ) were not clear and the methods for measuring localized reactive oxygen species ( ROS ) and NO were poorly developed. Similarly, the rationale for why decreased rates of endocytic delivery to lysosomes should enhance microbicidal activity was not obvious and required further explanation. It was also felt by one reviewer that the PI should place greater emphasis on how listericidal macrophages inhibit listeriolysin LLO function. The PI has now responded to all of these criticisms/concerns in a direct, straightforward manner. In particular, the experimental plan has been expanded to include biochemical and immunohistochemical studies to buttress the morphologic experiments. The PI has provided evidence that the probes for NO are highly selective and expanded the methods for monitoring ROS and NO production. The description of these techniques and the necessary controls are now very well developed. Similarly, the "Background and Significance" section has been rewritten and provides a much better explanation of how alterations in membrane trafficking can favor the generation of reactive oxygen and nitrogen species. Specific Aim #3 now contains detailed experiments for investigating the chemical reactions of activated macrophages that may inhibit the hemolytic activity of LLO. The new sections utilizing biochemical methods to monitor NO formation, protein nitrosylation and evaluating the effects of NO and ROS on isolated LLO and Listeria in vitro are state of the art and highly relevant to this proposal. In short, the PI has successfully addressed all of the earlier criticism. These changes have resulted in a more focused, stronger proposal. Progress During the Past Funding Period The PI successfully accomplished the research described in the specific aims of his last funded proposal. For example, he demonstrated that the chemistry of particles undergoing phagocytosis can affect the degree of postlysosomal interactions with other organelles, that increasing vacuolar pH reduced/prevented perforation of macrophages by Listeria monocytogenes, and that
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the formation of "spacious phagosomes" contributes to the survival and virulence of Salmonella. The PI also developed a highly efficient method for delivering macromolecules into the cytosol of macrophages using liposomes that contain LLO. This research resulted in ca. 10 papers published in first rate, peer-reviewed journals along with numerous reviews and book chapters. The PI now wishes to build on this strong record and extend these studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISM OF A FUNCTIONAL SWITCH IN GAMMA DELTA T CELLS Principal Investigator & Institution: O'brien, Rebecca L.; Associate Professor; National Jewish Medical & Res Ctr and Research Center Denver, Co 80206 Timing: Fiscal Year 2002; Project Start 01-APR-1999; Project End 31-MAR-2004 Summary: Recent observations indicate that GammaDelta T cells can undergo a functional switch during the course of disease. We believe that understanding the mechanism of this switch is important because it is probably central to any role these cells play in the regulation of the immune response. In this proposal, our overall objective is to determine what causes GammaDelta T cells to undergo a functional switch. Our specific aims are as follows: Aim 1: to test the hypothesis that responses of different GammaDelta TCR-defined subsets correlate with distinct functions. Using mice infected with the intracellular pathogen Listeria monocytogenes, we plan to examine whether the VGamma1, VGamma4, or VGamma6 subsets show differential cytokine production in infected mice, and to assess how selectively removing each subset affects the disease outcome. Aim 2: to test the hypothesis that functional switching in GammaDelta T cells is controlled by GammaDelta T cells themselves. Here, we will examine whether GammaDelta T cells either directly or indirectly control their own functional switching: 1) by responding as subsets with set functions when triggered by particular antigens or host signals; 2) by stimulating the responses of each other, such that one GammaDelta T cell subset having a set function induces the response of the next, whose set function differs; 3) by inducing FasL-mediated cell death among certain GammaDelta T cells to make way for responses by others having different functions; and 4) by inducing FasL- mediated cell death within other immune cells, thus altering the cytokine milieu and perhaps the subsequent function of GammaDelta T cells as well. Aim 3: to test the hypothesis that the functional switch in GammaDelta T cells is influenced or controlled by external factors. We plan examine the cytokines made by GammaDelta T cells in systems in which the normal cytokine milieu has been perturbed. We will focus on three different ways in which an externally induced switch could occur: 1) as an overall switch in the cytokines produced by GammaDelta T cells of all types; 2) as a subset-based switch in which external cytokines favor the stimulation of certain GammaDelta T cell subsets with a set cytokine profile over other subsets; and 3) via changes in infiltrating inflammatory cells that cause the same cytokines to have different effects, even though no actual switch in cytokines made by the GammaDelta T cells has occurred. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISM OF ETHANOL INDUCED IMPAIRMENTS IN IMMUNITY Principal Investigator & Institution: Jerrells, Thomas R.; Professor; Pediatrics; University of Nebraska Medical Center Omaha, Ne 681987835
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Listeria monocytogenes
Timing: Fiscal Year 2002; Project Start 01-SEP-1988; Project End 31-MAY-2004 Summary: (Adapted from the Investigator's Abstract) Study results from my laboratory and reported by other researchers have shown that ethanol (ETOH) consumption by experimental animals and human beings is associated with an increased susceptibility to infectious diseases. Overall, this is associated mostly with defects in the generation of cell-mediated immune responses and the effector functions of lymphoid cells, including T and natural killer cells as well as macrophages. We and others have shown that ETOH consumption is also associated with activation of the hypothalamic-pituitary- adrenal (HPA) axis and that many of the changes in lymphoid cell numbers and function can be attributed to the resulting corticosteroids produced as a result of this activation. The general hypothesis to be tested in the studies proposed in this application is that the corticosteroids produced by ETOH-fed animals suppress innate and acquired immune responses that are necessary for host defenses against infectious microorganisms. This hypothesis and other more specific hypotheses resulting from the general hypothesis will be tested by using a murine model of ETOH consumption in a liquid diet with a pair-feeding paradigm. With the use of adrenalectomized mice we will determine whether immune responses to model T-cell-dependent antigens such as phosphocholine conjugated to key hole limpet hemocyananin or infectious microorganisms, including Listeria monocytogenes, Salmonella typhimurium, Nippostrongylus brasiliensis, and murine cytomegalovirus, are decreased by corticosteroids produced as a result of ETOH consumption. With this approach the role of ETOH-associated corticosteroid production on the cellular effectors of immunity, including natural killer cells, CD4+ and CD8+T cells, and macrophages will be tested. By using the various infectious model systems in place in this laboratory the ETOH-mediated effects on the subsets of helper T cells (TH-1 and TH-2) will also be defined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS CD8 T CELL MEDIATED ANTIMICROBIAL ACTIVITY Principal Investigator & Institution: Tuma, Roman A.; Sloan-Kettering Institute for Cancer Res New York, Ny 100216007 Timing: Fiscal Year 2002; Project Start 01-JUL-2001; Project End 30-JUN-2004 Summary: In vivo mechanisms of CD8 T cell mediated protective immunity against viral and bacterial infection are incompletely defined. Nevertheless, adoptive transfer of pathogen specific T lymphocytes is under clinical investigation in transplant and HIV infected patients. Our goal is to characterize CD8 T cell mediated immunity in the murine model of Listeria monocytogenes (LM) infection. It is our hypothesis that the ability of CD8 T lymphocytes to confer protective immunity upon transfer into a naive recipient is determined by their antigen specificity and affinity, their activation/effector status, their ability to traffic and their context within the inflammatory response. Our preliminary data show that naive, effector, and memory T cells differ in their ability to repopulate and proliferate in response to infection upon adoptive transfer into naive mice. Furthermore, affinity maturation of the transferred T cell populations appear to increase their protective capacity. The first aim of this proposal will correlate T cell phenotypes, quantities and affinities with protective immunity. Transferred CD8 and CD4 T lymphocytes will be characterized for in vivo proliferation and trafficking properties. The second aim is to determine the impact of antigen specificity upon protective immunity. CD8 T cell lines specific for 7 different LM epitopes have been generated in vitro and will be characterized for their in vivo proliferation and trafficking characteristics. This section will also entail strategies to improve in vitro growth of T
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lymphocytes. The third aim is to dissect the in vivo mechanism of CD8 T cell mediated bacterial clearance. Previous studies have demonstrated that neutrophils are essential mediators of T cell mediated immunity to LM reinfection. We will test the hypothesis that LM specific T cells rapidly recruit neutrophils to sites of LM infection, resulting in bacterial clearance within 24 hours of rechallenge. In summary, the investigations will characterize the relative ability of phenotypically different, antigen specific T cells to mediate protective immunity, determine the impact of different antigen specificities upon protective immunity, and dissect the mechanism of CD8 mediated neutrophil recruitment to sites of bacterial infection. These studies are likely to provide valuable insights with potential implications for adoptive T cell therapy in the treatment of immunodeficiency and malignancy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS OF MEMBRANE DAMAGE BY LISTERIOLYSIN O Principal Investigator & Institution: Provoda, Chester J.; Pharmaceutical Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-MAR-2002 Summary: This proposal is designed to address questions concerning the mechanism of escape of the intracellular pathogen Listeria monocytogenes (LM), from the host cell's endosomal/lysosomal degradative pathway. The Gram-positive LM belongs to a class of facultative intracellular pathogens that are capable of growing and replicating within the cytosol of host cells. The ability of LM to escape from the endocytotic vacuole is due primarily to the presence of secreted listeriolysin O (LLO), and possibly to the presence of secreted phospholipases whose exact roles are unknown. Binding of LLO to cholesterol is postulated to be followed by membrane insertion and homooligomerization to form pores. Pore formation is thought to be at least partly responsible for the escape of LM into the cytosol, although the exact molecular nature and size of the pore are not completely understood. LLO is secreted as a water-soluble monomer that apparently undergoes a conformational change at a pH optimum of 5.5-5.9, resulting in the protein's ability to insert into lipid membranes. However, a complete understanding of the biochemical and biophysical events that account for the transition from a watersoluble state to one favoring the protein's presence in a hydrophobic environment is currently lacking. LLO has several features, particularly its low optimal pH, that make it a favorable candidate as a vehicle for cytosolic drug delivery. We plan to exploit these attributes of LLO, in combination with liposomes, to increase the efficiency of the delivery of therapeutic macromolecules such as plasmid DNA to the cytosol of mammalian cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MICROBIAL VECTORS FOR ANTIGEN DELIVERY Principal Investigator & Institution: Mekalanos, John J.; Professor; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: This proposal involves development of three very promising vector systems to facilitate immunization with antigens of BioDefense (BD) importance. The overall goal is to develop the expertise to rapidly construct vaccine prototypes and evaluate immune responses against expressed BD antigens. The vector systems will include safe, live vaccines based on Vibrio cholerae, killed vaccines based on Escherichia coli, and
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live, virus vectors based on replication-incompetent herpes simplex virus (HSV). Vaccine vectors will be tested for ability to promote antibody and cell-mediated immune responses to each of three BD antigens: the protective antigen (PA) of Bacillus anthracis, listeriolysin O (LLO) of Listeria monocytogenes, and the West Nile virus envelope protein (WNE). The proposed program will provide preclinical information needed to justify testing the antigen-vector constructs for safety and immunogenicity in human volunteers. For bacterial vectors, BD antigen constructs will be introduced as chromosomal insertions by transposition or by directed homologous recombination. Expression profiling using genomic microarrays will guide design of vectors for optimal constitutive or in vivo induced BD antigen expression. E. coli K-12 engineered to express cytoplasmic LLO will be used to deliver BD antigens to the MHC Class I pathway of antigen processing and presentation. Technology will also be developed for targeting E. coli and V. cholerae-based vectors into nonprofessional antigen presenting cells and promoting their in situ lysis to deliver BD antigens or DNA vaccine constructs into these host cells. Replication-incompetent HSV vectors engineered to express BD antigens will be studied in various cell lines for kinetics and levels of BD antigen expression. All BD antigen-expressing vaccines will be evaluated for their ability to induce neutralizing antibodies as well as CD8 + T-cell responses in mice. The vectors will also be tested for their ability to protect animals against anthrax toxin and/or bacterial and viral challenge. The most promising candidates will be evaluated for further development. This proj ect will use NERCE cores in Proteomics, Biological Molecule Production, and Animal and Clinical Testing (the latter, only after approval of human testing by IRB and appropriate committees). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MINORITY PREDOCTORAL FELLOWSHIP PROGRAM Principal Investigator & Institution: Gonzales, Ramona L.; Molecular and Cell Biology; University of California Berkeley Berkeley, Ca 947205940 Timing: Fiscal Year 2002; Project Start 01-AUG-2002 Summary: (provided by the applicant): I propose to study the host innate immune response to infection with the Gram-positive, facultative, intracellular bacterial pathogen, Listeria monocytogenes. The molecular details of the L. monocytogenes infectious cycle are well known, and defective mutants exist for each stage of infection. I will use cDNA microarrays and real-time, quantitative PCR to characterize the transcriptional response of primary murine bone marrow macrophages (BMM), isolated from wild type (C57BL/6) mice, over the time-course of infection by wild type or mutant L. monocytogenes. This will provide valuable information about the mechanisms used by host cells to control progressive infection, not only by Listeria, but also by intracellular pathogens in general. Toll-like receptor 2 (TLR2) has recently been identified as a key initial component in the host's recognition of and inflammatory response to Gram-positive bacteria. In order to explore the role of TLR2 in the host innate immune response to L. monocytogenes infection, I will characterize the transcriptional response of BMM isolated from tlr2-/- mice over the time-course of infection by wild type or mutant L. monocytogenes. I ultimately wish to determine the exact involvement of specific host cell factors, identified as significantly up- or downregulated in gene expression analyses, in nathwavs activated at each state of L. monocytogenes infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR TRAJECTORY/MOTILITY
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Principal Investigator & Institution: Lacayo, Catherine I.; Biochemistry; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2003; Project Start 01-JAN-2004; Project End 31-DEC-2006 Summary: Many motile prokaryotic and eukaryotic cells employ actin-based mechanisms to achieve movement. In particular, the bacteria Listeria monocytogenes move by assembling an actin filament-dense comet tail that propels them inside the cytoplasm of their host cells. Eukaryotic cells assemble actin networks that create membrane projections (lamellipodia,filopodia,etc.) that may drive whole-cell movement. Since quantitative cell motility studies have mainly analyzed the parameter of speed to evaluate molecular changes, this project seeks to explore molecular contributions that allow moving cells to change direction and achieve curvature in their trajectories using a systematic and quantitative approach. By analyzing protein distribution and actin network architecture in relation to Listeria monocytogenes movement in cell lines and during neutrophil chemotaxis and chemokinesis,we will specifically: 1. Characterize the molecular variations underlying Listeria monocytogenes directional motility 2. Determine the mechanism of action of molecules involved in bacterium-comet tail interactions influencing directional motility of Listeria monocytogenes 3. Characterize directional motility in neutrophils and begin analysis of molecular contributions by VASP (Vasodilator-stimulated phosphoprotein). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MONONUCLEAR LEUKOCYTES AND IMMUNITY Principal Investigator & Institution: Silverstein, Samuel C.; John C Dalton Professor and Chairman; Physiology/Cellualr Biophysics; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 01-JUL-1984; Project End 30-APR-2004 Summary: We are studying monocular and polymorphonuclear phagocytes in infection and inflammation. The studies proposed focus on functions of plasma membrane transporters, and of receptors for nucleotide and extracellular matrix proteins on these cells. The project has three aims: #1. To identify by expression cloning in Xenopus oocytes the plasma membrane receptors on mononuclear phagocytes for UTP and for ATP. Mononuclear phagocytes express two distinct types of surface receptors for nucleotide. 1. AP2u-type receptor that signals a rise in cytosolic calcium ([Ca+]i}, when it binds UTP. While UTP dose not signal any known effector function, it potentiates these cells effector system (e.g., H2O2 secretion). 2. A P3Z type receptor that responds to ATP-by opening a pore in the cells' plasma membrane. This pore is permeable to molecules of up to 900 daltons. It has been suggested that the pore is formed by the insertion of a gap junction protein, into the macrophage surface. We have expressed in Xenopus oocytes the P2u and P2Z-like activities of J774 macrophage receptors and are cloning the cDNAs encoding these activities. #2. To determine whether inhibitors of macrophage organic anion transport increase the efficacy of antibiotics against Mycobacterium, Avium complex, Legionella pneumophila, and Listeria monocytogenes, in human monocytes and macrophage to identify the transporter molecule by expression cloning, and to determine whether leukotriene C4 is an endogenous substrate for this transporter. We have discovered a pathway by which mouse macrophage secrete beta-lactam and quinoline antibiotics from their cytoplasm into the extracellular medium. (We have evidence that a similar pathway exists in
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human macrophage.) By this means, macrophage decrease the efficacy of these drugs against Listeria growing within their cytoplasm. We have discovered the gemfibrozil (GFZ) blocks this secretory pathway and increases the efficacy of quinoline antibiotics against intracellular listeria in Vitro. We will determine whether GFZ enhances the efficacy of quinoline antibiotics against Mycobacterium, Avium complex, Legionella pneumophila, and Listeria monocytogenes in human monocytes, and macrophage. We will identify the transporter molecule by expression cloning and determine whether it mediates the secretion of exogenous and endogenous substances from macrophage. #3 To characterize the mechanisms by which plasma membrane receptors of phagocytic phagocytes to crawl under some circumstances, and to become sessile under others. Whether they crawl or adhere appears to be a function of both the identify of the chemokine/chemoattractant and the substrate on, or in the which the cells are located. By blocking specific adhesion promoting receptors on phagocytes we have changed their response to one chemokine (tumor necrosis factor) from adhesion to migration through fibrin gel. We are exploring the mechanisms that control cell migration, and adhesion; and the effects of different matrix proteins on these processes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NOVEL IMMUNOTHERAPY FOR THE TREATMENT OF CERVICAL CANCER Principal Investigator & Institution: Verch, Thorten; Advaxis, Inc. 3701 Market St Philadelphia, Pa 19104 Timing: Fiscal Year 2004; Project Start 17-MAY-2004; Project End 30-APR-2006 Summary: (provided by applicant): Despite the demonstrated efficacy of screening programs, cervical cancer continues to be a significant health issue. In 1999 alone, 12,800 women were be diagnosed with advanced cervical cancer in the U.S. and approximately 4,000 died of the disease. These women are predominantly poor and have reduced access to the health care system. Cervical cancer is primarily related to the sexual transmission of human papilloma virus (HPV). HPV has been shown to be associated with 95 percent of cervical epithelial neoplasms, and 50 percent of all-cervical cancer derives from a single strain, HPV-16. Current treatment modalities for advanced cervical cancer include chemotherapy and surgery, but morbidity and mortality remain unacceptably high. However, most cervical tumors continue to express HPV-related antigens thus providing a target for immunotherapeutic approaches. To address this challenge, Dr. Paterson's laboratory has developed a potent therapeutic vaccine vector, Listeria monocytogenes, which can target antigens to the immune system with the induction of strong cell mediated immunity. Using this approach to target the E7 antigen of HPV-16 in a mouse model, they have demonstrated that HPV-transformed macroscopic tumors can be cured. One drawback of this technology, however, has been the need to introduce antibiotic resistance genes into Listeria as a selection factor for transformation of the bacterial vector. Vectors containing these genes may not be suitable for human use because of concerns about spreading such resistance to other bacteria. Advaxis is working to commercialize these approaches. The work to be completed during this grant period will test the following hypothesis: Listeria monocytogenes, genetically engineered to express the E7 antigen in combination with certain bacterial proteins and rendered safe for human usage by attenuation and by removing antibiotic resistance genes, will show specific antitumor activity against HPVtransformed cells in vivo and ultimately in patients. The specific aims of our work during this grant period are to (1) complete the work on the engineered bacterial vector needed for the clinical trial using a strain of Listeria that does not have antibiotic
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resistance genes; (2) retest the re-engineered vector in the mouse model for HPV transformed cancer; (3) determine biodistribution of the therapeutic, and (4) initiate toxicology testing in the mouse. The long-term goal of the current work is to advance this therapy into and through human clinical trials. This agent could become a useful therapy for cervical cancer, either as a primary therapy or as an adjunct to standard treatments. In addition, this technology can be applied to other cancers and infectious diseases, projects that are in preclinical development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NOVEL STRATEGIES FOR THE IMMUNOTHERAPY OF COLON CANCER Principal Investigator & Institution: Reisfeld, Ralph A.; Professor/ Head; Scripps Research Institute Tpc7 La Jolla, Ca 92037 Timing: Fiscal Year 2002; Project Start 08-MAY-2000; Project End 30-APR-2004 Summary: (Adapted from applicant's abstract) The overall objective is to construct and optimize novel human CEA-based DNA vaccines for the effective immunotherapy of colon carcinoma. The investigators will test the hypothesis that peripheral T cell tolerance to these tumor self-antigens can be overcome by DNA vaccines boosted by effective adjuvants designed to generate cytolytic T lymphocyte (CTLs) specific for CEA epitopes expressed as MHC class I complexes on colon carcinoma cells. Emphasis will be on optimizing antigen processing and presentation in mouse models either transgenic for CEA or double transgenic for CEA and HLA-A2.1Kb. Their aim is to use such models for optimization of vaccine by antibody-cytokine fusion proteins and to investigate basic concepts such as mechanisms of T cell co-stimulation, generation of tumor-specific CTLs and T memory cells and establish principles for adoptive immunotherapy. The specific aims designed to achieve these objectives are: 1) construction of optimal human CEA-specific DNA vaccines containing first the entire CEA gene and then minigenes encoding specific CEA peptides with HLA-A*0201 anchor residues. Delivery of the vaccines by injction of naked KNA or orally by galvage using attenuated strains of either Salmonella typhimurium or Listeria monocytogenes; 2) optimization of antigen processing in the 20S proteasome and presentation by using ubiquitinated versions of the entire CEA gene, minigenes encoding several CEA nonapeptides organized as as a string of beads or direct targeting of single CEA or repeat epitopes to the endoplasmic reticulum; 3) achievement of optimal adjuvanticity using either unmethylated CpG dinucleotide motifs or CD40 Ligand/Trimer coexpression; and 4) determination whether antibody-IL2 fusion proteins can effectively boost DNA vaccines to achieve optimal, long-lived tumor-protective immunity, as well as eradicate established metastases, and identification of immunological mechanisms involved in generating tumor-specific CTLs and T memory cells. The achievement of this proposal's objectives should lead to the design of effective DNA vaccines based on rational immunological principles that may ultimately lead to the improved treatment of colon cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NOVEL VACCINE STRATEGY FOR LISTERIA MONOCYTOGENES Principal Investigator & Institution: Higgins, Darren E.; Microbiol & Molecular Genetics; Harvard University (Medical School) Medical School Campus Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JAN-2008
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Summary: (provided by applicant): Listeria monocytogenes is an intracellular bacterial pathogen that causes serious foodborne illness in pregnant women, the elderly, infants and immunocompromised individuals. L. monocytogenes infections have the highest case fatality rate of all reported foodborne illnesses. L. monocytogenes can be easily cultured outside of host cells under standard laboratory conditions, making L. monocytogenes a significant public health risk and a significant potential threat as a biological weapons agent. Animal models show that protective immunity to L. monocytogenes is mediated by CD8+ effector cells that recognize and eliminate infected host cells. Vaccine studies have demonstrated that stimulation of protective CD8+ effector cells requires subclinical infection with live bacteria. However, immunization of humans with virulent bacteria fully capable of intracellular replication imposes a significant health risk to any population as a vaccine strategy, especially for those individuals inherently at risk to L. monocytogenes infection. We have recently developed a novel strategy for the generation of replication-deficient bacterial vaccine vectors that are capable of stimulating protective CD8+ effector cell responses. The focus of this proposal is to utilize this approach to produce non-replicating L. monocytogenes vaccine strains capable of generating protective CD8+ effector cell responses. In Specific Aim I, we will construct non-replicating L. monocytogenes vaccine vectors to deliver protective native bacterial antigens to the cytosol of professional and nonprofessional antigen presenting cells (APC) for endogenous processing and MHC Class I presentation. In Specific Aim II, we will determine the kinetics of antigen delivery to APC and the requirement of bacterial viability for efficient antigen delivery. In Specific Aim III, we will determine whether uptake of the vaccine constructs sensitizes APC for recognition by L. monocytogenes-specific effector cells. In Specific Aim IV, we will determine whether antigen specific effector cells are stimulated following immunization with the replication-deficient vaccine constructs, and assess stimulation of protective antilisterial immunity. Our goal is that following completion of the proposed studies, a safe and effective replication-deficient vaccine formulation will be identified that is suitable for clinical trials. It is also envisioned that these studies will provide a foundation for the development of replication-deficient vaccine vectors against other intracellular pathogens using a similar approach. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PHASE VARIATION IN LISTERIA MONOCYTOGENES Principal Investigator & Institution: Lenz, Laurel L.; Molecular and Cell Biology; University of California Berkeley Berkeley, Ca 947205940 Timing: Fiscal Year 2002; Project Start 01-MAY-2002 Summary: I propose to study a mechanism for regulation of reversible bacterial cell differentiation which L. monocytogenes exhibits both in vitro and in colonized animals. The studied differentiation step involves phase-variation in the completion of L. monocytogenes septation during cell-division, which manifests as smooth (S) or rough (R) colony morphologies. I will identify the lesion in a transposon mutagenized, Rphase-locked L. monocytogenes strain. The effect that expression of this disrupted locus (termed efs) has on L. monocytogenes morphology will be evaluated by studying the morphological consequences of efs deletion and overexpression. Subsequently, mutants locked in S-phase will be engineered by altering expression of the efs locus, or isolated in screens of mutagenized L. monocytogenes. These phase-locked strains will be used to study the effects of phase-variation on the ability of L. monocytogenes to compete for colonization of the gut and internal organs of orally and intravenously-infected mice. The phase-locked L. monocytogenes strains will also be used to evaluate the effects of
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phase-variation on development of host T cell immune responses to this pathogen. For this experiment, CTL responses to a subset of previously-defined peptide epitopes from bacterial proteins will be quantitated. The expression of these bacterial proteins is known to differ in S-phase and R-phase L. monocytogenes. The studies in this proposal should provide insight into a potentially novel mechanism for regulation of bacterial cell differentiation and will begin to address how this mechanism affects virulence and immunogenicity of L. monocytogenes in a murine host. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROPERTIES OF METALS MAY GOVERN TOXICITIES IN THE LUNGS Principal Investigator & Institution: Cohen, Mitchell D.; Environmental Medicine; New York University School of Medicine 550 1St Ave New York, Ny 10016 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2007 Summary: (provided by applicant): Research bridging inorganic chemistry and medicine is needed so principles can be established to permit rational design/screening of metallopharmaceuticals, particularly inhalable forms. An improved understanding of how metals act in situ would enable Investigators to improve the specificity, and control the toxicity, of such novel compounds. Studies to define mechanisms underlying adverse health effects from airborne metal pollutant exposure have provided information from which the types of studies needed can evolve. In studies showing that inhalation of some metals led to altered lung bacterial resistance and local immune cell function, it was clear that variations in degree of immunomodulation induced did not simply depend on amount of metal deposited in the lung, but also on the agent used. It follows that if agent specificity governs extent of immunomodulation induced, then physicochemical properties inherent to each metal may have contributing roles in eliciting the effects. Based on this premise, the goal of this project is two-fold - to improve understanding of reactions of metals in living systems and to help establish basic principles that may facilitate design of novel metallopharmaceuticals. Using induction of pulmonary immunomodulation as a parameter to reflect potential toxicity of an inhaled xenobiotic, we hypothesize that for any metal, major determinants of immunomodulatory potential in situ are its (A) redox behavior and valency, due, in part, to their governing the extent to which the metal might affect availability/utilizability of glutathione (GSH) and NAD(P)H reductants critical to optimal alveolar macrophage (PAM) and neutrophil (PMN) function and (B) solubility, in that it governs overall metal bioavailability to these cells. An integrated hierarchical approach is proposed to examine potential differences in pulmonary immunotoxicity within and between properties. Various vanadium, chromium, lead, and zinc agents will serve as models for ambient metal pollutants with diverse physicochemical properties. Each agent will first be tested for a clinical effect (i.e., impact of 5 d (5 hr/d) exposure on the lung innate immune response to a subsequent Listeria monocytogenes infection) as this yields data reflecting overall impact on lung immunocompetence and, importantly, lets agents with no effect to be dropped from analyses. To determine if there may be a common mechanism of effect among the demonstrably immunomodulatory agents, and to use variations in implementation as a means to examine influence of each property, studies will then examine exposure effects on PAM and PMN: GSH and NAD(P)H status; reductant-influenced production/expression of factors critical to cell recruitment/activation and, activation status, during innate responses. By establishing if certain properties of metals are more relevant to toxicity
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than others, this may provide Investigators a needed basis to preempt use of some metal ions/complexes in metallopharmaceuticals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROTEIN EXPORT AND SURFACE ANCHORING IN GRAM+ BACTERIA Principal Investigator & Institution: Scott, June R.; Professor; Microbiology and Immunology; Emory University 1784 North Decatur Road Atlanta, Ga 30322 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JAN-2008 Summary: (provided by applicant): Among the low G+C Gram+ bacteria are many important human pathogens, including some classified as potential bioterrorism agents (i.e. Bacillus anthracis, category A and Listeria monocytogenes, category B). Many of these organisms have proteins on their surface that lack typical Sec-dependent Nterminal secretion signals and thus use unknown mechanisms for export through the cell membrane (cm). Some of these proteins are apparently involved in pathogenesis since they are effective for passive immunization of mice. Aims 1 and 2 of this work are directed at identification and characterization of new Sec-independent protein secretion systems in these organisms. Once secreted through the cm in Gram+ organisms, proteins are either released into the extracellular milieu or anchored to the cell surface. The general mechanism for anchoring proteins to the cell wall (cw) in Gram+ bacteria requires a transpeptidase, called sortase, that recognizes and cleaves a short amino acid motif preceding a C-terminal hydrophobic region and charged tail. We recently characterized two sortases in the group A streptococcus (GAS) that anchor distinct subsets of proteins with the LPXTG motif. At a similar location in the genome of other GAS strains, we have identified genes encoding additional proteins with homology to sortase. In Aim 3 we will characterize the function in the GAS of these proposed new sortases and test their ability to anchor their predicted substrate proteins, which we find encoded nearby. We will also characterize a predicted protein with homology to signal peptidase I (encoded in the same region) that we propose will be needed for secretion of these proteins. The greater understanding of secretion and cell wall anchoring in Gram+ bacteria that results from this work should provide new targets for broad spectrum antibacterial therapy and potential new vaccine vectors. In addition, it should provide commercially useful new methods for large-scale production of proteins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RAPID DETECTION OF MAJOR FOOD-BORNE PATHOGENS Principal Investigator & Institution: Zhu, Peixuan; Creatv Microtech, Inc. 11609 Lake Potomac Dr Potomac, Md 20854 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant): Our food is a major source of illness. The Centers for Disease Control (CDC) estimates that food-borne diseases cause approximately 76 million incidents of illness, resulting in 325,000 hospitalizations and 5,000 deaths annually in the U.S. Known pathogens were implicated in 14 million of these incidents, 60,000 associated hospitalizations, and 1,800 deaths. Four pathogens alone (E. coli, Salmonella, Listeria, and Campylobacter) are believed to account for over two-thirds of deaths caused by known pathogens. The goal of our research is to achieve rapid, sensitive, and simple detection of pathogenic bacteria and toxins commonly found in foods by applying a new, very sensitive technology known as the "Integrating Waveguide Biosensor". This technology was recently developed by the Naval Research
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Laboratory (NRL) and is being licensed to Creatv MicroTech for application in the fields of water and food safety testing. NRL's initial experimental results for two molecules showed the Integrating Waveguide Biosensor to be 100 times more sensitive than the previous generation of biosensors based on optical fibers and planar arrays. We expect to achieve a similar improvement in sensitivity for detection of pathogens in food in a test that can be completed in less than 30 minutes. The resulting device will be ideally suited to the prevention of food-borne diseases. The initial scope in Phase I will focus on E. coli O157:H7 and Salmonella bacteria in ground beef and apple juice. A test instrument will be constructed incorporating the biosensor technology, assays will be developed and verified for the specified pathogens, and tests performed on food samples. In Phase II the scope will be expanded to include the pathogens Listeria monocytogenes and Campylobacter jejuni and the food groups poultry and fresh produce. The instrument will be redesigned to be more compact and portable, and assays developed for use outside a laboratory setting. Tests will be performed on location where these foods are produced, transported and/or prepared. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RECOMBINANT LISTERIA MONOCYTOGENES AS AN SIV VACCINE Principal Investigator & Institution: Mcchesney, Michael B.; Adjunct Associate Professor; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 956165200 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 30-APR-2003 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RECOMBINANT LISTERIA VACCINES FOR MELANOMA Principal Investigator & Institution: Miller, Jeffery F.; Professor and Chair; Microbiol, Imm & Molec Genetics; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 05-FEB-2000; Project End 31-JAN-2004 Summary: Listeria monocytogenes is a gram positive bacterium that is able to enter host cells, escape from the endocytic vesicle, multiply within the cytoplasm and spread directly from cell-to-cell without encountering the extracellular milieu. The ability to gain access to the host cell cytosol allows proteins secreted by the bacterium to efficiently the MHC class I antigen processing and presentation pathway leading to the induction of CD8+ cytotoxic T cells (CTL). We developed a genetic system for expression and secretion of foreign antigens by L. monocytogenes. Recombinant vaccine strains expressing the lymphocytic choriomeningitis virus (LCMV) nucleoprotein (NP), or a specific MHC class I restricted NP epitope, are able to induce LCMV specific CD8+ cytotoxic T lymphocyte (CTL) responses in mice following vaccination. These strains confer antiviral protection as indicated by the ability of immunized mice to efficiently clear LCMV infection. Listeria strains that express the E11 protein cottontail rabbit papillomavirus (CRP) have also been constructed. Immunization of rabbits with these recombinants causes regression of CRPV induced papillomas and protection from carcinoma. These and other results demonstrate the utility of Listeria vaccine strains for inducing antiviral and anti-tumor immunity. Our objectives are to explore the utility of recombinant Listeria strains as anti-tumor vaccines and determine optimal strategies for attenuation and antigen delivery. The specific aims are to: 1. Construct L.
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monocytogenes vaccine strains expressing tumor rejection antigens. L. monocytogenes strains expressing the melanoma associated tumor rejection antigens gp100, MART1, TRP2, or an H-2K/b restricted TRP2 181-188 epitope will be constructed. 2. Determine the effects of prophylactic or therapeutic administration of recombinant Listeria vaccine strains on tumor establishment, growth and regression. Two murine tumor models will be used to test vaccine efficacy. 3. Construct Listeria innocua vaccine strains and compare their immunogenicity with wild type and attenuated L. monocytogenes. L. innocua is a non-pathogenic member of the Listeria genus. By transferring genes from L. monocytogenes, we will attempt to construct chimeric strains that are immunogenic yet avirulent. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF ANTIGEN PRESENTATION BY APLP-2 Principal Investigator & Institution: Morris, Chantey R.; Eppley Institute for Research in Cancer & Allied Diseases; University of Nebraska Medical Center Omaha, Ne 681987835 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2006 Summary: (provided by the applicant): Major histocompatibility complex (MHC) presentation of peptides to cytotoxic T lymphocytes results in killing of infected cells. Thus assembly and peptide loading of MHC class I molecules is required to achieve cellular immune responses against infections. The binding of the MHC heavy chain to a peptide follows interactions with several endoplasmic reticulum (ER) proteins, such as calnexin, the transporter associated with antigen processing (TAP), calreticulin, tapasin, and ERp57. Recent studies have shown that amyloid precursor-like protein 2 (APLP-2) also associates with MHC class I molecules. We have found that APLP-2 down regulates the quantity of MHC class I molecules at the cell surface. Based on these preliminary findings, we hypothesize that APLP-2 regulates MHC class I maturation and presentation of peptides, including known epitopes from NIAID priority pathogens (Hantaan virus, Mycobacterium tuberculosis, influenza A virus, dengue virus, Japanese encephalitis virus, and Listeria monocytogenes). Results from these studies will clarify the role of APLP-2 in the MHC class I assembly pathway and may result in new means to prevent or treat infections. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: REGULATION OF ANTIGEN PRESENTATION BY APLP-2 Principal Investigator & Institution: Solheim, Joyce C.; Assistant Professor; Eppley Institute for Research in Cancer & Allied Diseases; University of Nebraska Medical Center Omaha, Ne 681987835 Timing: Fiscal Year 2004; Project Start 01-JAN-2004; Project End 31-DEC-2005 Summary: (provided by applicant): The cellular immune response against infections is initiated at the level of peptide loading and assembly of major histocompatibility complex (MHC) class I molecules. MHC class I presentation of nonself peptides triggers killing of infected cells by cytolytic T lymphocytes. The assembly of the MHC class I heavy chain with antigenic peptide and beta2-microglobulin (Beta2m) occurs via association with endoplasmic reticulum (ER) proteins such as calnexin, TAP, calreticulin, tapasin, and ERp57. Another cellular protein, amyloid precursor-like protein 2 (APLP-2), has recently been shown to associate with MHC class I molecules, and our preliminary findings indicate that APLP-2 down regulates the quantity of MHC class I molecules at the cell surface. The long-range goal of our laboratory is to comprehend the regulation of antigen presentation by MHC class I molecules. The
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objective of this Exploratory/Developmental Research (R21) Grant proposal is to define the effect of APLP-2 on the presentation of pathogen-derived epitopes. Our central hypothesis is that APLP-2 regulates MHC class I maturation and presentation of pathogen-derived peptides, including known epitopes from NIAID biodefense priority pathogens (Hantaan virus, Mycobacterium tuberculosis, influenza A, dengue virus, Japanese encephalitis virus, and Listeria monocytogenes). New insights obtained from this study will clarify the role of APLP-2 in the regulation of the MHC class I assembly pathway and may lead to new immune-based means to prevent or treat infections. The Specific Aims of this proposal are: Aim 1. To ascertain the cellular location of interacting APLP-2/MHC class I molecules and the influence of APLP-2 on MHC class I presentation of peptide. We hypothesize that APLP-2 regulates MHC class l peptide presentation at a late stage in MHC class I maturation. Aim 2. To determine the effect of APLP-2 on T lymphocyte recognition of pathogen epitopes. We hypothesize that the presentation of epitopes from NIAID priority pathogens is affected by APLP-2 interaction with the MHC class I molecule. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF GLUTAMATE SYNTHESIS IN BACILLUS SUBTILIS Principal Investigator & Institution: Sonenshein, Abraham L.; Professor; Molecular Biol & Microbiology; Tufts University Boston Boston, Ma 02111 Timing: Fiscal Year 2004; Project Start 01-SEP-1986; Project End 31-JUL-2008 Summary: (provided by applicant): The biosynthesis of glutamate lies at the intersection of carbon and nitrogen metabolism, linking the Krebs citric acid cycle to nitrogen assimilation through glutamine synthetase. In Bacillus subtilis, the genes for glutamate synthesis and for the pathways leading to the precursors of glutamate are tightly regulated by a host of proteins that respond to a variety of metabolic signals. The longterm goal of this project is to unravel and understand the network of genes, enzymes, and regulatory proteins that allow the cell to maintain tight control over glutamate accumulation. Building on knowledge gained from previous work, this proposal aims to focus on the roles of two of these regulatory proteins, CcpC and GItC. Two aspects of CcpC function will be investigated: interaction with the inducer, citrate, and the role of multimerization in repression. For GItC, the metabolite or protein that regulates its activity will be identified, in addition, the broad role of GltC in gene regulation and its functional interaction with other regulatory proteins will be explored. One of the Krebs cycle enzymes, aconitase, may have a second, non-enzymatic activity, perhaps as an RNA binding protein. The putative secondary activity of aconitase will be tested by seeking targets of such a function and by creating mutants that retain enzymatic activity but have lost the non-enzymatic activity. The implications of this second activity for sporulation in B. subtilis will receive particular attention. Since B. subtilis is a model organism for the gram-positive branch of the bacterial world, the knowledge gained here will be applied to a related, pathogenic species, Listeria monocytogenes. Thus, this proposal seeks to take advantage of the apparent conservation of regulatory proteins, gene organization and regulatory sites between B. subtilis and L. monocytogenes and thereby make rapid progress in an unexplored aspect of the life of an important pathogen. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: REGULATION OF IFN-G-INDUCED INNATE IMMUNITY BY LRG-47 Principal Investigator & Institution: Taylor, Gregory A.; Medicine; Duke University Durham, Nc 27710 Timing: Fiscal Year 2004; Project Start 01-MAR-2004; Project End 28-FEB-2009 Summary: (provided by applicant): Recently, a new family of IFN-gamma-induced p47 GTPases has been identified that is essential for innate immunity against intracellular pathogens. Knock-out (KO) mouse studies have shown that three of these proteins (LRG-47, IGTP, and IRG-47) are critical for resistance to multiple category A, B, and C biodefense priority pathogens. In particular, LRG-47, but not IGTP or IRG-47, is absolutely required for resistance to the intracellular bacteria Salmonella typhimurium, Mycobacterium tuberculosis, Listeria monocytogenes, and Francisella tularensis. In contrast, all three proteins are required for resistance to the protozoan parasite Toxoplasma gondii. The underlying mechanism for the antibacterial actions of LRG-47 is unknown. It is hypothesized here that LRG-47 regulates host resistance to intracellular bacteria by promoting IFN-gamma-induced bacterial killing in macrophages. It is further hypothesized that the protein localizes to the early endosomal compartment, where it catalyzes endosomal fusion with nascent bacteria-containing phagosomes, promoting phagosomal maturation and bacterial killing. In contrast, it is proposed that IGTP and IRG-47 localize to lysosomes and catalyze different facets of phagosomal processing. These hypotheses will be tested with the following aims: Aim I. The subcellular mechanism that underlies the impaired ability of LRG-47 KO macrophages to elicit IFN-gamma-induced bacterial killing will be defined, by determining: (a) the precise localization of LRG-47 within endosomal compartments; (b) the kinetics of LRG47 trafficking to S. typhimurium-containing phagosomes; and (c) the effect of LRG-47 on maturation of the phagosome maturation, including lysosomal fusion, phagosomal acidification, and trafficking of endosomal markers. Aim II. Molecular domains of LRG47 that determine its activity will be defined. Extensive mutational analysis and functional assays will define domains required for: (a) association with endosomes and trafficking to phagosomes; (b) endosome/phagosome fusion; (c) modulation of phagosomal maturation; and (d) bacterial killing in cultured macrophages and in vivo. Thus, this research will elucidate a mechanism that is critical for IFN-gamma- induced innate resistance to intracellular bacteria, with the ultimate goal of creating broadly effective anti-bacterial agents for biodefense. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: REGULATION OF MUCOSAL MEMORY T CELL INDUCTION Principal Investigator & Institution: Lefrancois, Leo J.; Professor; Medicine; University of Connecticut Sch of Med/Dnt Bb20, Mc 2806 Farmington, Ct 060302806 Timing: Fiscal Year 2003; Project Start 30-SEP-1992; Project End 31-MAY-2007 Summary: (provided by applicant): The generation of memory lymphocytes is essential for protection against many infectious pathogens and is the goal of vaccination. Although much has been learned regarding the generation and quantification of memory T cells, how memory cell populations are regulated in terms of migratory abilities and functional differentiation in vivo remain subjects of great interest and importance. The patrolling of mucosal tissues by memory T cells is critical to protection against infection, since these sites are in close proximity to the environment. Our results suggest that microbe-specific CD8 and CD4 memory T cells exhibit tissue-specific differences in the intestinal mucosa and other non-lymphoid tissues. However, whether the generation of memory cells in a particular tissue occurs in lymphoid tissue
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associated with that site is unknown. Also, whether memory cells in a given tissue are part of a larger recirculating pool or resident in that site has not been determined. Moreover, whether memory cells can modify their functional behavior upon entry into a particular tissue remains unclear. Thus, the studies proposed will test the hypothesis that the site of initial T cell activation regulates homing molecule expression and will examine the role of such molecules in memory cell migration to the intestinal mucosa and elsewhere. The aims of the proposal are: Aim 1. To determine whether the site of activation of naive or memory T cells directs the pattern of homing molecule expression. Studies will test the hypothesis that the pattern of homing molecule expression by T cells responding to Listeria monocytogenes infection is dependent on the site of antigen encounter. Aim 2. To determine the migratory abilities of microbe-specific memory T cells in vivo. Experiments will compare the efficiency of migration of microbe-specific CD8 versus CD4 memory T cells into the intestinal mucosa and the functional consequences of migration will be assessed. Aim 3. To determine the molecular requirements for migration of effector and memory antimicrobial T cells to the intestinal mucosa. Whether candidate homing molecules are involved in primary and memory cell migration to the intestinal mucosa will be examined using T cells deficient in these molecules. Overall, these studies will provide significant new information regarding the population dynamics of T cell memory generation and migration in vivo in response to infection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF ADAPTER PROTEIN IN INFECTIOUS DISEASES Principal Investigator & Institution: Diakonova, Maria; Molecular/Cell/Develop Biology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2004; Project Start 01-JUN-2004; Project End 31-MAY-2006 Summary: (provided by applicant): Listeria monocytogenes is a food-borne pathogen that can cause meningitis, meningoencephalitis, septicemias, abortions and, in some cases, gastroenteritis. The overall mortality rate is >20% and fetal or neonatal infection with Listeria has an even higher mortality. Listeria invades a broad range of cell types. Intracellular Listeria replicates in the cytoplasm of host cells and induces the polymerization of host actin filaments ("actin tails") at the bacteria surface using bacterial protein ActA. Actin-based motility allows Listeria to spread from cell to cell without leaving the protective intracellular niche, and is essential for pathogenesis. However, the mechanism underlying Listeria motility and spreading remains elusive. The adapter protein SH2- Bbeta regulates cell motility. I have implicated SH2- Bbeta in the motility of Listeria. Preliminary data revealed that Listeria in cells overexpressing wild type SH2- Bbeta demonstrates increased velocity (225% of control) while expression of SH2 domain-deficient mutants of SH2- Bbeta in host cells inhibits Listeria movement (by approximately 60%). In a cell-free system using Xenopus ooeyte extracts and purified GST-SH2-Bbeta, SH2-Ba increased the velocity of Listeria by 140% of control. I have shown that SH2- Bbeta binds to VASP/profilin two proteins that have been shown to participate in actin-dependent Listeria motility. This application tests the hypothesis that SH2- Bbeta promotes Listeria infection by stimulating actin-based motility. The first aim will determine whether VASP/ profilin directly bind(s) to SH2Bbeta. The second aim will determine whether SH2- Bbeta interaction with VASP/profilin is required for Listeria motility. The third aim will test whether SH2- Ba is required for spreading of Listeria infection. The fourth aim will examine whether SH2- Bbeta is required for the virulence of Listeria. In addition to providing insight into
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the molecular mechanism by which SH2- Bbeta contributes to Listeria motility, the results of the application studies will increase our understanding of the fundamental mechanism by which Listeria spreads. These studies designed to identify new proteins and signaling pathways involved in Listeria motility may identify new therapeutic targets for preventing the rapid distribution of Listeria infection and thereby protect people from listeriosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF CD8+ T CELLS IN INNATE IMMUNE RESPONSES Principal Investigator & Institution: Berg, Rance E.; Microbiology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2005 Summary: (provided by the applicant): We have recently uncovered a role for CD8+ T cells in the innate immune response and this proposal is designed to understand the mechanisms by which CD8+ T cells contribute to innate immunity. Specifically, we have shown that a subset of CD8+ T cells rapidly secrete IFN-gamma in response to infection with Listeria monocytogenes (LM). This IFN-? secretion is antigen/TCR independent and is promoted by cytokine stimulation. The specific aims are as follows: I) To characterize the CD8+ T cells that secrete IFN-gamma, II) To determine the contribution of CD8+ T cells in innate immune responses, and III) To use microarray analysis to determine which genes are involved in controlling responsiveness of CD8+ T cells to IL12 and IL-18. To achieve specific aim I, we will further characterize the cell surface phenotype of the CD8+ T cells secreting IFN-? with regard to their activation/memory status. Furthermore, we will determine the levels of the cytokine receptors responsible for inducing IFN-gamma secretion and see if this correlates with responsiveness. Specific aim II will require in vivo studies to analyze what role CD8+ T cells play in the innate immune response. Once a surface phenotype has been established from specific aim I, we will use this knowledge to transfer purified populations of CD8+ T cells into IFN gamma, knock-out mice to overcome the natural defect in IFN-gamma which results in mortality upon infection with LM. Using microarray analysis for specific aim III will allow us to identify genes which are involved in controlling the responsiveness of CD8+ T cells to innate stimulation mediated by IL-12 and IL-18. The results of the experiments outlined in this proposal will advance our knowledge concerning the role of CD8+ T cells in innate responses to bacteria, viruses and tumors. Armed with this knowledge, we can use these CD8+ T cells to help combat infectious diseases and tumors early in the disease state. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF HEMOLYSINS IN ESCAPE OF ANTHRAX FROM MACROPHAGES Principal Investigator & Institution: Popov, Serguei G.; Senior Scientist; Advanced Biosystems, Inc. 10900 University Blvd Manassas, Va 201102201 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 30-JUN-2004 Summary: (provided by applicant): This proposal studies the role of hemolysins as virulence factors for Bacillus anthracis. Hemolysins allow certain virulent bacterial species to escape the phagosome of macrophages. Using the sequence of Listeria monocytogenes hemolysins for comparison, the incomplete genome of B. anthracis was screened for the presence of hemolysin genes. Five open reading frames containing protein-coding sequences homologous to Listeria hemolysins or associated proteins
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were discovered in the B. anthracis chromosome. These hemolytic proteins, named anthralysins 0, A, B (AnLO, AnLA, AnLB); p3058, and p3201, have not been previously characterized. The goals of this proposal are to: (1) Characterize these hemolytic genes by studying gene expression patterns and regulation; (2) Address the role of each individual anthralysin gene in anthrax pathogenesis; and (3) Study means to inhibit the activity of anthralysins. Such understanding could lead to the development of new antibiotic compounds which act by inhibiting hemolytic proteins and preventing release of anthrax bacilli from the macrophage phagosome, preventing anthrax-associated macrophage death and blocking the infection before it can become systemic. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF MUCOSAL IMMUNITY IN VACCINE PROTECTION Principal Investigator & Institution: Howard, Kristina E.; Population Health and Pathobiology; North Carolina State University Raleigh 2230 Stinson Drive Raleigh, Nc 27695 Timing: Fiscal Year 2004; Project Start 01-JUL-2004; Project End 30-APR-2008 Summary: (provided by applicant): The intermediate goal of the candidate, Kristina E. Howard, DVM, is to complete a mentored training program in retrovirus pathogenesis research, culminating in the PhD degree and providing the opportunity for continued postdoctoral study. Dr. Howard's long-term goal is to become a principal investigator employing animal models to investigate the mucosal immune pathogenesis of infectious diseases. The research training program will be conducted under the guidance of Dr. Gregg A. Dean and Dr. Wayne Tompkins, at North Carolina State University. The FlV research group, of which the co-sponsors are part, has a strong record of extramural funding and scientist training. The candidate's plan emphasizes laboratory training in the current molecular techniques and immunological research methods applied to an animal model of AIDS. This proposal employs the feline immunodeficiency virus (FIV) animal model in the testing of a novel oral vaccine strategy utilizing recombinant Listeria monocytogenes to express FIV proteins. The FIV/cat model is a wellestablished model of lentiviral immunodeficiency in a natural host that is characterized by the ability to initiate transmucosal infection utilizing either cell-associated or cell-free inoculum. Using a recombinant L. monocytogenes, we have recently shown that a single oral vaccination provided protection against vaginal FIV challenge. This proposal will characterize mucosal immunity conferred by this vaccine and assess potential mechanisms of protection. In the first aim we will assess mucosal and systemic immune responses following vaccination to better understand the specific responses induced by the vaccine. Aim 2 will assess the ability of the oral vaccine to protect against homologous versus heterologous mucosal FIV challenge and determine what specific humoral and cell-mediated immune responses may correlate with protection. Aim 3 addresses potential mechanisms by which this vaccine may protect the host from FIV infection. The results of these studies will provide establish whether or not this vaccine can protect against diverse FIV challenge, will identify mucosal immune responses that may be responsible for protection, and may identify additional immune system targets for enhanced vaccine development and therapeutic intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF RIP2 IN BIODEFENSE AGAINST LISTERIA INFECTION Principal Investigator & Institution: Cheng, Genhong; Associate Professor; Microbiol, Imm & Molec Genetics; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024
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Listeria monocytogenes
Timing: Fiscal Year 2004; Project Start 15-MAY-2004; Project End 30-APR-2009 Summary: (provided by applicant): The long-term objective of this proposal is to gain insight into the mechanisms of action of the receptor interacting protein 2 (RIP2) in host biodefense against Listeria monocytogenes infection. RIP2 is a member of the RIP family of serine/threonine (Ser/Thr) kinases. It has been implicated in the signal transduction pathways activated by the Nod receptor family proteins, potential receptors for intracellular pathogens. We recently created knockout mice lacking the RIP2 gene, and found that RIP2-/- mice are severely impaired in their ability to defend against infection with L. monocytogenes. Our preliminary results also indicated that RIP2-/- macrophages have lost their ability to respond to muramyl dipeptide (MDP), the minimal immunostimulatory subunit of peptidoglycan from gram positive bacteria. In addition, RIP2-/- T helper 1 (Thl) and natural killer (NK) cells have reduced interferon gamma (IFN-gamma) production upon IL-12 stimulation. We hypothesize that RIP2 may be involved in multiple signaling and cellular events to coordinate innate and adaptive immune responses in host biodefense against pathogen infection. We propose experiments to investigate RIP2- mediated signal transduction pathways and to determine the in vivo role of RIP2 in immune responses during pathogen infections. First, we hypothesize that RIP2 is involved in MDP-induced activation of innate immune responses. We will determine the role and the mechanism of RIP2 in mediating signal transduction and cytokine production by macrophages in response to MDP stimulation. Second, we hypothesize that RIP2 is involved in Thl differentiation by modulating the activity of IL-12-induced STAT4 activation and interferon gamma (IFNgamma) production. We will first confirm the intrinsic defects of RIP2-/- Thl cells, and then explore potential signaling events where RIP2 might be involved in IL-12-induced STAT4 activation and interferon IFN-(, production. Third, we hypothesize that RIP2 is involved in host defense against microbial infections by affecting both innate and adaptive immune responses. We will determine the susceptibility of RIP2-/- mice to gram-positive and gram-negative extracellular and intracellular bacteria to understand the role of RIP2 in determining the pathogen specificity. We will also use L. monocytogenes infection of RIP2-/- mice as a model to determine the contribution of RIP2 in innate and adaptive immune responses against microbial infections. We believe that the insights obtained from these studies will provide new knowledge about pathogen recognition and coordination between innate and adaptive immune systems, and suggest new avenues of immunologic intervention to prevent and treat many human infectious diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF THE BLTR1 RECEPTOR IN LYMPHOCYTE TRAFFICKING Principal Investigator & Institution: Islam, Sabina A.; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): With the proposed Mentored Clinical Scientist Development Award, the applicant will build upon her prior experiences studying antigen-specific human CD8+ cells to expand her scientific skills in immunology, cell biology and molecular biology. Dr. Andrew Luster will mentor the principal investigator's scientific development. Dr. Luster is a recognized leader in the field of chemokine biology. He is the Chief of Rheumatology, Allergy and Immunology and has trained numerous postdoctoral fellows. The laboratory of Dr. Luster will provide a rich intellectual environment to foster the candidate's scientific development toward her goal of independent investigation. The proposed study will provide the applicant with an
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opportunity to utilize in vivo molecular genetic approaches to study basic questions in T lymphocyte trafficking. Leukocyte recruitment and activation are critical for orchestrating host inflammatory responses, and mediators regulating these responses are attractive targets for therapeutic intervention. Leukotriene B4 (LTB4) is a potent lipid chemo-attractant synthesized primarily by myeloid cells. The sponsor identified murine BLTR1 as the high affinity receptor for LTB4 and generated a mouse strain with a targeted deletion of the BLTR1 gene. While BLTR1 has been described as an important functional receptor on myeloid cells that mediates LTB4 function, its expression and function on T cells has not been previously characterized. In preliminary experiments the applicant has demonstrated that BLTR1 is induced upon in vitro T cell activation in effector CD4+ and CD8+ T cells. Additional preliminary data from human subjects and animal models suggests that BLTR1 expressing T lymphocytes may be recruited to sites of inflammation. The applicant will investigate the novel hypothesis that BLTR1 and LTB4 are important for effector T cell trafficking to inflammatory sites, thus serving to link the acquired immune response to the activation of innate immune cells such as neutrophils and macrophages. The applicant specifically proposes to: (1) determine the role of BLTR1 in antigen generated CD4+ and CD8+ trafficking in vivo; (2) determine the role of BLTR1 in Th1 and Th2 cell trafficking; (3) determine the role of BLTR1 in effector CD8+ cell trafficking in a murine model of Listeria monocytogenes infection; (4) determine if BLTR1 expression defines a unique population of human effector T cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: S. TYPHIMIURIUM ENTEROPATHOGENS
VACCINE
AGAINST
BACTERIAL
Principal Investigator & Institution: Curtiss, Roy Iii.; Professor; Biology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-MAR-2008 Summary: Of the 18.9 million annual deaths (1997) due to infectious diseases, about 2 million are the result of infections by Salmonella and other related bacterial enteropathogens including Escherichia coli and Shigella species, and less closely related enteropathogens such as Vibrio cholerae, Campylobacter jejuni and Listeria monocytogenes. In addition, these bacteria are responsible are responsible for significant morbidity causing diarrheal and systemic diseases that can be transmitted to humans by contamination of food products and/or the water supply and such contamination can be willful. In the belief that improving health, nutrition and economic well-being (the latter dependent on the first two) provide the best means to enhance the quality of life globally and thus reduce conditions that result in warlike and terrorist behavior, we propose a vaccine developmental program based on our recent technical developments in using non-recombinant and recombinant attenuated Salmonella veterinary vaccines to prevent-reduce diarrheal diseases caused by bacterial enteropathogens. Our objectives include: (i) to further genetically modify a strain of Salmonella typhimurium that has been designed to minimize induction of immune responses to serotype-specific antigens and to maximize induction of cross protective immunity to common related antigens of S. enterica strains of diverse serotype and then fully evaluate this modified strain as a vaccine to reduce diarrheal diseases in humans caused by S. enterica serotypes and possibly by other bacterial enteric pathogens, especially Escherichia coli of the EPEC, ETEC and EHEC types and Shigella; (ii) to design, construct and fully evaluate an attenuated derivative of S. paratyphi A, with similar genetic attributes as the S. typhimurium vaccine designed for the same purpose, to induce cross protective immunity in humans to prevent enteric fever and to
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Listeria monocytogenes
significantly reduce diarrheal diseases due to infection by diverse S. enterica serotypes and possibly by other bacterial enteric pathogens, especially E. coli of the EPEC, ETEC and EHEC types and Shigella; (iii) to further genetically modify the S. typhimurium and S. paratyphi A vaccines designed to induce cross protective immunity to also display biological containment so that they are less able to survive in the intestinal tract or in nature and/or die by lysis after approximately ten cell divisions following delivery to the immunized individual; and (iv) to design, construct and evaluate recombinant attenuated Salmonella vaccines, using optimal attributes for immunogenicity, biological containment and antigen delivery, to express antigens to further enhance induction of cross protective immunity to Salmonella-related bacterial enteropathogens or to confer protective immunity to one of the less Salmonella-related enteropathogens. We will also collaboratively work to develop our Master File, prepare and fully characterize candidate vaccine Master Seeds for stability and safety, prepare and submit protocols for IRB approvals, submit information necessary to obtain INDs, and perform any other work needed to arrange that the best candidate vaccines by clinically evaluated in human volunteers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SECRETION MECHANISMS OF LISTERIA MONOCYTOGENES Principal Investigator & Institution: Cheng, Luisa W.; Molecular and Cell Biology; University of California Berkeley Berkeley, Ca 947205940 Timing: Fiscal Year 2002; Project Start 01-JUN-2002 Summary: Listeria spp. are Gram-positive intracellular pathogens that cause severe food-borne diseases in humans. Their pathogenic strategy entails the regulated export of a series of virulence determinants that induce internalization by host cells, phagosomal escape and intracellular cell- cell spreading. However, little is known about the mechanisms for protein secretion in Gram-positive bacteria and no specialized secretion machine for the export of virulence factors has yet been identified. In light of our lack of understanding of these processes, this proposal will address the following questions: 1. What are the Listeria genes required for the secretion of virulence factors? 2. Are there specialized secretion mechanisms responsible for that secretion of virulence factors? Listeria is an excellent model organism for these studies as many molecular and cellular tools are available. The almost complete Listeria genome and availably of relevant animal models will further help us understand Listeria pathogenesis and its interaction with the host. Better understanding of Listeria secretion mechanisms may help us in the identification of better anti-microbial targets, and the development of intracellular delivery vectors for antigens in the fight of not only microbial diseases, but that of human diseases as well. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SIGMA MONOCYTOGENES
B
AND
STRESS
RESPONSE
IN
LISTERIA
Principal Investigator & Institution: Boor, Kathryn J.; Food Science; Cornell University Ithaca Office of Sponsored Programs Ithaca, Ny 14853 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JAN-2007 Summary: (provided by applicant): Listeria monocytogenes (L. m.) causes serious invasive diseases in humans and animals, with a human case mortality rate of approximately 20%. One goal of the US Dept. of Health and Human Services Healthy People 2010 Initiative is to reduce human listeriosis cases by 50%. The long-term
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objective of our research program is to contribute to that end through identification of factors that influence L. m. pathogenesis, which ultimately will enable development of novel and effective intervention strategies for preventing listerial infections. The work proposed in this application is designed to test the specific hypotheses that (i) the sigma/B general stress response system in gram-positive bacterial pathogens (and specifically in L. monocytogenes) provides a key transcriptional regulatory mechanism that facilitates environmental survival and virulence through induction of stress response genes; and that (ii) bacterial stress response systems contribute to pathogenesis by responding to specific environments, including those encountered in the host, through initiation of stress response and virulence gene expression (e.g., prfA). The specific aims of these studies are to: (1) Define the L. m. sigmaB regulon through proteomic and genetic approaches. (2) Determine sigmaB regulon expression patterns under environmental stress conditions, sigma/B -dependent gene expression patterns will be evaluated using microarrays and reporter (-3) Measure sigmaB-dependent gene expression during host cell infection. Reporter fusions to selected sigmaB-dependent genes (e.g., prfA) in wildtype L. m. and selected null mutant strains (e.g., AsigB) will be used to identify gene expression patterns during cellular infection in tissue culture models. (4) Characterize deltasigmaB mutant virulence in tissue culture and animal models. At the conclusion of these studies, we will have developed an understanding of the contribution of cyB and the sigmaB-dependent stress response system to L. monocytogenes environmental survival and infection. More broadly, L. monocytogenes will serve as a model system for examining the role of alternative sigma factor-directed general stress response systems in survival and pathogenesis of gram-positive foodborne pathogens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SYNDECAN AND BACTERIAL TRANSLOCATION IN SHOCK AND TRAUMA Principal Investigator & Institution: Wells, Carol L.; Professor; Lab Medicine and Pathology; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2007 Summary: (provided by applicant): Normal enteric bacteria, such as Escherichia coli and Enterococcus faecalis, frequently cause complicating infections in patients with shock and trauma. A common finding in these patients is increased intestinal epithelial permeability, and experiments with cultured enterocytes have shown that bacterial adherence to and internalization by enterocytes is increased following opening of enterocyte tight junctions, exposing the enterocyte lateral surface. Syndecan-1, expressed on the basolateral surface of human enterocytes, is a cell surface transmembrane proteoglycan that expresses heparan sulfate (HS) on its extracellular domain. Our working hypothesis is that HS chains of cell surface proteoglycans, and specifically syndecan-1, may act as an enterocyte receptor or co-receptor for a variety of enteric bacteria. Preliminary data indicated that,like human enterocytes, HS and syndecan-1 are prominently expressed on the basolateral surface of cultured HT-29 enterocytes but not Caco-2 enterocytes. Experiments with HT-29 enterocytes (designed to open enterocyte tight junctions and interfere with bacterial binding to the HS chains on syndecan-1) suggested that HS may be a receptor for gram-positive but not gram-negative bacteria. The HS analog heparin, and HS itself, inhibited adherence and internalization of grampositive Listeria monocytogenes by HT-29 enterocytes, and experiments with related glycosaminoglycans indicated that this inhibition was specific for HS. Additional
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Listeria monocytogenes
preliminary experiments with HT-29 enterocytes indicated that heparin and HS similarly inhibited internalization of gram-positive E. faecalis and Staphylococcus aureus, but not gram-negative Salmonella typhimurium, Proteus mirabilis, and E. coli. Heparin did not have a noticeable effect on internalization of any bacterial species using Caco-2 enterocytes, which express low levels of HS and syndecan-1 Other preliminary experiments indicated that heparin-treated L. monocytogenes was less invasive in orally inoculated mice than was untreated L monocytogenes. In this proposal several experimental tools are used to clarify the interactions of cultured enterocytes with a variety of gram-negative bacteria, while focusing on gram-positive L. monocytogenes, E. faecalis, and S. aureus. These tools include monoclonal antibodies, glycosamino glycans, and heparin disaccharides, and two cell lines transfected to over express syndecan-1, namely ARH-77 myeloma cells and Caco-2 enterocytes. Data from in vitro studies are used to design experiments in mice (outbred and syndecan-1 knockout) to clarify the role of HS and syndecan-1 in intestinal colonization and extra intestinal dissemination of enteric bacteria. Data from these experiments may indicate that enterocytes have a receptor (related to cell surface HS and perhaps syndecan-1) involved in adherence and internalization of a variety of gram-positive bacteria including E. faecalis and S. aureus. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: T CELL- MEDIATED IMMUNITY TO MYCOBACTERIAL INFECTION Principal Investigator & Institution: Williams, Matthew A.; Immunology; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2006 Summary: provided by the applicant): Acute infection of mice with intracellular pathogens such as Vaccinia virus (W) and Listeria monocytogenes (LM) results in potent T cell responses, rapid clearance of the pathogen, and the establishment of longlived memory. In contrast, Mycobacterium bovis bacillus Calmette-Guerin (BCG) persists in the face of detectable CD4 and CD8 T cell responses, with much less known about their relative size, duration, and ability to generate memory. A key advance in the study of LM and W has been the generation of recombinant pathogens expressing model antigens such as chicken ovalbumin (OVA). Combined with the use of TCR transgenic T cells specific for Class I- and Class II-restricted OVA epitopes, these recombinants have helped facilitate the characterization of in vivo immune responses to acute infection. We propose to: 1) adapt this technology to characterize antimycobacterial T cell responses by the creation of a BCG-OVA recombinant; 2) dissect underlying differences of T cell responses in their ability to generate sterilizing, protective immunity to chronically infecting intracellular pathogens such as BCG and acutely infecting pathogens such as LM and W; and 3) assess the activation, expansion, and protective capacity of mycobacteria-specific memory CD4 and/or CD8 T cells following infection. An enhanced understanding of how immune responses to these infections differ will provide insight into the mechanisms governing the generation of optimal CD4 and CD8 T cell responses in vivo. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TARGETED OLIGONUCLEOTIDE
CYTOSOLIC
DELIVERY
OF
ANTISENSE
Principal Investigator & Institution: Lee, Kyung-Dall D.; Associate Professor; Pharmaceutical Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274
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Timing: Fiscal Year 2002; Project Start 01-MAR-2001; Project End 28-FEB-2005 Summary: (Verbatim from Applicant's Abstract): Nucleic acid-based drugs have recently emerged as powerful solutions to many of medicine's most enduring problems. These therapeutic agents, and antisense oligodeoxynucleotides (ODN) in particular, possess enormous potential to complement or replace conventional pharmaceutical therapies based traditionally on small molecular weight drugs. With the uncanny ability to selectively downregulate the expression level of a specific protein, antisense ODN can modulate disease states in a highly specialized manner. Recent efforts to enhance ODN stability and advances in the selection method and design of effective ODN sequences have produced ODN molecules that are increasingly potent once delivered to their site of action in the cytosol or the nucleus. Despite the outstanding pharmacological characteristics, their full potential awaits resolution of critical pharmaceutical challenges, due primarily to the low membrane permeability of ODN molecules. Similar to the difficulties facing gene therapy in general, the success of ODN drug therapies relies on delivery to specific cell types at high enough concentrations, followed by efficient cellular uptake and transport into the cytoplasm of the cells. This proposal takes two main approaches to address these delivery problems. First, a listeriolysin O (LLO)-containing liposomal delivery system will be utilized to overcome the membrane barrier for cytosolic delivery. LLO, the hemolysin of Listeria monocytogenes, confers upon the lipsome formulation the mechanism that is utilized by Listeria to escape the endosomal/lysosomal degradation pathway and enter the cytosol. Second, the LLOliposomes carrying ICAM1 or B7-1/2 specific antisense ODN will be targeted to antigen presenting cells (APC) by conjugating a targeting motif, CTLA4Ig, onto the liposomes. CTLA4Ig, a high affinity, competitive ligand for the B7 molecules on the surface of APC, has been shown to block the essential, CD28/B7-mediated co-stimulatory signal for T cell activation. The effectiveness of B7-specific antisense ODN delivered by this targeted cytosolic delivery vehicle, the CTLA4Ig-conjugated LLO-liposomes, will be assessed for efficient inhibition of alloreactive immune responses using the mixed lymphocyte reaction assay. Several approaches will be taken to optimize various parameters for achieving the special balance of long circulation and targeting of CTLA4Ig-liposomes in vivo. The results will then be extended to in vivo mouse models of transplantation. Efficient blockade of the T cell co-stimulatory signal at multiple levels, as rendered by the ODN delivery systsem characterized and developed in this project, is an ideal modality of immunosuppressive treatments for transplant recipients. Development of such a delivery strategy for ODN can be further generalized beyond immune response modulation to a wide range of diseases mediated by specific proteins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: T-CELL DEPENDENT IMMUNE RESPONSES AND ETHANOL Principal Investigator & Institution: Cook, Robert T.; Professor; Pathology; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): This work is part of a long-term strategy to define the alterations leading to the immunologic abnormalities of the alcoholic. In addition to the widely reported clinical immune deficiency and disorders with possible autoimmune origins, we and others have demonstrated that chronic alcoholics have (a) persistently activated T lymphocytes, (b) lymphocyte fine subset losses in B cells, T cells, and NK cells, (c) monocyte activation, and (d) a range of functional changes in vivo and in vitro. We now propose five interactive projects (IRPG) to evaluate chronic ethanol effects on innate and adaptive immune system components and the interactions of both
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Listeria monocytogenes
with infectious disease agents. In brief, the projects are: (1) T cell dependent immune responses and ethanol; (2) Effect of ethanol on the murine B cell compartment; (3) Dendritic cell function and ethanol; (4) Natural killer cells and ethanol; (5) The role of immune responses in alcoholic liver disease. A key feature of all projects is the use of a model of chronic ethanol administration which we have shown to be well tolerated by mice, can be administered for prolonged periods of time proportional to that seen in humans, and importantly, produces changes similar in many immunologic parameters to changes observed in chronic human alcoholics. This project, (1) T-cell dependent immune responses and ethanol, will investigate T cell dependent alterations by chronic ethanol exposure. We have shown elsewhere that chronic ethanol mice have activated T cells. The literature clearly shows that alcoholics have diminished T dependent immunity, and we have found in preliminary data that mice exposed to chronic ethanol have both decreased antigen-specific T cell responses to Listeria monocytogenes LLO antigen, and altered T dependent humoral response to TNP-KLH. We now propose to evaluate both CD4+ and CD8+ T cell antigen-specific responses to Listeria antigens after prolonged ethanol ingestion, the effect of boosting immunizations and withdrawal on these ethanol-diminished responses, and several experimental protocols to evaluate memory cell survival in chronic ethanol exposure. In other experiments, the effect of chronic ethanol on TH1 and TH2-driven humoral responses will be measured, in both TH1- and TH2-dominant mice. Experiments to distinguish clearly whether T cells from chronic ethanol mice have diminished capacity to respond to normal peptide-loaded bone marrow dendritic cells will be carried out both in vitro and in vivo. DNA vaccines encoding the Listeria LLO protein will be used to attempt to boost ethanol-diminished antigen-specific T cell responses, and to increase both memory cells and antigen-specific cytolytic T cell responses, which are important in protection. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE A2B1 INTEGRIN: INNATE IMMUNITY TO PATHOGENS & TUMORS Principal Investigator & Institution: Zutter, Mary M.; Professor; Pathology and Immunology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 01-JAN-2003; Project End 30-JUN-2003 Summary: (provided by applicant): The a2a1 integrin is a collagen/laminin receptor expressed on platelets, endothelial cells, fibroblasts, epithelial cells, and subsets of leukocytes. To define the role of the a2a1 integrin in vivo, we created a genetically engineered mouse in which expression of the a2a1 integrin was completely eliminated. Mice deficient in the a2a1 integrin are viable and fertile and develop relatively normally. Quantitative analysis of mammary gland branching morphogenesis demonstrated that branching complexity is markedly diminished in the a2-deficient animals. Although the a2-deficient mice do not manifest a bleed diathesis, platelets from a2-null mice fail to adhere to type I collagen under either static or shear-stress conditions. The a2a1 integrin-null mouse thus exhibits diverse, sometimes subtle, phenotypes consistent with the widespread pattern of integrin expression. Leukocyte integrins are required for development and activation of the immune system and for leukocyte migration to sites of injury, infection, and tumor formation. The a2a1 integrin has not previously been considered to play a major role in immune function. Our exciting preliminary data clearly demonstrate that the a2a1 integrin is required for innate immunity to infectious organisms and possibly tumors. This proposal will directly address the hypothesis that a2a1 integrin expression is required for innate immune function. The specific aims are (1) To define the role of the a2a1 integrin in the immune response to bacteria using
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Listeria monocytogenes as a model. (2) To define the mechanisms involved in a2a1 integrin mediated immune response to MCMV infection. (3) To determine whether the a2a1 integrin plays a role in tumor immunoediting. In summary, this proposal will determine the role of the a2a1 integrin expression in the innate immune response to bacteria, viruses, and tumors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE ROLE OF H2-M3 IN T CELL DEVELOPMENT AND IMMUNITY Principal Investigator & Institution: Wang, Chyung-Ru; Associate Professor; Pathology; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2002; Project Start 01-JUL-1996; Project End 31-MAY-2006 Summary: (provided by applicant): H2-M3 is an MHC class Ib molecule which preferentially binds N-Formylated peptides. Since all prokaryotes initiate protein synthesis with N-formylated methionine, the peptide binding specificity of M3 is especially suited for presenting these unique microbial antigens to T cells. Consistent with this notion, mice infected with Listeria monocytogenes, generate CD8+ CTLs that recognize N-formylated Listeria peptides presented by M3. Recent studies have shown that M3-restricted T cells expand rapidly during primary Listeria infection, prior to the expansion of class Ia-restricted T cells. However, the expansion of M3-restricted T cells following secondary Listeria infection was rather limited compared with the vigorous recall response of class Ia-restricted T cells. The mechanisms underlying the distinct kinetics of the M3-restricted response are not clear and the significance of M3-restricted T cells in bacterial infection remains to be defined. This application seeks to understand how M3 presents bacterial antigens and how M3 contributes to shaping the T cell repertoire during bacterial infections. First, we will use biochemical and cell biology approaches to examine the structural requirements for controlling intracellular trafficking of M3 and to elucidate the pathway for presentation of both endogenous and exogenous listerial antigens by M3. Secondly, we will compare T cell development in the M3-deficient and control mice to determine whether M3 is responsible for selecting unique subset(s) of T cells. Adoptive transfer of naive and memory T cells from D7 transgenic mice, expressing TCR specific for M3/LemA complexes, will be performed to investigate whether M3-restricted T cells have requirements similar to class Ia-restricted T cells for the maintenance of the periphery T cell pools. Thirdly, we will infect M3deficient, class Ia-deficient and control mice with Listeria to examine the relative contribution of class Ia-restricted and M3-restricted responses during Listeria infection, and to determine whether lack of an early M3 response could alter the kinetics and magnitude of class Ia-restricted response. Finally, we will extend our study to explore the functional role of M3-restricted T cells in immunity against Mycobaterium tuberculosis. Study of M3-restricted T cells responses against two distinct groups of intracellular bacteria would shed light on whether early and potent M3-restricted T cell response is unique to Listeria infection or is a general host defense mechanism against intracellular bacterial infection. Understanding the inter-relationship between class Iarestricted and class Ib-restricted responses during the generation of specific immunity may facilitate the development of more effective vaccines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE ROLE OF PROFILIN IN LISTERIA ACTIN-BASED MOTILITY Principal Investigator & Institution: Larson, Laura L.; Medicine; University of Florida Gainesville, Fl 32611
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Timing: Fiscal Year 2002; Project Start 28-FEB-2002 Summary: Listeria monocytogenes is able to spread from cell-to-cell by utilizing the host-cell's mechanism of actin polymerization to propel it through the cytoplasm. Despite years of extensive investigation, this mechanism is still poorly understood, and the roles of several actin regulatory proteins have yet to be established. The function of one of these proteins, profilin, remains controversial. We propose that profilin plays a critical role in actin-based motility in Listeria and must be concentrated on the surface of the bacterium to support the rapid rates of actin assembly associated with the migration of Listeria through the host-cell cytoplasm. We believe that the profilin-actin complex is the preferred species for addition of actin monomers to the growing actin filament. To that end, we will study the function of this complex utilizing two experimental approaches. In the first approach, we will introduce profilin, actin, profilin-actin complex, or mutated profilin-actin complex into PtK2 cells infected with Listeria. We expect than the addition of the profilin-actin complex will enhance bacterial motility more than the other additions. To complement these experiments, we will also introduce the same proteins into profilin-depleted Xenopus egg extracts supporting Listeria. In cell-free model, we also expect the profilin-actin complex to be the most effective component restoring bacterial motility. Finally, we will explore the interaction of profilin with other proteins found in the actin polymerization zone using fluorescent energy transfer. These investigations are central in determining the role of profilin in actin- based motility of Listeria, which will provide further insight into how this bacteria causes disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: USE OF LISTERIA AS COLON CANCER VACCINE ADJUVANTS Principal Investigator & Institution: Giedlin, Martin A.; Cerus Corporation 2411 Stanwell Dr Concord, Ca 945204810 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 30-SEP-2003 Summary: (provided by the applicant): Colorectal cancer is the second leading cause of cancer death in the US. There is a 40 percent recurrence in patients treated surgically. Patients with distal metastatic disease have a low 5 yr survival rate with current chemotherapy. Therefore there is a critical need for improved options in the adjuvant setting. The principal goal of this SBIR Phase I proposal is to identify a panel of attenuated Listeria monocytogenes (Listeria) strains that can potentiate the immune response to cellular vaccines for colon cancer. Preliminary studies have suggested that Listeria administered following a therapeutic vaccination can target anti-tumor immune response specifically to liver metastases in a murine model of metastatic colon cancer, increasing the effectiveness of the vaccine by almost 5-fold. The various Listeria strains will be screened for relative pathogenicity and immunogenicity that characterize the innate and adaptive immune response. The immune response to these strains will also be assessed in the murine colorectal liver metastasis model. Appropriate attenuated strains of Listeria will be constructed to secrete GM-CSF and be evaluated for their ability to further augment the immune response to the vaccine in mice. Ultimately, this work will lead to novel adjuvant approaches to treating patients with advanced colon cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: USING DROSPHILA MACROPHAGES TO STUDY INNATE IMMUNITY Principal Investigator & Institution: Schneider, David S.; Assistant Professor; Microbiology and Immunology; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2003; Project Start 01-DEC-2002; Project End 30-NOV-2007 Summary: (provided by applicant): Infections caused by such intracellular pathogens as mycobacteria, Salmonella, and Listeria annually claim millions of lives worldwide. This proposal develops the fruit fly, Drosophila melanogaster as a model organism to study these infections. Mutations in both the host and pathogens will be tested. The fruit fly has been used previously to study innate immune responses to gram positive and negative bacteria as well as fungi. Past work focused only on microorganisms that grow freely in the extracellular space. This proposal describes experiments that will use Drosophila to study intracellular infections of macrophages. Growth characteristics including growth rate, lethality and location will be measured for several bacteria that cause infections of Drosophila macrophages (Mycobacterium marinum, Salmonella typhimurium, Listeria monocytogenes). Drosophila mutants expected to have difficulty fighting intracellular pathogens will be tested for their ability to defend against intracellular infections. Salmonella typhimurium mutants will be tested for their ability to infect the fly, to determine the role bacterial genes play in virulence. These experiments will provide tools to analyze a collection of Drosophila mutants isolated based upon a phenotype that is likely to involve the cellular immune response. 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 “Listeria monocytogenes” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for Listeria monocytogenes in the PubMed Central database: •
16S rRNA-based probes and polymerase chain reaction method to detect Listeria monocytogenes cells added to foods. by Wang RF, Cao WW, Johnson MG.; 1992 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183014
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A di- and tripeptide transport system can supply Listeria monocytogenes Scott A with amino acids essential for growth. by Verheul A, Hagting A, Amezaga MR, Booth IR, Rombouts FM, Abee T.; 1995 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167277
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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A Homolog of CcpA Mediates Catabolite Control in Listeria monocytogenes but Not Carbon Source Regulation of Virulence Genes. by Behari J, Youngman P.; 1998 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=107718
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A mutant of Listeria monocytogenes LO28 unable to induce an acid tolerance response displays diminished virulence in a murine model. by Marron L, Emerson N, Gahan CG, Hill C.; 1997 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168821
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A new method for direct detection of Listeria monocytogenes from foods by PCR. by Makino S, Okada Y, Maruyama T.; 1995 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167673
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A nonvirulent mutant of Listeria monocytogenes does not move intracellularly but still induces polymerization of actin. by Kuhn M, Prevost MC, Mounier J, Sansonetti PJ.; 1990 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313686
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A Novel Serotype-Specific Gene Cassette (gltA-gltB) Is Required for Expression of Teichoic Acid-Associated Surface Antigens in Listeria monocytogenes of Serotype 4b. by Lei XH, Fiedler F, Lan Z, Kathariou S.; 2001 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=94985
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A novel strictly anaerobic recovery and enrichment system incorporating lithium for detection of heat-injured Listeria monocytogenes in pasteurized milk containing background microflora. by Mendonca AF, Knabel SJ.; 1994 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201928
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A nucleic acid sequence-based amplification system for detection of Listeria monocytogenes hlyA sequences. by Blais BW, Turner G, Sooknanan R, Malek LT.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168321
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A Pediocin-Producing Lactobacillus plantarum Strain Inhibits Listeria monocytogenes in a Multispecies Cheese Surface Microbial Ripening Consortium. by Loessner M, Guenther S, Steffan S, Scherer S.; 2003 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150062
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A recombinant minigene vaccine containing a nonameric cytotoxic-T-lymphocyte epitope confers limited protection against Listeria monocytogenes infection. by An LL, Pamer E, Whitton JL.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173980
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A ribosomal DNA fragment of Listeria monocytogenes and its use as a genus-specific probe in an aqueous-phase hybridization assay. by Emond E, Fliss I, Pandian S.; 1993 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182340
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A simple RNA probe system for analysis of Listeria monocytogenes polymerase chain reaction products. by Blais BW, Phillippe LM.; 1993 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182368
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Adaptation to sublethal environmental stresses protects Listeria monocytogenes against lethal preservation factors. by Lou Y, Yousef AE.; 1997 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168417
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Adhesion, Invasion, and Translocation Characteristics of Listeria monocytogenes Serotypes in Caco-2 Cell and Mouse Models. by Jaradat ZW, Bhunia AK.; 2003 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=161501
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Administration of Superantigens Protects Mice from Lethal Listeria monocytogenes Infection by Enhancing Cytotoxic T Cells. by Okamoto S, Kawabata S, Nakagawa I, Hamada S.; 2001 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=100037
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Analysis of clinical and food-borne isolates of Listeria monocytogenes in the United States by multilocus enzyme electrophoresis and application of the method to epidemiologic investigations. by Bibb WF, Gellin BG, Weaver R, Schwartz B, Plikaytis BD, Reeves MW, Pinner RW, Broome CV.; 1990 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184572
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Antibacterial activity of hen egg white lysozyme against Listeria monocytogenes Scott A in foods. by Hughey VL, Wilger PA, Johnson EA.; 1989 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184171
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Antibodies against Listerial Protein 60 Act as an Opsonin for Phagocytosis of Listeria monocytogenes by Human Dendritic Cells. by Kolb-Maurer A, Pilgrim S, Kampgen E, McLellan AD, Brocker EB, Goebel W, Gentschev I.; 2001 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98265
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Antimicrobial Activities against 84 Listeria monocytogenes Isolates from Patients with Systemic Listeriosis at a Comprehensive Cancer Center (1955-1997). by Safdar A, Armstrong D.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149630
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Application of 5[prime prime or minute]-Nuclease PCR for Quantitative Detection of Listeria monocytogenes in Pure Cultures, Water, Skim Milk, and Unpasteurized Whole Milk. by Nogva HK, Rudi K, Naterstad K, Holck A, Lillehaug D.; 2000 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92295
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Application of multilocus enzyme electrophoresis and restriction fragment length polymorphism analysis to the typing of Listeria monocytogenes strains isolated from raw milk, nondairy foods, and clinical and veterinary sources. by Harvey J, Gilmour A.; 1994 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201515
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Application of multilocus enzyme electrophoresis in studies of the epidemiology of Listeria monocytogenes in Denmark. by Norrung B, Skovgaard N.; 1993 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182371
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Assessment of Photodynamic Destruction of Escherichia coli O157:H7 and Listeria monocytogenes by Using ATP Bioluminescence. by Romanova NA, Brovko LY, Moore L, Pometun E, Savitsky AP, Ugarova NN, Griffiths MW.; 2003 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=262251
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Assessment of the Accuprobe Listeria monocytogenes culture identification reagent kit for rapid colony confirmation and its application in various enrichment broths. by Ninet B, Bannerman E, Bille J.; 1992 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183227
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Attachment of Listeria monocytogenes to Radish Tissue Is Dependent upon Temperature and Flagellar Motility. by Gorski L, Palumbo JD, Mandrell RE.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152467
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Automated Ribotyping Using Different Enzymes To Improve Discrimination of Listeria monocytogenes Isolates, with a Particular Focus on Serotype 4b Strains. by De Cesare A, Bruce JL, Dambaugh TR, Guerzoni ME, Wiedmann M.; 2001 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=88281
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Behavior of Listeria monocytogenes during fabrication and storage of experimentally contaminated smoked salmon. by Guyer S, Jemmi T.; 1991 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182979
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Behavior of Listeria monocytogenes in wiener exudates in the presence of Pediococcus acidilactici H or pediocin AcH during storage at 4 or 25 degrees C. by Yousef AE, Luchansky JB, Degnan AJ, Doyle MP.; 1991 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182970
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Betaine and L-carnitine transport by Listeria monocytogenes Scott A in response to osmotic signals. by Verheul A, Glaasker E, Poolman B, Abee T.; 1997 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=179637
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Bile Stress Response in Listeria monocytogenes LO28: Adaptation, Cross-Protection, and Identification of Genetic Loci Involved in Bile Resistance. by Begley M, Gahan CG, Hill C.; 2002 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=134417
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Biocontrol of Listeria monocytogenes on Fresh-Cut Produce by Treatment with Lytic Bacteriophages and a Bacteriocin. by Leverentz B, Conway WS, Camp MJ, Janisiewicz WJ, Abuladze T, Yang M, Saftner R, Sulakvelidze A.; 2003 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=169090
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Biological inactivation of adhering Listeria monocytogenes by listeriaphages and a quaternary ammonium compound. by Roy B, Ackermann HW, Pandian S, Picard G, Goulet J.; 1993 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182386
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Catalase, superoxide dismutase, and hemolysin activities and heat susceptibility of Listeria monocytogenes after growth in media containing sodium chloride. by Dallmier AW, Martin SE.; 1990 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184847
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CD8 + T-Cell Priming against a Nonsecreted Listeria monocytogenes Antigen Is Independent of the Antimicrobial Activities of Gamma Interferon. by Tvinnereim AR, Harty JT.; 2000 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97404
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CD8 +-T-Cell Response to Secreted and Nonsecreted Antigens Delivered by Recombinant Listeria monocytogenes during Secondary Infection. by Tvinnereim AR, Hamilton SE, Harty JT.; 2002 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=127606
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Cell Wall Teichoic Acid Glycosylation in Listeria monocytogenes Serotype 4b Requires gtcA, a Novel, Serogroup-Specific Gene. by Promadej N, Fiedler F, Cossart P, Dramsi S, Kathariou S.; 1999 Jan 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=93394
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Changes in cell morphology of Listeria monocytogenes and Shewanella putrefaciens resulting from the action of protamine. by Johansen C, Gill T, Gram L.; 1996 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167869
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Changes in serum colony-stimulating factor and monocytic progenitor cells during Listeria monocytogenes infection in mice. by Wing EJ, Waheed A, Shadduck RK.; 1984 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=263297
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Characterization and Pathogenic Potential of Listeria monocytogenes Isolates from the Smoked Fish Industry. by Norton DM, Scarlett JM, Horton K, Sue D, Thimothe J, Boor KJ, Wiedmann M.; 2001 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92631
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Characterization by DNA restriction endonuclease analysis of Listeria monocytogenes strains related to the Swiss epidemic of listeriosis. by Nocera D, Bannerman E, Rocourt J, Jaton-Ogay K, Bille J.; 1990 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=268158
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Characterization of a Listeria monocytogenes Scott A Isolate with High Tolerance towards High Hydrostatic Pressure. by Karatzas KA, Bennik MH.; 2002 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126791
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Characterization of an aromatic amino acid-dependent Listeria monocytogenes mutant: attenuation, persistence, and ability to induce protective immunity in mice. by Alexander JE, Andrew PW, Jones D, Roberts IS.; 1993 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=280833
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Characterization of an Extracellular Virulence Factor Made by Group A Streptococcus with Homology to the Listeria monocytogenes Internalin Family of Proteins. by Reid SD, Montgomery AG, Voyich JM, DeLeo FR, Lei B, Ireland RM, Green NM, Liu M, Lukomski S, Musser JM.; 2003 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=308899
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Characterization of five esterases from Listeria monocytogenes and use of their electrophoretic polymorphism for strain typing. by Gilot P, Andre P.; 1995 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167427
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Characterization of Glycine Betaine Porter I from Listeria monocytogenes and Its Roles in Salt and Chill Tolerance. by Mendum ML, Smith LT.; 2002 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126668
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Characterization of Listeria monocytogenes isolated from poultry products and from the poultry-processing environment by random amplification of polymorphic DNA and multilocus enzyme electrophoresis. by Lawrence LM, Gilmour A.; 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167487
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Characterization of Listeria monocytogenes isolates by esterase electrophoresis. by Harvey J, Gilmour A.; 1996 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167918
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Characterization of Listeria monocytogenes pathogenesis in a strain expressing perfringolysin O in place of listeriolysin O. by Jones S, Portnoy DA.; 1994 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=303309
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Characterization of Listeria monocytogenes Strains Involved in Invasive and Noninvasive Listeriosis Outbreaks by PCR-Based Fingerprinting Techniques. by Franciosa G, Tartaro S, Wedell-Neergaard C, Aureli P.; 2001 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92799
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Characterization of Recurrent and Sporadic Listeria monocytogenes Isolates from Raw Milk and Nondairy Foods by Pulsed-Field Gel Electrophoresis, Monocin Typing, Plasmid Profiling, and Cadmium and Antibiotic Resistance Determination. by Harvey J, Gilmour A.; 2001 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92656
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Chemical composition and biological functions of Listeria monocytogenes cell wall preparations. by Hether NW, Campbell PA, Baker LA, Jackson LL.; 1983 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=348071
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Chemokine Receptor 5 Is Dispensable for Innate and Adaptive Immune Responses to Listeria monocytogenes Infection. by Zhong MX, Kuziel WA, Pamer EG, Serbina NV.; 2004 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=321636
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Cloning and Expression of the Listeria monocytogenes Scott A ptsH and ptsI Genes, Coding for HPr and Enzyme I, Respectively, of the Phosphotransferase System. by Christensen DP, Benson AK, Hutkins RW.; 1998 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=106702
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Cloning of a gene encoding a major secreted polypeptide of Listeria monocytogenes and its potential use as a species-specific probe. by Flamm RK, Hinrichs DJ, Thomashow MF.; 1989 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203064
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Cloning of rel from Listeria monocytogenes as an Osmotolerance Involvement Gene. by Okada Y, Makino SI, Tobe T, Okada N, Yamazaki S.; 2002 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123880
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clpB, a Novel Member of the Listeria monocytogenes CtsR Regulon, Is Involved in Virulence but Not in General Stress Tolerance. by Chastanet A, Derre I, Nair S, Msadek T.; 2004 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=344206
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Cold stress proteins induced in Listeria monocytogenes in response to temperature downshock and growth at low temperatures. by Bayles DO, Annous BA, Wilkinson BJ.; 1996 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167876
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Collapse of the proton motive force in Listeria monocytogenes caused by a bacteriocin produced by Pediococcus acidilactici. by Christensen DP, Hutkins RW.; 1992 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183096
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Colony-Stimulating Factor 1-Dependent Cells Protect against Systemic Infection with Listeria monocytogenes but Facilitate Neuroinvasion. by Jin Y, Dons L, Kristensson K, Rottenberg ME.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128173
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Comparative Analysis of Multilocus Sequence Typing and Pulsed-Field Gel Electrophoresis for Characterizing Listeria monocytogenes Strains Isolated from Environmental and Clinical Sources. by Revazishvili T, Kotetishvili M, Stine OC, Kreger AS, Morris JG Jr, Sulakvelidze A.; 2004 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=321703
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Comparison of cold enrichment and U.S. Department of Agriculture methods for isolating Listeria monocytogenes from naturally contaminated foods. The Listeria Study Group. by Hayes PS, Graves LM, Ajello GW, Swaminathan B, Weaver RE, Wenger JD, Schuchat A, Broome CV.; 1991 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183536
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Comparison of Host Resistance to Primary and Secondary Listeria monocytogenes Infections in Mice by Intranasal and Intravenous Routes. by Mizuki M, Nakane A, Sekikawa K, Tagawa YI, Iwakura Y.; 2002 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128264
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Comparison of media and methods for detecting and enumerating Listeria monocytogenes in refrigerated cabbage. by Hao DY, Beuchat LR, Brackett RE.; 1987 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203793
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Comparison of methods for discrimination between strains of Listeria monocytogenes from epidemiological surveys. by Baloga AO, Harlander SK.; 1991 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183571
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Comparison of ribotyping and multilocus enzyme electrophoresis for subtyping of Listeria monocytogenes isolates. by Graves LM, Swaminathan B, Reeves MW, Hunter SB, Weaver RE, Plikaytis BD, Schuchat A.; 1994 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=264203
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Construction of the temperature-sensitive vectors pLUCH80 and pLUCH88 for delivery of Tn917::NotI/SmaI and use of these vectors to derive a circular map of Listeria monocytogenes Scott A, a serotype 4b isolate. by He W, Luchansky JB.; 1997 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168654
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Construction, Characterization, and Use of Two Listeria monocytogenes Site-Specific Phage Integration Vectors. by Lauer P, Chow MY, Loessner MJ, Portnoy DA, Calendar R.; 2002 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=135211
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Control of natural killer cell-mediated innate resistance against the intracellular pathogen Listeria monocytogenes by gamma/delta T lymphocytes. by Ladel CH, Blum C, Kaufmann SH.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173987
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Coordinate regulation of virulence genes in Listeria monocytogenes requires the product of the prfA gene. by Chakraborty T, Leimeister-Wachter M, Domann E, Hartl M, Goebel W, Nichterlein T, Notermans S.; 1992 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=205751
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Correlation of bioenergetic parameters with cell death in Listeria monocytogenes cells exposed to nisin. by Winkowski K, Bruno ME, Montville TJ.; 1994 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201958
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Critical role of anteiso-C15:0 fatty acid in the growth of Listeria monocytogenes at low temperatures. by Annous BA, Becker LA, Bayles DO, Labeda DP, Wilkinson BJ.; 1997 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168698
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Depletion of proton motive force by nisin in Listeria monocytogenes cells. by Bruno ME, Kaiser A, Montville TJ.; 1992 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195764
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Detection of a prfA-independent promoter responsible for listeriolysin gene expression in mutant Listeria monocytogenes strains lacking the PrfA regulator. by Domann E, Wehland J, Niebuhr K, Haffner C, Leimeister-Wachter M, Chakraborty T.; 1993 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=280962
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Detection of hemolytic Listeria monocytogenes by using DNA colony hybridization. by Datta AR, Wentz BA, Hill WE.; 1987 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=204091
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Detection of Listeria monocytogenes by direct colony hybridization on hydrophobic grid-membrane filters by using a chromogen-labeled DNA probe. by Peterkin PI, Idziak ES, Sharpe AN.; 1991 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182753
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Detection of Listeria monocytogenes by using the polymerase chain reaction. by Bessesen MT, Luo QA, Rotbart HA, Blaser MJ, Ellison RT 3rd.; 1990 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184869
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Detection of Listeria monocytogenes from a Model Food by Fluorescence Resonance Energy Transfer-Based PCR with an Asymmetric Fluorogenic Probe Set. by Koo K, Jaykus LA.; 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=143584
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Detection of Listeria monocytogenes in cheese with the magnetic immunopolymerase chain reaction assay. by Fluit AC, Torensma R, Visser MJ, Aarsman CJ, Poppelier MJ, Keller BH, Klapwijk P, Verhoef J.; 1993 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182079
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Detection of Listeria monocytogenes in foods by immunomagnetic separation. by Skjerve E, Rorvik LM, Olsvik O.; 1990 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184991
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Detection of Listeria monocytogenes with a nonisotopic polymerase chain reactioncoupled ligase chain reaction assay. by Wiedmann M, Barany F, Batt CA.; 1993 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182352
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Detection of multiple virulence-associated genes of Listeria monocytogenes by PCR in artificially contaminated milk samples. by Cooray KJ, Nishibori T, Xiong H, Matsuyama T, Fujita M, Mitsuyama M.; 1994 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201759
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Detection of Salmonella spp. and Listeria monocytogenes in Suspended Organic Waste by Nucleic Acid Extraction and PCR. by Burtscher C, Fall PA, Wilderer PA, Wuertz S.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91323
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Detection of Viable Listeria monocytogenes with a 5[prime prime or minute] Nuclease PCR Assay. by Norton DM, Batt CA.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91307
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Determination of virulence of different strains of Listeria monocytogenes and Listeria innocua by oral inoculation of pregnant mice. by Lammerding AM, Glass KA, Gendron-Fitzpatrick A, Doyle MP.; 1992 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183216
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Development of a Competitive Index Assay To Evaluate the Virulence of Listeria monocytogenes actA Mutants during Primary and Secondary Infection of Mice. by Auerbuch V, Lenz LL, Portnoy DA.; 2001 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98721
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Development of a Listeria monocytogenes EGDe Partial Proteome Reference Map and Comparison with the Protein Profiles of Food Isolates. by Ramnath M, Rechinger KB, Jansch L, Hastings JW, Knochel S, Gravesen A.; 2003 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=161492
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Development of a Multilocus Sequence Typing Method for Analysis of Listeria monocytogenes Clones. by Salcedo C, Arreaza L, Alcala B, de la Fuente L, Vazquez JA.; 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149676
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Development of a repair-enrichment broth for resuscitation of heat-injured Listeria monocytogenes and Listeria innocua. by Busch SV, Donnelly CW.; 1992 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195165
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Development of polymerase chain reaction assays for detection of Listeria monocytogenes in clinical cerebrospinal fluid samples. by Jaton K, Sahli R, Bille J.; 1992 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=265418
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Diagnosis and epidemiological association of Listeria monocytogenes strains in two outbreaks of listerial encephalitis in small ruminants. by Wiedmann M, Czajka J, Bsat N, Bodis M, Smith MC, Divers TJ, Batt CA.; 1994 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=267168
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Differences in Gamma Interferon Production Induced by Listeriolysin O and Ivanolysin O Result in Different Levels of Protective Immunity in Mice Infected with Listeria monocytogenes and Listeria ivanovii. by Kimoto T, Kawamura I, Kohda C, Nomura T, Tsuchiya K, Ito Y, Watanabe I, Kaku T, Setianingrum E, Mitsuyama M.; 2003 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153848
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Differences in virulence and in expression of PrfA and PrfA-regulated virulence genes of Listeria monocytogenes strains belonging to serogroup 4. by Sokolovic Z, Schuller S, Bohne J, Baur A, Rdest U, Dickneite C, Nichterlein T, Goebel W.; 1996 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=174330
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Differential activation of virulence gene expression by PrfA, the Listeria monocytogenes virulence regulator. by Sheehan B, Klarsfeld A, Msadek T, Cossart P.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=177497
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Differentiation of epidemic-associated strains of Listeria monocytogenes by restriction fragment length polymorphism in a gene region essential for growth at low temperatures (4 degrees C). by Zheng W, Kathariou S.; 1995 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167742
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Differentiation of Listeria monocytogenes and Listeria innocua by 16S rRNA genes and intraspecies discrimination of Listeria monocytogenes strains by random amplified polymorphic DNA polymorphisms. by Czajka J, Bsat N, Piani M, Russ W, Sultana K, Wiedmann M, Whitaker R, Batt CA.; 1993 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202095
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Direct detection of Listeria monocytogenes in 25 milliliters of raw milk by a two-step PCR with nested primers. by Herman LM, De Block JH, Moermans RJ.; 1995 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167343
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Discrimination of Listeria monocytogenes from other Listeria species by ligase chain reaction. by Wiedmann M, Czajka J, Barany F, Batt CA.; 1992 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183127
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Disruption of Putative Regulatory Loci in Listeria monocytogenes Demonstrates a Significant Role for Fur and PerR in Virulence. by Rea RB, Gahan CG, Hill C.; 2004 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=321596
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Division of Listeria monocytogenes Serovar 1/2a Strains into Two Groups by PCR and Restriction Enzyme Analysis. by Unnerstad H, Nilsson I, Ericsson H, DanielssonTham ML, Bille J, Bannerman E, Tham W.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91297
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Division of Listeria monocytogenes serovar 4b strains into two groups by PCR and restriction enzyme analysis. by Ericsson H, Stalhandske P, Danielsson-Tham ML, Bannerman E, Bille J, Jacquet C, Rocourt J, Tham W.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167691
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DNA fragments from regions involved in surface antigen expression specifically identify Listeria monocytogenes serovar 4 and a subset thereof: cluster IIB (serotypes 4b, 4d, and 4e). by Lei XH, Promadej N, Kathariou S.; 1997 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168398
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Effect of Acid Adaptation on the Fate of Listeria monocytogenes in THP-1 Human Macrophages Activated by Gamma Interferon. by Conte MP, Petrone G, Di Biase AM, Longhi C, Penta M, Tinari A, Superti F, Fabozzi G, Visca P, Seganti L.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128136
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Effect of exogenous proline, betaine, and carnitine on growth of Listeria monocytogenes in a minimal medium. by Beumer RR, Te Giffel MC, Cox LJ, Rombouts FM, Abee T.; 1994 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201482
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Effect of liposome-entrapped ampicillin on survival of Listeria monocytogenes in murine peritoneal macrophages. by Bakker-Woudenberg IA, Lokerse AF, Vink-van den Berg JC, Roerdink FH, Michel MF.; 1986 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=180537
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Effect of recombinant human gamma interferon on intracellular activities of antibiotics against Listeria monocytogenes in the human macrophage cell line THP-1. by Scorneaux B, Ouadrhiri Y, Anzalone G, Tulkens PM.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=163296
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Effect of the lactoperoxidase system on Listeria monocytogenes behavior in raw milk at refrigeration temperatures. by Gaya P, Medina M, Nunez M.; 1991 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183971
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Effective Induction of Acquired Resistance to Listeria monocytogenes by Immunizing Mice with In Vivo-Infected Dendritic Cells. by Sashinami H, Nakane A, Iwakura Y, Sasaki M.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=143424
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Effectiveness of nanoparticle-bound ampicillin in the treatment of Listeria monocytogenes infection in athymic nude mice. by Youssef M, Fattal E, Alonso MJ, Roblot-Treupel L, Sauzieres J, Tancrede C, Omnes A, Couvreur P, Andremont A.; 1988 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=172377
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Effects of Above-Optimum Growth Temperature and Cell Morphology on Thermotolerance of Listeria monocytogenes Cells Suspended in Bovine Milk. by Rowan NJ, Anderson JG.; 1998 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=106279
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Effects of growth temperature and strictly anaerobic recovery on the survival of Listeria monocytogenes during pasteurization. by Knabel SJ, Walker HW, Hartman PA, Mendonca AF.; 1990 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183347
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Effects of growth temperature on the ingestion and killing of clinical isolates of Listeria monocytogenes by human neutrophils. by Stecha PF, Heynen CA, Roll JT, Brown JF, Czuprynski CJ.; 1989 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=267617
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Elucidation of Listeria monocytogenes Contamination Routes in Cold-Smoked Salmon Processing Plants Detected by DNA-Based Typing Methods. by Fonnesbech Vogel B, Huss HH, Ojeniyi B, Ahrens P, Gram L.; 2001 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92911
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Emergence of the trimethoprim resistance gene dfrD in Listeria monocytogenes BM4293. by Charpentier E, Courvalin P.; 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=163863
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Endogenous Interleukin-10 Is Required for Prevention of a Hyperinflammatory Intracerebral Immune Response in Listeria monocytogenes Meningoencephalitis. by Deckert M, Soltek S, Geginat G, Lutjen S, Montesinos-Rongen M, Hof H, Schluter D.; 2001 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98533
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Enhanced control of Listeria monocytogenes by in situ-produced pediocin during dry fermented sausage production. by Foegeding PM, Thomas AB, Pilkington DH, Klaenhammer TR.; 1992 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195349
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Enhanced Immunological Memory Responses to Listeria monocytogenes in Rodents, as Measured by Delayed-Type Hypersensitivity (DTH), Adoptive Transfer of DTH, and Protective Immunity, following Lactobacillus casei Shirota Ingestion. by de Waard R, Claassen E, Bokken GC, Buiting B, Garssen J, Vos JG.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=145274
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Enhanced Levels of Cold Shock Proteins in Listeria monocytogenes LO28 upon Exposure to Low Temperature and High Hydrostatic Pressure. by WemekampKamphuis HH, Karatzas AK, Wouters JA, Abee T.; 2002 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126669
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Enhanced sensitivity in PCR detection of Listeria monocytogenes in soft cheese through use of an aqueous two-phase system as a sample preparation method. by Lantz PG, Tjerneld F, Borch E, Hahn-Hagerdal B, Radstrom P.; 1994 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201820
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Enteral Immunization with Attenuated Recombinant Listeria monocytogenes as a Live Vaccine Vector: Organ-Dependent Dynamics of CD4 T Lymphocytes Reactive to a Leishmania major Tracer Epitope. by Saklani-Jusforgues H, Fontan E, Soussi N, Milon G, Goossens PL.; 2003 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=148854
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Evaluation of hybridization characteristics of a cloned pRF106 probe for Listeria monocytogenes detection and development of a nonisotopic colony hybridization assay. by Kim CM, Graves LM, Swaminathan B, Mayer LW, Weaver RE.; 1991 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182700
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Evaluation of luciferase reporter bacteriophage A511::luxAB for detection of Listeria monocytogenes in contaminated foods. by Loessner MJ, Rudolf M, Scherer S.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168593
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Evaluation of selective direct plating media for their suitability to recover uninjured, heat-injured, and freeze-injured Listeria monocytogenes from foods. by Golden DA, Beuchat LR, Brackett RE.; 1988 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202678
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Evaluation of the ability of primary selective enrichment to resuscitate heat-injured and freeze-injured Listeria monocytogenes cells. by Budu-Amoako E, Toora S, Ablett RF, Smith J.; 1992 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183068
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Examination of Listeria monocytogenes Intracellular Gene Expression by Using the Green Fluorescent Protein of Aequorea victoria. by Freitag NE, Jacobs KE.; 1999 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96536
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Expression and Phosphorylation of the Listeria monocytogenes ActA Protein in Mammalian Cells. by Brundage RA, Smith GA, Camilli A, Theriot JA, Portnoy DA.; 1993 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48090
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Expression of ActA, Ami, InlB, and Listeriolysin O in Listeria monocytogenes of Human and Food Origin. by Jacquet C, Gouin E, Jeannel D, Cossart P, Rocourt J.; 2002 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126661
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Expression of the Listeria monocytogenes EGD inlA and inlB genes, whose products mediate bacterial entry into tissue culture cell lines, by PrfA-dependent and independent mechanisms. by Lingnau A, Domann E, Hudel M, Bock M, Nichterlein T, Wehland J, Chakraborty T.; 1995 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173548
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Expression of Truncated Internalin A Is Involved in Impaired Internalization of Some Listeria monocytogenes Isolates Carried Asymptomatically by Humans. by Olier M, Pierre F, Rousseaux S, Lemaitre JP, Rousset A, Piveteau P, Guzzo J.; 2003 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=148840
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Fate of Listeria monocytogenes in murine macrophages: evidence for simultaneous killing and survival of intracellular bacteria. by de Chastellier C, Berche P.; 1994 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186140
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Functional Similarities between the Listeria monocytogenes Virulence Regulator PrfA and Cyclic AMP Receptor Protein: the PrfA* (Gly145Ser) Mutation Increases Binding Affinity for Target DNA. by Vega Y, Dickneite C, Ripio MT, Bockmann R, Gonzalez-Zorn B, Novella S, Dominguez-Bernal G, Goebel W, Vazquez-Boland JA.; 1998 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=107770
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Gbu Glycine Betaine Porter and Carnitine Uptake in Osmotically Stressed Listeria monocytogenes Cells. by Mendum ML, Smith LT.; 2002 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129888
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Gene Cloning and Expression and Secretion of Listeria monocytogenes Bacteriophage-Lytic Enzymes in Lactococcus lactis. by Gaeng S, Scherer S, Neve H, Loessner MJ.; 2000 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92096
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Gene Fragments Distinguishing an Epidemic-Associated Strain from a Virulent Prototype Strain of Listeria monocytogenes Belong to a Distinct Functional Subset of Genes and Partially Cross-Hybridize with Other Listeria Species. by Herd M, Kocks C.; 2001 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98459
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Genetic characterization of clones of the bacterium Listeria monocytogenes causing epidemic disease. by Piffaretti JC, Kressebuch H, Aeschbacher M, Bille J, Bannerman E, Musser JM, Selander RK, Rocourt J.; 1989 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=287232
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Glucose uptake by Listeria monocytogenes Scott A and inhibition by pediocin JD. by Christensen DP, Hutkins RW.; 1994 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201899
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Glucose-1-phosphate utilization by Listeria monocytogenes is PrfA dependent and coordinately expressed with virulence factors. by Ripio MT, Brehm K, Lara M, Suarez M, Vazquez-Boland JA.; 1997 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=179662
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Growth Limits of Listeria monocytogenes as a Function of Temperature, pH, NaCl, and Lactic Acid. by Tienungoon S, Ratkowsky DA, McMeekin TA, Ross T.; 2000 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92408
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Growth of Listeria monocytogenes and Yersinia enterocolitica on Cooked ModifiedAtmosphere-Packaged Poultry in the Presence and Absence of a Naturally Occurring Microbiota. by Barakat RK, Harris LJ.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91029
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Gut Colonization of Mice with actA-Negative Mutant of Listeria monocytogenes Can Stimulate a Humoral Mucosal Immune Response. by Manohar M, Baumann DO, Bos NA, Cebra JJ.; 2001 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98330
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GW domains of the Listeria monocytogenes invasion protein InlB are SH3-like and mediate binding to host ligands. by Marino M, Banerjee M, Jonquieres R, Cossart P, Ghosh P.; 2002 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=131055
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Hemolysin is required for extraintestinal dissemination of Listeria monocytogenes in intragastrically inoculated mice. by Roll JT, Czuprynski CJ.; 1990 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313625
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Hemolytic activity reevaluation of putative nonpathogenic Listeria monocytogenes strains. by Lachica RV.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168254
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Highly selective medium for isolation of Listeria monocytogenes from food. by alZoreky N, Sandine WE.; 1990 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184914
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Host cell responses to Listeria monocytogenes infection include differential transcription of host stress genes involved in signal transduction. by Schwan WR, Goebel W.; 1994 Jul 5; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=44215
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Human Endothelial Cell Activation and Mediator Release in Response to Listeria monocytogenes Virulence Factors. by Rose F, Zeller SA, Chakraborty T, Domann E, Machleidt T, Kronke M, Seeger W, Grimminger F, Sibelius U.; 2001 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97967
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Identification and characterization of a novel PrfA-regulated gene in Listeria monocytogenes whose product, IrpA, is highly homologous to internalin proteins, which contain leucine-rich repeats. by Domann E, Zechel S, Lingnau A, Hain T, Darji A, Nichterlein T, Wehland J, Chakraborty T.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=174562
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Identification and Disruption of BetL, a Secondary Glycine Betaine Transport System Linked to the Salt Tolerance of Listeria monocytogenes LO28. by Sleator RD, Gahan CG, Abee T, Hill C.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91301
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Identification and enumeration of Listeria monocytogenes by nonradioactive DNA probe colony hybridization. by Datta AR, Moore MA, Wentz BA, Lane J.; 1993 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202069
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Identification in Listeria monocytogenes of MecA, a Homologue of the Bacillus subtilis Competence Regulatory Protein. by Borezee E, Msadek T, Durant L, Berche P.; 2000 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=94723
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Identification of a new operon involved in Listeria monocytogenes virulence: its first gene encodes a protein homologous to bacterial metalloproteases. by Mengaud J, Geoffroy C, Cossart P.; 1991 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=258365
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Identification of an extracellular protein of Listeria monocytogenes possibly involved in intracellular uptake by mammalian cells. by Kuhn M, Goebel W.; 1989 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313040
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Identification of four new members of the internalin multigene family of Listeria monocytogenes EGD. by Dramsi S, Dehoux P, Lebrun M, Goossens PL, Cossart P.; 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=175184
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Identification of Listeria monocytogenes Genes Expressed in Response to Growth at Low Temperature. by Liu S, Graham JE, Bigelow L, Morse PD II, Wilkinson BJ.; 2002 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123842
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Identification of Listeria monocytogenes Genes Involved in Salt and Alkaline-pH Tolerance. by Gardan R, Cossart P, Labadie J.; 2003 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=161542
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Identification of Listeria monocytogenes In Vivo-Induced Genes by FluorescenceActivated Cell Sorting. by Wilson RL, Tvinnereim AR, Jones BD, Harty JT.; 2001 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98595
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Identification of New Genes Involved in the Virulence of Listeria monocytogenes by Signature-Tagged Transposon Mutagenesis. by Autret N, Dubail I, Trieu-Cuot P, Berche P, Charbit A.; 2001 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98130
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Identification of the Gene Encoding the Alternative Sigma Factor [final sigma]B from Listeria monocytogenes and Its Role in Osmotolerance. by Becker LA, Cetin MS, Hutkins RW, Benson AK.; 1998 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=107466
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Incidence of Listeria spp. and Listeria monocytogenes in a poultry processing environment and in poultry products and their rapid confirmation by multiplex PCR. by Lawrence LM, Gilmour A.; 1994 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202027
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Induction of Human Immunodeficiency Virus (HIV)-Specific CD8 T-Cell Responses by Listeria monocytogenes and a Hyperattenuated Listeria Strain Engineered To Express HIV Antigens. by Friedman RS, Frankel FR, Xu Z, Lieberman J.; 2000 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=102037
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Induction of immunity with avirulent Listeria monocytogenes 19113 depends on bacterial replication. by Baldridge JR, Thomashow MF, Hinrichs DJ.; 1988 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=259530
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Induction of Protective Immunity to Listeria monocytogenes with Dendritic Cells Retrovirally Transduced with a Cytotoxic T Lymphocyte Epitope Minigene. by Nakamura Y, Suda T, Nagata T, Aoshi T, Uchijima M, Yoshida A, Chida K, Koide Y, Nakamura H.; 2003 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152038
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Induction of Protective T Cells against Listeria monocytogenes in Mice by Immunization with a Listeriolysin O-Negative Avirulent Strain of Bacteria and Liposome-Encapsulated Listeriolysin O. by Tanabe Y, Xiong H, Nomura T, Arakawa M, Mitsuyama M.; 1999 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96356
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Influence of preadsorbed milk proteins on adhesion of Listeria monocytogenes to hydrophobic and hydrophilic silica surfaces. by al-Makhlafi H, McGuire J, Daeschel M.; 1994 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201855
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Influence of the Natural Microbial Flora on the Acid Tolerance Response of Listeria monocytogenes in a Model System of Fresh Meat Decontamination Fluids. by Samelis J, Sofos JN, Kendall PA, Smith GC.; 2001 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92889
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Inhibition of intracellular growth of Listeria monocytogenes by antibiotics. by Michelet C, Avril JL, Cartier F, Berche P.; 1994 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=284477
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Inhibition of Listeria monocytogenes by fatty acids and monoglycerides. by Wang LL, Johnson EA.; 1992 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195293
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Inhibition of Listeria monocytogenes by Lactobacillus bavaricus MN in beef systems at refrigeration temperatures. by Winkowski K, Crandall AD, Montville TJ.; 1993 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182319
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Inhibition of Listeria monocytogenes growth by the lactoperoxidase-thiocyanateH2O2 antimicrobial system. by Siragusa GR, Johnson MG.; 1989 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203172
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Interaction of Listeria monocytogenes with Human Brain Microvascular Endothelial Cells: an Electron Microscopic Study. by Greiffenberg L, Goebel W, Kim KS, Daniels J, Kuhn M.; 2000 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97578
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Interaction of Listeria monocytogenes with Human Brain Microvascular Endothelial Cells: InlB-Dependent Invasion, Long-Term Intracellular Growth, and Spread from Macrophages to Endothelial Cells. by Greiffenberg L, Goebel W, Kim KS, Weiglein I, Bubert A, Engelbrecht F, Stins M, Kuhn M.; 1998 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108657
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Internalin B promotes the replication of Listeria monocytogenes in mouse hepatocytes. by Gregory SH, Sagnimeni AJ, Wing EJ.; 1997 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=175740
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Intracellular hemolysin-producing Listeria monocytogenes strains inhibit macrophage-mediated antigen processing. by Cluff CW, Garcia M, Ziegler HK.; 1990 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313704
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Intracellular Induction of Listeria monocytogenes actA Expression. by Shetron-Rama LM, Marquis H, Bouwer HG, Freitag NE.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=127770
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Intracellular killing of Listeria monocytogenes in the J774.1 macrophage-like cell line and the lipopolysaccharide (LPS)-resistant mutant LPS1916 cell line defective in the generation of reactive oxygen intermediates after LPS treatment. by Inoue S, Itagaki S, Amano F.; 1995 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173238
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Intracellular methicillin selection of Listeria monocytogenes mutants unable to replicate in a macrophage cell line. by Camilli A, Paynton CR, Portnoy DA.; 1989 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=297655
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Intracytoplasmic growth and virulence of Listeria monocytogenes auxotrophic mutants. by Marquis H, Bouwer HG, Hinrichs DJ, Portnoy DA.; 1993 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=281074
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Introduction of pAM beta 1 into Listeria monocytogenes by conjugation and homology between native L. monocytogenes plasmids. by Flamm RK, Hinrichs DJ, Thomashow MF.; 1984 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=263486
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Investigation of the effect of combined variations in temperature, pH, and NaCl concentration on nisin inhibition of Listeria monocytogenes and Staphylococcus aureus. by Thomas LV, Wimpenny JW.; 1996 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167979
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Iron availability affects entry of Listeria monocytogenes into the enterocytelike cell line Caco-2. by Conte MP, Longhi C, Polidoro M, Petrone G, Buonfiglio V, Di Santo S, Papi E, Seganti L, Visca P, Valenti P.; 1996 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=174316
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Isolation of Listeria monocytogenes from raw milk. by Hayes PS, Feeley JC, Graves LM, Ajello GW, Fleming DW.; 1986 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=238890
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Isolation of Listeria monocytogenes small-plaque mutants defective for intracellular growth and cell-to-cell spread. by Sun AN, Camilli A, Portnoy DA.; 1990 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313727
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Isolation of Rifampin-Resistant Mutants of Listeria monocytogenes and Their Characterization by rpoB Gene Sequencing, Temperature Sensitivity for Growth, and Interaction with an Epithelial Cell Line. by Morse R, O'Hanlon K, Virji M, Collins MD.; 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=85412
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Localization of the ActA polypeptide of Listeria monocytogenes in infected tissue culture cell lines: ActA is not associated with actin "comets". by Niebuhr K, Chakraborty T, Rohde M, Gazlig T, Jansen B, Kollner P, Wehland J.; 1993 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=280923
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Loss of catalase activity in Tn1545-induced mutants does not reduce growth of Listeria monocytogenes in vivo. by Leblond-Francillard M, Gaillard JL, Berche P.; 1989 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313489
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Low Sensitivity of Listeria monocytogenes to Quaternary Ammonium Compounds. by Mereghetti L, Quentin R, Marquet-Van Der Mee N, Audurier A.; 2000 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92423
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Mechanism of the Intracellular Killing and Modulation of Antibiotic Susceptibility of Listeria monocytogenes in THP-1 Macrophages Activated by Gamma Interferon. by Ouadrhiri Y, Scorneaux B, Sibille Y, Tulkens PM.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=89140
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Membranes of Class IIa Bacteriocin-Resistant Listeria monocytogenes Cells Contain Increased Levels of Desaturated and Short-Acyl-Chain Phosphatidylglycerols. by Vadyvaloo V, Hastings JW, van der Merwe MJ, Rautenbach M.; 2002 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=129904
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Method for flow cytometric detection of Listeria monocytogenes in milk. by Donnelly CW, Baigent GJ.; 1986 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239098
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Methods for improved recovery of Listeria monocytogenes from cheese. by Yousef AE, Ryser ET, Marth EH.; 1988 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=204349
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Microtiter Plate Assay for Assessment of Listeria monocytogenes Biofilm Formation. by Djordjevic D, Wiedmann M, McLandsborough LA.; 2002 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123944
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Mobilization of Protein Kinase C in Macrophages Induced by Listeria monocytogenes Affects Its Internalization and Escape from the Phagosome. by Wadsworth SJ, Goldfine H.; 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128209
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Modifications of membrane phospholipid composition in nisin-resistant Listeria monocytogenes Scott A. by Verheul A, Russell NJ, Van'T Hof R, Rombouts FM, Abee T.; 1997 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168652
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Modulation of Enzymatic Activity and Biological Function of Listeria monocytogenes Broad-Range Phospholipase C by Amino Acid Substitutions and by Replacement with the Bacillus cereus Ortholog. by Zuckert WR, Marquis H, Goldfine H.; 1998 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108596
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Molecular cloning, sequencing, and identification of a metalloprotease gene from Listeria monocytogenes that is species specific and physically linked to the listeriolysin gene. by Domann E, Leimeister-Wachter M, Goebel W, Chakraborty T.; 1991 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=257706
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Molecular determinants of Listeria monocytogenes pathogenesis. by Portnoy DA, Chakraborty T, Goebel W, Cossart P.; 1992 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=256991
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Molecular Epidemiological Survey of Listeria monocytogenes in Seafoods and Seafood-Processing Plants. by Rorvik LM, Aase B, Alvestad T, Caugant DA.; 2000 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92379
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Molecular Epidemiology of an Outbreak of Febrile Gastroenteritis Caused by Listeria monocytogenes in Cold-Smoked Rainbow Trout. by Miettinen MK, Siitonen A, Heiskanen P, Haajanen H, Bjorkroth KJ, Korkeala HJ.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=85164
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Molecular Studies on the Ecology of Listeria monocytogenes in the Smoked Fish Processing Industry. by Norton DM, McCamey MA, Gall KL, Scarlett JM, Boor KJ, Wiedmann M.; 2001 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92546
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Molecular Typing by Pulsed-Field Gel Electrophoresis of Spanish Animal and Human Listeria monocytogenes Isolates. by Vela AI, Fernandez-Garayzabal JF, Vazquez JA, Latre MV, Blanco MM, Moreno MA, de la Fuente L, Marco J, Franco C, Cepeda A, Rodriguez Moure AA, Suarez G, Dominguez L.; 2001 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=93380
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Monoclonal antibodies with a high degree of specificity for Listeria monocytogenes serotype 4b. by Kathariou S, Mizumoto C, Allen RD, Fok AK, Benedict AA.; 1994 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201853
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Morphological and Physiological Characterization of Listeria monocytogenes Subjected to High Hydrostatic Pressure. by Ritz M, Tholozan JL, Federighi M, Pilet MF.; 2001 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92862
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Multiple Deletions of the Osmolyte Transporters BetL, Gbu, and OpuC of Listeria monocytogenes Affect Virulence and Growth at High Osmolarity. by WemekampKamphuis HH, Wouters JA, Sleator RD, Gahan CG, Hill C, Abee T.; 2002 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126390
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Multiplication of Listeria monocytogenes in a murine hepatocyte cell line. by Wood S, Maroushek N, Czuprynski CJ.; 1993 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=280961
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Mutagenesis of Active-Site Histidines of Listeria monocytogenes Phosphatidylinositol-Specific Phospholipase C: Effects on Enzyme Activity and Biological Function. by Bannam T, Goldfine H.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96294
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Mutants of Listeria monocytogenes Defective in In Vitro Invasion and Cell-to-Cell Spreading Still Invade and Proliferate in Hepatocytes of Neutropenic Mice. by Appelberg R, Leal IS.; 2000 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97221
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Neural Route of Cerebral Listeria monocytogenes Murine Infection: Role of Immune Response Mechanisms in Controling Bacterial Neuroinvasion. by Jin Y, Dons L, Kristensson K, Rottenberg ME.; 2001 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=97990
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New Aspects Regarding Evolution and Virulence of Listeria monocytogenes Revealed by Comparative Genomics and DNA Arrays. by Doumith M, Cazalet C, Simoes N, Frangeul L, Jacquet C, Kunst F, Martin P, Cossart P, Glaser P, Buchrieser C.; 2004 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=321639
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Nisin Resistance in Listeria monocytogenes ATCC 700302 Is a Complex Phenotype. by Crandall AD, Montville TJ.; 1998 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124699
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Nonhemolytic Listeria monocytogenes mutants that are also noninvasive for mammalian cells in culture: evidence for coordinate regulation of virulence. by Kathariou S, Pine L, George V, Carlone GM, Holloway BP.; 1990 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313766
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Nucleotide sequence of the lecithinase operon of Listeria monocytogenes and possible role of lecithinase in cell-to-cell spread. by Vazquez-Boland JA, Kocks C, Dramsi S, Ohayon H, Geoffroy C, Mengaud J, Cossart P.; 1992 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=257526
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Osmotic and Chill Activation of Glycine Betaine Porter II in Listeria monocytogenes Membrane Vesicles. by Gerhardt PN, Tombras Smith L, Smith GM.; 2000 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111319
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Pathogenicity and Immunogenicity of a Listeria monocytogenes Strain That Requires d-Alanine for Growth. by Thompson RJ, Bouwer HG, Portnoy DA, Frankel FR.; 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108386
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Pathogenicity and immunogenicity of Listeria monocytogenes small-plaque mutants defective for intracellular growth and cell-to-cell spread. by Barry RA, Bouwer HG, Portnoy DA, Hinrichs DJ.; 1992 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=257039
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Pathogenicity of Listeria monocytogenes grown on crabmeat. by Brackett RE, Beuchat LR.; 1990 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184385
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Pathogenicity test for Listeria monocytogenes using immunocompromised mice. by Stelma GN Jr, Reyes AL, Peeler JT, Francis DW, Hunt JM, Spaulding PL, Johnson CH, Lovett J.; 1987 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=269416
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Penicillin-binding protein 3 of Listeria monocytogenes as the primary lethal target for beta-lactams. by Vicente MF, Perez-Daz JC, Baquero F, Angel de Pedro M, Berenguer J.; 1990 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=171640
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Peptide epitopes from noncytosolic Listeria monocytogenes can be presented by major histocompatibility complex class I molecules. by Zwickey HL, Potter TA.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=174008
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Phosphatidylcholine-Specific Phospholipase C from Listeria monocytogenes Is an Important Virulence Factor in Murine Cerebral Listeriosis. by Schluter D, Domann E, Buck C, Hain T, Hof H, Chakraborty T, Deckert-Schluter M.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108751
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Phosphatidylinositol-specific phospholipase C from Listeria monocytogenes contributes to intracellular survival and growth of Listeria innocua. by Schwan WR, Demuth A, Kuhn M, Goebel W.; 1994 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=303189
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Plasmids in Listeria monocytogenes in relation to cadmium resistance. by Lebrun M, Loulergue J, Chaslus-Dancla E, Audurier A.; 1992 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183070
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Positive Selection of Mutations Leading to Loss or Reduction of Transcriptional Activity of PrfA, the Central Regulator of Listeria monocytogenes Virulence. by Herler M, Bubert A, Goetz M, Vega Y, Vazquez-Boland JA, Goebel W.; 2001 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=95447
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Prevalence and Fingerprinting of Listeria monocytogenes Strains Isolated from Raw Whole Milk in Farm Bulk Tanks and in Dairy Plant Receiving Tanks. by Waak E, Tham W, Danielsson-Tham ML.; 2002 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126782
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Prevention by gamma interferon of fatal infection with Listeria monocytogenes in mice treated with cyclosporin A. by Nakane A, Minagawa T, Yasuda I, Yu C, Kato K.; 1988 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=259516
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Production of Monoclonal Antibodies to Listeria monocytogenes and Their Application To Determine the Virulence of Isolates from Channel Catfish. by Erdenlig S, Ainsworth AJ, Austin FW.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91424
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Pulsed-field fingerprinting of listeriae: identification of genomic divisions for Listeria monocytogenes and their correlation with serovar. by Brosch R, Chen J, Luchansky JB.; 1994 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201687
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Purification and characterization of Listeria monocytogenes phosphatidylinositolspecific phospholipase C. by Goldfine H, Knob C.; 1992 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=257436
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Pyrosequencing as a Method for Grouping of Listeria monocytogenes Strains on the Basis of Single-Nucleotide Polymorphisms in the inlB Gene. by Unnerstad H, Ericsson H, Alderborn A, Tham W, Danielsson-Tham ML, Mattsson JG.; 2001 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=93312
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Quantifying Translocation of Listeria monocytogenes in Rats by Using Urinary Nitric Oxide-Derived Metabolites. by Sprong RC, Hulstein MF, van der Meer R.; 2000 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92459
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Rapid confirmation of Listeria monocytogenes isolated from foods by a colony blot assay using a digoxigenin-labeled synthetic oligonucleotide probe. by Kim C, Swaminathan B, Cassaday PK, Mayer LW, Holloway BP.; 1991 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183440
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Real-Time Measurements of the Interaction between Single Cells of Listeria monocytogenes and Nisin on a Solid Surface. by Budde BB, Jakobsen M.; 2000 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92188
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Reduced virulence of a Listeria monocytogenes phospholipase-deficient mutant obtained by transposon insertion into the zinc metalloprotease gene. by Raveneau J, Geoffroy C, Beretti JL, Gaillard JL, Alouf JE, Berche P.; 1992 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=257573
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Regulation of hly Expression in Listeria monocytogenes by Carbon Sources and pH Occurs through Separate Mechanisms Mediated by PrfA. by Behari J, Youngman P.; 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108396
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Relationship of bacterial growth phase to killing of Listeria monocytogenes by oxidative agents generated by neutrophils and enzyme systems. by Bortolussi R, Vandenbroucke-Grauls CM, van Asbeck BS, Verhoef J.; 1987 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=260049
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Replica plating of colonies from Listeria-selective agars to blood agar to improve the isolation of Listeria monocytogenes from foods. by Cassiday PK, Graves LM, Swaminathan B.; 1990 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184600
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Responses of Listeria monocytogenes to Acid Stress and Glucose Availability Revealed by a Novel Combination of Fluorescence Microscopy and Microelectrode Ion-Selective Techniques. by Shabala L, Budde B, Ross T, Siegumfeldt H, Jakobsen M, McMeekin T.; 2002 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123830
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Restriction Fragment Length Polymorphisms Detected with Novel DNA Probes Differentiate among Diverse Lineages of Serogroup 4 Listeria monocytogenes and Identify Four Distinct Lineages in Serotype 4b. by Tran HL, Kathariou S.; 2002 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126560
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Ribotype diversity of Listeria monocytogenes strains associated with outbreaks of listeriosis in ruminants. by Wiedmann M, Bruce JL, Knorr R, Bodis M, Cole EM, McDowell CI, McDonough PL, Batt CA.; 1996 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=228960
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Ribotypes and virulence gene polymorphisms suggest three distinct Listeria monocytogenes lineages with differences in pathogenic potential. by Wiedmann M, Bruce JL, Keating C, Johnson AE, McDonough PL, Batt CA.; 1997 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=175382
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Role of [final sigma]B in Adaptation of Listeria monocytogenes to Growth at Low Temperature. by Becker LA, Evans SN, Hutkins RW, Benson AK.; 2000 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=94839
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Role of ctc from Listeria monocytogenes in Osmotolerance. by Gardan R, Duche O, Leroy-Setrin S, Labadie J.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152465
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Role of Listeria monocytogenes [sigma]B in Survival of Lethal Acidic Conditions and in the Acquired Acid Tolerance Response. by Ferreira A, Sue D, O'Byrne CP, Boor KJ.; 2003 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154505
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Roles of Listeria monocytogenes virulence factors in survival: virulence factors distinct from listeriolysin are needed for the organism to survive an early neutrophilmediated host defense mechanism. by Conlan JW, North RJ.; 1992 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=257579
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Safety and Shedding of an Attenuated Strain of Listeria monocytogenes with a Deletion of actA/plcB in Adult Volunteers: a Dose Escalation Study of Oral Inoculation. by Angelakopoulos H, Loock K, Sisul DM, Jensen ER, Miller JF, Hohmann EL.; 2002 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=128066
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Salmonella enterica Serovar Typhimurium and Listeria monocytogenes Acid Tolerance Response Induced by Organic Acids at 20[deg]C: Optimization and Modeling. by Greenacre EJ, Brocklehurst TF, Waspe CR, Wilson DR, Wilson PD.; 2003 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165179
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SecA2-dependent secretion of autolytic enzymes promotes Listeria monocytogenes pathogenesis. by Lenz LL, Mohammadi S, Geissler A, Portnoy DA.; 2003 Oct 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=218775
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Selection and Identification of a Listeria monocytogenes Target Strain for Pulsed Electric Field Process Optimization. by Lado BH, Yousef AE.; 2003 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154796
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Sensitive and specific detection of Listeria monocytogenes in milk and ground beef with the polymerase chain reaction. by Thomas EJ, King RK, Burchak J, Gannon VP.; 1991 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183622
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Sensitive detection of viable Listeria monocytogenes by reverse transcription-PCR. by Klein PG, Juneja VK.; 1997 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168763
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Sensitivity of Listeria monocytogenes to Sanitizers Used in the Meat Processing Industry. by Romanova N, Favrin S, Griffiths MW.; 2002 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=134375
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Sensitization of heat-treated Listeria monocytogenes to added lysozyme in milk. by Kihm DJ, Leyer GJ, An GH, Johnson EA.; 1994 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201895
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Sensitization of Listeria monocytogenes to Low pH, Organic Acids, and Osmotic Stress by Ethanol. by Barker C, Park SF.; 2001 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92774
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Separation of pathogenic from apathogenic Listeria monocytogenes by three in vitro reactions. by Groves RD, Welshimer HJ.; 1977 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=274655
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Sequence Variations within PrfA DNA Binding Sites and Effects on Listeria monocytogenes Virulence Gene Expression. by Williams JR, Thayyullathil C, Freitag NE.; 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=94353
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Serological diagnosis of bovine, caprine, and ovine mastitis caused by Listeria monocytogenes by using an enzyme-linked immunosorbent assay. by Bourry A, Cochard T, Poutrel B.; 1997 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=229800
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Serotyping and esterase typing for analysis of Listeria monocytogenes populations recovered from foodstuffs and from human patients with listeriosis in Belgium. by Gilot P, Genicot A, Andre P.; 1996 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=228941
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Serotyping of Listeria monocytogenes by Enzyme-Linked Immunosorbent Assay and Identification of Mixed-Serotype Cultures by Colony Immunoblotting. by Palumbo JD, Borucki MK, Mandrell RE, Gorski L.; 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149718
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Simple color tests based on an alanyl peptidase reaction which differentiate Listeria monocytogenes from other Listeria species. by Clark AG, McLaughlin J.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=229924
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Sodium-driven, osmotically activated glycine betaine transport in Listeria monocytogenes membrane vesicles. by Gerhardt PN, Smith LT, Smith GM.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=178477
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Sources of Listeria monocytogenes Contamination in a Cold-Smoked Rainbow Trout Processing Plant Detected by Pulsed-Field Gel Electrophoresis Typing. by Autio T, Hielm S, Miettinen M, Sjoberg AM, Aarnisalo K, Bjorkroth J, Mattila-Sandholm T, Korkeala H.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=90996
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Species-specific detection of Listeria monocytogenes by DNA amplification. by Deneer HG, Boychuk I.; 1991 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182759
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Specific Identification of Listeria welshimeri and Listeria monocytogenes by PCR Assays Targeting a Gene Encoding a Fibronectin-Binding Protein. by Gilot P, Content J.; 2002 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153408
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Stress-Induced ClpP Serine Protease of Listeria monocytogenes Is Essential for Induction of Listeriolysin O-Dependent Protective Immunity. by Gaillot O, Bregenholt S, Jaubert F, Di Santo JP, Berche P.; 2001 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98585
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Subtyping Listeria monocytogenes isolates genetically related to the Swiss epidemic clone. by Boerlin P, Bannerman E, Jemmi T, Bille J.; 1996 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=229207
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Suppression of Listeria monocytogenes colonization following adsorption of nisin onto silica surfaces. by Bower CK, McGuire J, Daeschel MA.; 1995 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167359
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Survival and Heat Resistance of Listeria monocytogenes after Exposure to Alkali and Chlorine. by Taormina PJ, Beuchat LR.; 2001 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92907
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Synthesis of listeriolysin in Listeria monocytogenes under heat shock conditions. by Sokolovic Z, Goebel W.; 1989 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=313092
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Synthetic peptides derived from the Listeria monocytogenes p60 protein as antigens for the generation of polyclonal antibodies specific for secreted cell-free L. monocytogenes p60 proteins. by Bubert A, Schubert P, Kohler S, Frank R, Goebel W.; 1994 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201779
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Temperature- and Surfactant-Induced Membrane Modifications That Alter Listeria monocytogenes Nisin Sensitivity by Different Mechanisms. by Li J, Chikindas ML, Ludescher RD, Montville TJ.; 2002 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=134382
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The ActA polypeptides of Listeria ivanovii and Listeria monocytogenes harbor related binding sites for host microfilament proteins. by Gerstel B, Grobe L, Pistor S, Chakraborty T, Wehland J.; 1996 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=174018
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The broad-range phospholipase C and a metalloprotease mediate listeriolysin Oindependent escape of Listeria monocytogenes from a primary vacuole in human epithelial cells. by Marquis H, Doshi V, Portnoy DA.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173647
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The bvr Locus of Listeria monocytogenes Mediates Virulence Gene Repression by [beta]-Glucosides. by Brehm K, Ripio MT, Kreft J, Vazquez-Boland JA.; 1999 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=93992
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The expression of virulence genes in Listeria monocytogenes is thermoregulated. by Leimeister-Wachter M, Domann E, Chakraborty T.; 1992 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=206174
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The iap gene of Listeria monocytogenes is essential for cell viability, and its gene product, p60, has bacteriolytic activity. by Wuenscher MD, Kohler S, Bubert A, Gerike U, Goebel W.; 1993 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=204749
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The inlA Gene of Listeria monocytogenes LO28 Harbors a Nonsense Mutation Resulting in Release of Internalin. by Jonquieres R, Bierne H, Mengaud J, Cossart P.; 1998 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=108362
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The LisRK Signal Transduction System Determines the Sensitivity of Listeria monocytogenes to Nisin and Cephalosporins. by Cotter PD, Guinane CM, Hill C.; 2002 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=127401
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The Listeria monocytogenes lemA Gene Product Is Not Required for Intracellular Infection or To Activate fMIGWII-Specific T Cells. by D'Orazio SE, Velasquez M, Roan NR, Naveiras-Torres O, Starnbach MN.; 2003 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=308916
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The Macrocyclic Peptide Antibiotic Micrococcin P1 Is Secreted by the Food-Borne Bacterium Staphylococcus equorum WS 2733 and Inhibits Listeria monocytogenes on Soft Cheese. by Carnio MC, Holtzel A, Rudolf M, Henle T, Jung G, Scherer S.; 2000 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=110537
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The rpoN (sigma54) gene from Listeria monocytogenes is involved in resistance to mesentericin Y105, an antibacterial peptide from Leuconostoc mesenteroides. by Robichon D, Gouin E, Debarbouille M, Cossart P, Cenatiempo Y, Hechard Y.; 1997 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=179715
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The Sortase SrtA of Listeria monocytogenes Is Involved in Processing of Internalin and in Virulence. by Garandeau C, Reglier-Poupet H, Dubail I, Beretti JL, Berche P, Charbit A.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=127754
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The two distinct phospholipases C of Listeria monocytogenes have overlapping roles in escape from a vacuole and cell-to-cell spread. by Smith GA, Marquis H, Jones S, Johnston NC, Portnoy DA, Goldfine H.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=173601
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The virulence gene cluster of Listeria monocytogenes is also present in Listeria ivanovii, an animal pathogen, and Listeria seeligeri, a nonpathogenic species. by Gouin E, Mengaud J, Cossart P.; 1994 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=302991
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The zinc metalloprotease of Listeria monocytogenes is required for maturation of phosphatidylcholine phospholipase C: direct evidence obtained by gene complementation. by Poyart C, Abachin E, Razafimanantsoa I, Berche P.; 1993 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=281405
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Thermotolerance of heat-shocked Listeria monocytogenes in milk exposed to hightemperature, short-time pasteurization. by Bunning VK, Crawford RG, Tierney JT, Peeler JT.; 1992 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195733
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Three Transporters Mediate Uptake of Glycine Betaine and Carnitine by Listeria monocytogenes in Response to Hyperosmotic Stress. by Angelidis AS, Smith GM.; 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=143676
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Transcriptional activation of the Listeria monocytogenes hemolysin gene in Bacillus subtilis. by Freitag NE, Youngman P, Portnoy DA.; 1992 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=206424
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Transcriptional enhancement of the Listeria monocytogenes PCR and simple immunoenzymatic assay of the product using anti-RNA:DNA antibodies. by Blais BW.; 1994 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201312
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Transcriptional Regulation and Posttranslational Activity of the Betaine Transporter BetL in Listeria monocytogenes Are Controlled by Environmental Salinity. by Sleator RD, Wood JM, Hill C.; 2003 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=296249
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Transposon-Induced Mutations in Two Loci of Listeria monocytogenes Serotype 1/2a Result in Phage Resistance and Lack of N-Acetylglucosamine in the Teichoic Acid of the Cell Wall. by Tran HL, Fiedler F, Hodgson DA, Kathariou S.; 1999 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91646
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Types of Listeria monocytogenes Predicted by the Positions of EcoRI Cleavage Sites Relative to Ribosomal RNA Sequences. by Hubner RJ, Cole EM, Bruce JL, McDowell CI, Webster JA.; 1995 May 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41883
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Typing of human, animal, food, and environmental isolates of Listeria monocytogenes by multilocus enzyme electrophoresis. by Boerlin P, Piffaretti JC.; 1991 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183442
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Typing of Listeria monocytogenes Strains by Repetitive Element Sequence-Based PCR. by Jersek B, Gilot P, Gubina M, Klun N, Mehle J, Tcherneva E, Rijpens N, Herman L.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=84179
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Unstable Expression and Thermal Instability of a Species-Specific Cell Surface Epitope Associated with a 66-Kilodalton Antigen Recognized by Monoclonal Antibody EM-7G1 within Serotypes of Listeria monocytogenes Grown in Nonselective and Selective Broths. by Nannapaneni R, Story R, Bhunia AK, Johnson MG.; 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=106818
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Use of a bacteriocin produced by Pediococcus acidilactici to inhibit Listeria monocytogenes associated with fresh meat. by Nielsen JW, Dickson JS, Crouse JD.; 1990 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184573
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Use of molecular typing methods to trace the dissemination of Listeria monocytogenes in a shrimp processing plant. by Destro MT, Leitao MF, Farber JM.; 1996 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167838
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Use of polymerase chain reaction for detection of Listeria monocytogenes in food. by Niederhauser C, Candrian U, Hofelein C, Jermini M, Buhler HP, Luthy J.; 1992 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195641
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Utilization of Oligopeptides by Listeria monocytogenes Scott A. by Verheul A, Rombouts FM, Abee T.; 1998 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=106367
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Variation in the Infectivity of Listeria monocytogenes Isolates following Intragastric Inoculation of Mice. by Barbour AH, Rampling A, Hormaeche CE.; 2001 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=98544
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Verification of causal relationships between Listeria monocytogenes isolates implicated in food-borne outbreaks of listeriosis by randomly amplified polymorphic DNA patterns. by Czajka J, Batt CA.; 1994 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=263669
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Virulent Rough Filaments of Listeria monocytogenes from Clinical and Food Samples Secreting Wild-Type Levels of Cell-Free p60 Protein. by Rowan NJ, Candlish AA, Bubert A, Anderson JG, Kramer K, McLauchlin J.; 2000 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=86987
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 Listeria monocytogenes, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “Listeria monocytogenes” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for Listeria monocytogenes (hyperlinks lead to article summaries):
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 comparative heat inactivation study of indigenous microflora in beef with that of Listeria monocytogenes, Salmonella serotypes and Escherichia coli O157:H7. Author(s): Juneja VK. Source: Letters in Applied Microbiology. 2003; 37(4): 292-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12969491
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A gene-expression program reflecting the innate immune response of cultured intestinal epithelial cells to infection by Listeria monocytogenes. Author(s): Baldwin DN, Vanchinathan V, Brown PO, Theriot JA. Source: Genome Biology. 2003; 4(1): R2. Epub 2002 December 23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12537547
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A molecular marker for evaluating the pathogenic potential of foodborne Listeria monocytogenes. Author(s): Jacquet C, Doumith M, Gordon JI, Martin PM, Cossart P, Lecuit M. Source: The Journal of Infectious Diseases. 2004 June 1; 189(11): 2094-100. Epub 2004 May 14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15143478
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A three-tiered approach to differentiate Listeria monocytogenes biofilm-forming abilities. Author(s): Marsh EJ, Luo H, Wang H. Source: Fems Microbiology Letters. 2003 November 21; 228(2): 203-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14638425
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A/J mice are susceptible and C57BL/6 mice are resistant to Listeria monocytogenes infection by intragastric inoculation. Author(s): Czuprynski CJ, Faith NG, Steinberg H. Source: Infection and Immunity. 2003 February; 71(2): 682-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12540546
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Activities of ABT-773 against Listeria monocytogenes and coryneform bacteria of clinical interest. Author(s): Conejo Mdel C, Martinez-Martinez L, Pascual A, Suarez AI, Perea EJ. Source: Antimicrobial Agents and Chemotherapy. 2003 April; 47(4): 1403-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12654678
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Activity of beta-lactams (ampicillin, meropenem), gentamicin, azithromycin and moxifloxacin against intracellular Listeria monocytogenes in a 24 h THP-1 human macrophage model. Author(s): Carryn S, Van Bambeke F, Mingeot-Leclercq MP, Tulkens PM. Source: The Journal of Antimicrobial Chemotherapy. 2003 April; 51(4): 1051-2. Epub 2003 March 13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12654747
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Adhesion, invasion, and translocation characteristics of Listeria monocytogenes serotypes in Caco-2 cell and mouse models. Author(s): Jaradat ZW, Bhunia AK. Source: Applied and Environmental Microbiology. 2003 June; 69(6): 3640-5. Erratum In: Appl Environ Microbiol. 2003 September; 69(9): 5736. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12788773
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ADSA Foundation Scholar Award--An integrated science-based approach to dairy food safety: Listeria monocytogenes as a model system. Author(s): Wiedmann M; ADSA Foundation. Source: Journal of Dairy Science. 2003 June; 86(6): 1865-75. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12836921
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An improved cloning vector for construction of gene replacements in Listeria monocytogenes. Author(s): Li G, Kathariou S. Source: Applied and Environmental Microbiology. 2003 May; 69(5): 3020-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12732583
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An improved selective isolation medium for the recovery of Listeria monocytogenes from smoked fish. Author(s): Neamatallah AA, Dewar SJ, Austin B. Source: Letters in Applied Microbiology. 2003; 36(4): 230-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12641717
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An SNP-based PCR assay to differentiate between Listeria monocytogenes lineages derived from phylogenetic analysis of the sigB gene. Author(s): Moorhead SM, Dykes GA, Cursons RT. Source: Journal of Microbiological Methods. 2003 November; 55(2): 425-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14529964
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Antimicrobial activities against 84 Listeria monocytogenes isolates from patients with systemic listeriosis at a comprehensive cancer center (1955-1997). Author(s): Safdar A, Armstrong D. Source: Journal of Clinical Microbiology. 2003 January; 41(1): 483-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12517901
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Antimicrobial effects of mustard flour and acetic acid against Escherichia coli O157:H7, Listeria monocytogenes, and Salmonella enterica serovar Typhimurium. Author(s): Rhee MS, Lee SY, Dougherty RH, Kang DH. Source: Applied and Environmental Microbiology. 2003 May; 69(5): 2959-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12732572
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Antimicrobial resistance of Listeria monocytogenes. Author(s): Poros-Gluchowska J, Markiewicz Z. Source: Acta Microbiol Pol. 2003; 52(2): 113-29. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14594399
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Aromatic amino acids at the surface of InlB are essential for host cell invasion by Listeria monocytogenes. Author(s): Machner MP, Frese S, Schubert WD, Orian-Rousseau V, Gherardi E, Wehland J, Niemann HH, Heinz DW. Source: Molecular Microbiology. 2003 June; 48(6): 1525-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12791136
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Assessment of control measures to achieve a food safety objective of less than 100 CFU of Listeria monocytogenes per gram at the point of consumption for fresh precut iceberg lettuce. Author(s): Szabo EA, Simons L, Coventry MJ, Cole MB. Source: J Food Prot. 2003 February; 66(2): 256-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12597486
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Attachment of Listeria monocytogenes to radish tissue is dependent upon temperature and flagellar motility. Author(s): Gorski L, Palumbo JD, Mandrell RE. Source: Applied and Environmental Microbiology. 2003 January; 69(1): 258-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12514003
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Atypical colonial morphology and low recoveries of Listeria monocytogenes strains on Oxford, PALCAM, Rapid'L.mono and ALOA solid media. Author(s): Leclercq A. Source: Journal of Microbiological Methods. 2004 May; 57(2): 251-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15063065
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Auto, a surface associated autolysin of Listeria monocytogenes required for entry into eukaryotic cells and virulence. Author(s): Cabanes D, Dussurget O, Dehoux P, Cossart P. Source: Molecular Microbiology. 2004 March; 51(6): 1601-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15009888
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Bacterial endocarditis caused by Listeria monocytogenes. Author(s): Clark RA. Source: The Western Journal of Medicine. 1977 May; 126(5): 403-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=405800
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Bacterial endocarditis due to Listeria monocytogenes in a pregnant diabetic. Author(s): Holshouser CA, Ansbacher R, McNitt T, Steele R. Source: Obstetrics and Gynecology. 1978 January; 51(1 Suppl): 9S-10S. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=618485
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Bacteriocin-producing Enterococcus casseliflavus IM 416K1, a natural antagonist for control of Listeria monocytogenes in Italian sausages ("cacciatore"). Author(s): Sabia C, de Niederhausern S, Messi P, Manicardi G, Bondi M. Source: International Journal of Food Microbiology. 2003 October 15; 87(1-2): 173-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12927720
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Behavior of Listeria monocytogenes during processing and storage of experimentally contaminated hot-smoked trout. Author(s): Jemmi T, Keusch A. Source: International Journal of Food Microbiology. 1992 March-April; 15(3-4): 339-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1419540
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Behavior of Listeria monocytogenes in pasteurized milk during fermentation with lactic acid bacteria. Author(s): Pitt WM, Harden TJ, Hull RR. Source: J Food Prot. 2000 July; 63(7): 916-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10914660
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Betaine and carnitine uptake systems in Listeria monocytogenes affect growth and survival in foods and during infection. Author(s): Sleator RD, Francis GA, O'Beirne D, Gahan CG, Hill C. Source: Journal of Applied Microbiology. 2003; 95(4): 839-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12969299
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Bile stress response in Listeria monocytogenes LO28: adaptation, cross-protection, and identification of genetic loci involved in bile resistance. Author(s): Begley M, Gahan CG, Hill C. Source: Applied and Environmental Microbiology. 2002 December; 68(12): 6005-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12450822
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Biocide use in the food industry and the disinfectant resistance of persistent strains of Listeria monocytogenes and Escherichia coli. Author(s): Holah JT, Taylor JH, Dawson DJ, Hall KE. Source: Journal of Applied Microbiology. 2002; 92 Suppl: 111S-20S. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12000620
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Biological inactivation of adhering Listeria monocytogenes by listeriaphages and a quaternary ammonium compound. Author(s): Roy B, Ackermann HW, Pandian S, Picard G, Goulet J. Source: Applied and Environmental Microbiology. 1993 September; 59(9): 2914-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8215364
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Brain abscess caused by Listeria monocytogenes. Author(s): Brown PH, Ingram CW, van der Horst C. Source: Reviews of Infectious Diseases. 1991 July-August; 13(4): 768-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1925300
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Brain abscess due to Listeria monocytogenes: case report and literature review. Author(s): Dee RR, Lorber B. Source: Reviews of Infectious Diseases. 1986 November-December; 8(6): 968-77. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3099364
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Brain abscess due to Listeria monocytogenes: five cases and a review of the literature. Author(s): Eckburg PB, Montoya JG, Vosti KL. Source: Medicine; Analytical Reviews of General Medicine, Neurology, Psychiatry, Dermatology, and Pediatrics. 2001 July; 80(4): 223-35. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11470983
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Brainstem abscess and meningitis due to Listeria monocytogenes in an adult with juvenile chronic arthritis. Author(s): Turner D, Fried M, Hoffman M, Paleacu D, Reider I, Yust I. Source: Neurology. 1995 May; 45(5): 1020-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7746378
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Brainstem encephalitis (rhombencephalitis) due to Listeria monocytogenes: case report and review. Author(s): Armstrong RW, Fung PC. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1993 May; 16(5): 689-702. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8507761
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Brainstem encephalitis due to Listeria monocytogenes. Favourable outcome after early antibiotic therapy. Author(s): Barontini F, Leoncini F. Source: Italian Journal of Neurological Sciences. 1989 February; 10(1): 85-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2925348
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Capacity of ivanolysin O to replace listeriolysin O in phagosomal escape and in vivo survival of Listeria monocytogenes. Author(s): Frehel C, Lety MA, Autret N, Beretti JL, Berche P, Charbit A. Source: Microbiology (Reading, England). 2003 March; 149(Pt 3): 611-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12634330
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Carriage of Listeria monocytogenes and related species in pregnant and non-pregnant women in Aberdeen, Scotland. Author(s): Lamont RJ, Postlethwaite R. Source: The Journal of Infection. 1986 September; 13(2): 187-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3093591
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Cerebellar abscess due to Listeria monocytogenes. Author(s): Addas BM, Jan MS. Source: Saudi Med J. 2002 February; 23(2): 226-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11938402
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Characterization and pathogenic potential of Listeria monocytogenes isolates from the smoked fish industry. Author(s): Norton DM, Scarlett JM, Horton K, Sue D, Thimothe J, Boor KJ, Wiedmann M. Source: Applied and Environmental Microbiology. 2001 February; 67(2): 646-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11157227
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Characterization of an extracellular virulence factor made by group A Streptococcus with homology to the Listeria monocytogenes internalin family of proteins. Author(s): Reid SD, Montgomery AG, Voyich JM, DeLeo FR, Lei B, Ireland RM, Green NM, Liu M, Lukomski S, Musser JM. Source: Infection and Immunity. 2003 December; 71(12): 7043-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14638794
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Characterization of Listeria monocytogenes recovered from 41 cases of sporadic listeriosis in Austria by serotyping and pulsed-field gel electrophoresis. Author(s): Wagner M, Allerberger F. Source: Fems Immunology and Medical Microbiology. 2003 April 1; 35(3): 227-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12648841
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Characterization of Listeria monocytogenes strains involved in invasive and noninvasive listeriosis outbreaks by PCR-based fingerprinting techniques. Author(s): Franciosa G, Tartaro S, Wedell-Neergaard C, Aureli P. Source: Applied and Environmental Microbiology. 2001 April; 67(4): 1793-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11282635
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Characterization of natural killer cells induced in the peritoneal exudates of mice infected with Listeria monocytogenes: a study of their tumor target specificity and their expression of murine differentiation antigens and human NK-associated antigens. Author(s): Holmberg LA, Ault KA. Source: Cellular Immunology. 1984 November; 89(1): 151-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6435890
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Chronic active hepatitis, haemolytic anaemia and Listeria monocytogenes bacteraemia. Author(s): Chadwick RG, Graham JM. Source: Postgraduate Medical Journal. 1978 January; 54(627): 55-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=625461
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Cloning, sequencing and characterisation of a Listeria monocytogenes gene encoding a fibronectin-binding protein. Author(s): Gilot P, Jossin Y, Content J. Source: Journal of Medical Microbiology. 2000 October; 49(10): 887-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11023185
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Comparative analysis of multilocus sequence typing and pulsed-field gel electrophoresis for characterizing Listeria monocytogenes strains isolated from environmental and clinical sources. Author(s): Revazishvili T, Kotetishvili M, Stine OC, Kreger AS, Morris JG Jr, Sulakvelidze A. Source: Journal of Clinical Microbiology. 2004 January; 42(1): 276-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14715765
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Comparative genetic characterization of Listeria monocytogenes isolates from human and animal listeriosis cases. Author(s): Jeffers GT, Bruce JL, McDonough PL, Scarlett J, Boor KJ, Wiedmann M. Source: Microbiology (Reading, England). 2001 May; 147(Pt 5): 1095-104. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11320113
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Comparative intracellular (THP-1 macrophage) and extracellular activities of betalactams, azithromycin, gentamicin, and fluoroquinolones against Listeria monocytogenes at clinically relevant concentrations. Author(s): Carryn S, Van Bambeke F, Mingeot-Leclercq MP, Tulkens PM. Source: Antimicrobial Agents and Chemotherapy. 2002 July; 46(7): 2095-103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12069960
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Comparison of sludge and clinical isolates of Listeria monocytogenes. Author(s): Lozniewski A, Humbert A, Corsaro D, Schwartzbrod J, Weber M, Le Faou A. Source: Letters in Applied Microbiology. 2001 May; 32(5): 336-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11328501
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Comparison of the genome sequences of Listeria monocytogenes and Listeria innocua: clues for evolution and pathogenicity. Author(s): Buchrieser C, Rusniok C, Kunst F, Cossart P, Glaser P; Listeria Consortium. Source: Fems Immunology and Medical Microbiology. 2003 April 1; 35(3): 207-13. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12648839
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Construction, characterization, and use of two Listeria monocytogenes site-specific phage integration vectors. Author(s): Lauer P, Chow MY, Loessner MJ, Portnoy DA, Calendar R. Source: Journal of Bacteriology. 2002 August; 184(15): 4177-86. Erratum In: J Bacteriol. 2003 February; 185(4): 1484. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12107135
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Control of Listeria monocytogenes in the food-processing environment. Author(s): Tompkin RB. Source: J Food Prot. 2002 April; 65(4): 709-25. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11952224
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Control options for Listeria monocytogenes in seafoods. Author(s): Huss HH, Jorgensen LV, Vogel BF. Source: International Journal of Food Microbiology. 2000 December 20; 62(3): 267-74. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11156271
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Corneal ulcer due to Listeria monocytogenes. Author(s): Holland S, Alfonso E, Gelender H, Heidemann D, Mendelsohn A, Ullman S, Miller D. Source: Cornea. 1987; 6(2): 144-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3608514
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Correlations between molecular subtyping and serotyping of Listeria monocytogenes. Author(s): Nadon CA, Woodward DL, Young C, Rodgers FG, Wiedmann M. Source: Journal of Clinical Microbiology. 2001 July; 39(7): 2704-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11427601
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Delayed presentation of prosthetic joint infection due to Listeria monocytogenes. Author(s): Chougle A, Narayanaswamy V. Source: Int J Clin Pract. 2004 April; 58(4): 420-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15161131
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Deletion of the gene encoding p60 in Listeria monocytogenes leads to abnormal cell division and loss of actin-based motility. Author(s): Pilgrim S, Kolb-Maurer A, Gentschev I, Goebel W, Kuhn M. Source: Infection and Immunity. 2003 June; 71(6): 3473-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12761132
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Detection of Listeria monocytogenes by polymerase chain reaction in intestinal mucosal biopsies from patients with inflammatory bowel disease and controls. Author(s): Chen W, Li D, Paulus B, Wilson I, Chadwick VS. Source: Journal of Gastroenterology and Hepatology. 2000 October; 15(10): 1145-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11106094
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Detection of Listeria monocytogenes in humans, animals and foods. Author(s): Iida T, Kanzaki M, Nakama A, Kokubo Y, Maruyama T, Kaneuchi C. Source: The Journal of Veterinary Medical Science / the Japanese Society of Veterinary Science. 1998 December; 60(12): 1341-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9879536
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Development of a Listeria monocytogenes EGDe partial proteome reference map and comparison with the protein profiles of food isolates. Author(s): Ramnath M, Rechinger KB, Jansch L, Hastings JW, Knochel S, Gravesen A. Source: Applied and Environmental Microbiology. 2003 June; 69(6): 3368-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12788738
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Development of a multilocus sequence typing method for analysis of Listeria monocytogenes clones. Author(s): Salcedo C, Arreaza L, Alcala B, de la Fuente L, Vazquez JA. Source: Journal of Clinical Microbiology. 2003 February; 41(2): 757-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12574278
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Differences in pathogenicity for chick embryos and growth kinetics at 37 degrees C between clinical and meat isolates of Listeria monocytogenes previously stored at 4 degrees C. Author(s): Avery SM, Buncic S. Source: International Journal of Food Microbiology. 1997 March 3; 34(3): 319-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9039576
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Differential chemokine response of murine macrophages stimulated with cytokines and infected with Listeria monocytogenes. Author(s): Flesch IE, Barsig J, Kaufmann SH. Source: International Immunology. 1998 June; 10(6): 757-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9678756
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Differential diagnosis between Streptococcus agalactiae and Listeria monocytogenes in the clinical laboratory. Author(s): Kontnick C, von Graevenitz A, Piscitelli V. Source: Ann Clin Lab Sci. 1977 May-June; 7(3): 269-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=404952
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Differential expression of Listeria monocytogenes virulence genes in mammalian host cells. Author(s): Bubert A, Sokolovic Z, Chun SK, Papatheodorou L, Simm A, Goebel W. Source: Molecular & General Genetics : Mgg. 1999 March; 261(2): 323-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10102368
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Differential roles of multiple signal peptidases in the virulence of Listeria monocytogenes. Author(s): Bonnemain C, Raynaud C, Reglier-Poupet H, Dubail I, Frehel C, Lety MA, Berche P, Charbit A. Source: Molecular Microbiology. 2004 March; 51(5): 1251-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14982622
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Discrimination among Listeria monocytogenes isolates using a mixed genome DNA microarray. Author(s): Borucki MK, Krug MJ, Muraoka WT, Call DR. Source: Veterinary Microbiology. 2003 April 29; 92(4): 351-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12554104
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Discrimination of Listeria monocytogenes strains of serotype 4b by restriction enzyme analysis of chromosomal DNA. Author(s): Saito A, Sawada T, Tokumaru Y, Hondo R. Source: Jpn J Med Sci Biol. 1997 April; 50(2): 63-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9559441
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Dissemination of Listeria monocytogenes by infected phagocytes. Author(s): Drevets DA. Source: Infection and Immunity. 1999 July; 67(7): 3512-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10377133
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Distinct protein patterns associated with Listeria monocytogenes InlA- or InlBphagosomes. Author(s): Pizarro-Cerda J, Jonquieres R, Gouin E, Vandekerckhove J, Garin J, Cossart P. Source: Cellular Microbiology. 2002 February; 4(2): 101-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11896766
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Dithiothreitol enhances Listeria monocytogenes mediated cell cytotoxicity. Author(s): Westbrook DG, Bhunia AK. Source: Microbiology and Immunology. 2000; 44(6): 431-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10941925
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Division of Listeria monocytogenes serovar 1/2a strains into two groups by PCR and restriction enzyme analysis. Author(s): Unnerstad H, Nilsson I, Ericsson H, Danielsson-Tham ML, Bille J, Bannerman E, Tham W. Source: Applied and Environmental Microbiology. 1999 May; 65(5): 2054-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10224000
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Does etanercept monotherapy enhance the risk of Listeria monocytogenes meningitis? Author(s): Pagliano P, Attanasio V, Fusco U, Mohamed DA, Rossi M, Faella FS. Source: Annals of the Rheumatic Diseases. 2004 April; 63(4): 462-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15020347
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Effect of acid adaptation on the fate of Listeria monocytogenes in THP-1 human macrophages activated by gamma interferon. Author(s): Conte MP, Petrone G, Di Biase AM, Longhi C, Penta M, Tinari A, Superti F, Fabozzi G, Visca P, Seganti L. Source: Infection and Immunity. 2002 August; 70(8): 4369-78. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12117947
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Effect of gamma irradiation on Listeria monocytogenes in frozen, artificially contaminated sandwiches. Author(s): Clardy S, Foley DM, Caporaso F, Calicchia ML, Prakash A. Source: J Food Prot. 2002 November; 65(11): 1740-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12430695
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Effect of Listeria monocytogenes septicemia during pregnancy on the offspring. Author(s): Zervoudakis IA, Cederqvist LL. Source: American Journal of Obstetrics and Gynecology. 1977 October 15; 129(4): 465-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=910831
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Effect of oxygen concentration and redox potential on recovery of sublethally heatdamaged cells of Escherichia coli O157:H7, Salmonella enteritidis and Listeria monocytogenes. Author(s): George SM, Richardson LC, Pol IE, Peck MW. Source: Journal of Applied Microbiology. 1998 May; 84(5): 903-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9674145
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Effect of superatmospheric oxygen packaging on sensorial quality, spoilage, and Listeria monocytogenes and Aeromonas caviae growth in fresh processed mixed salads. Author(s): Allende A, Jacxsens L, Devlieghere F, Debevere J, Artes F. Source: J Food Prot. 2002 October; 65(10): 1565-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380740
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Effects of a bacteriocin-like inhibitory substance from Carnobacterium piscicola against human and salmon isolates of Listeria monocytogenes. Author(s): Schobitz R, Suazo V, Costa M, Ciampi L. Source: International Journal of Food Microbiology. 2003 July 25; 84(2): 237-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12781946
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Effects of trimethoprim and co-trimoxazole on the morphology of Listeria monocytogenes in culture medium and after phagocytosis. Author(s): Minkowski P, Staege H, Groscurth P, Schaffner A. Source: The Journal of Antimicrobial Chemotherapy. 2001 August; 48(2): 185-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11481287
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Effects of vegetable type, package atmosphere and storage temperature on growth and survival of Escherichia coli O157:H7 and Listeria monocytogenes. Author(s): Francis GA, O'Beirne D. Source: Journal of Industrial Microbiology & Biotechnology. 2001 August; 27(2): 111-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11641769
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Efflux pump Lde is associated with fluoroquinolone resistance in Listeria monocytogenes. Author(s): Godreuil S, Galimand M, Gerbaud G, Jacquet C, Courvalin P. Source: Antimicrobial Agents and Chemotherapy. 2003 February; 47(2): 704-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12543681
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Engineered Listeria monocytogenes as an AIDS vaccine. Author(s): Lieberman J, Frankel FR. Source: Vaccine. 2002 May 6; 20(15): 2007-10. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11983264
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Enzyme release of antigen from Streptococcus faecalis and Listeria monocytogenes cross-reactive with Lancefield group G typing reagents. Author(s): Hopfer RL, Pinzon R, Wenglar M, Rolston KV. Source: Journal of Clinical Microbiology. 1985 October; 22(4): 677-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3935666
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Epidural abscess and vertebral osteomyelitis caused by Listeria monocytogenes: case report and literature review. Author(s): Khan KM, Pao W, Kendler J. Source: Scandinavian Journal of Infectious Diseases. 2001; 33(9): 714-6. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11669234
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Eukaryotic expression plasmid transfer from the intracellular bacterium Listeria monocytogenes to host cells. Author(s): Hense M, Domann E, Krusch S, Wachholz P, Dittmar KE, Rohde M, Wehland J, Chakraborty T, Weiss S. Source: Cellular Microbiology. 2001 September; 3(9): 599-609. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11553012
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Evaluation of the pH-dependent, stationary-phase acid tolerance in Listeria monocytogenes and Salmonella Typhimurium DT104 induced by culturing in media with 1% glucose: a comparative study with Escherichia coli O157:H7. Author(s): Samelis J, Ikeda JS, Sofos JN. Source: Journal of Applied Microbiology. 2003; 95(3): 563-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12911705
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Experimental mixed infection of rabbits with Yersinia enterocolitica and Listeria monocytogenes. Author(s): Najdenski H, Vesselinova A. Source: Journal of Veterinary Medicine. B, Infectious Diseases and Veterinary Public Health. 2002 March; 49(2): 97-104. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12002426
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Experimental validation of low virulence in field strains of Listeria monocytogenes. Author(s): Roche SM, Gracieux P, Albert I, Gouali M, Jacquet C, Martin PM, Velge P. Source: Infection and Immunity. 2003 June; 71(6): 3429-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12761127
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Exploitation of host cell cytoskeleton and signalling during Listeria monocytogenes entry into mammalian cells. Author(s): Pizarro-Cerda J, Sousa S, Cossart P. Source: Comptes Rendus Biologies. 2004 February; 327(2): 115-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15060982
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Exposure of Listeria monocytogenes within an epidemic caused by butter in Finland. Author(s): Maijala R, Lyytikainen O, Autio T, Aalto T, Haavisto L, Honkanen-Buzalski T. Source: International Journal of Food Microbiology. 2001 October 22; 70(1-2): 97-109. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11759767
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Expression of ActA, Ami, InlB, and listeriolysin O in Listeria monocytogenes of human and food origin. Author(s): Jacquet C, Gouin E, Jeannel D, Cossart P, Rocourt J. Source: Applied and Environmental Microbiology. 2002 February; 68(2): 616-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11823199
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Expression of truncated Internalin A is involved in impaired internalization of some Listeria monocytogenes isolates carried asymptomatically by humans. Author(s): Olier M, Pierre F, Rousseaux S, Lemaitre JP, Rousset A, Piveteau P, Guzzo J. Source: Infection and Immunity. 2003 March; 71(3): 1217-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12595435
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Factors controlling acid tolerance of Listeria monocytogenes: effects of nisin and other ionophores. Author(s): Datta AR, Benjamin MM. Source: Applied and Environmental Microbiology. 1997 October; 63(10): 4123-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9327581
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Fatal endocarditis due to Listeria monocytogenes. Author(s): Carvajal A, Frederiksen W. Source: Reviews of Infectious Diseases. 1988 May-June; 10(3): 616-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3293164
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Fatal Listeria monocytogenes meningitis in two previously healthy adults. Author(s): Uprichard AC, Logan KR. Source: Ulster Med J. 1986 April; 55(1): 70-3. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3739064
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Fatal meningitis due to Listeria monocytogenes in elderly patients with underlying malignancy. Author(s): Levidiotou S, Charalabopoulos K, Vrioni G, Chaidos A, Polysoidis K, Bourantas K, Stefanou D. Source: Int J Clin Pract. 2004 March; 58(3): 292-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15117098
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Fatal pericarditis due to Listeria monocytogenes. Author(s): Revathi G, Suneja A, Talwar V, Aggarwal N. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 1995 March; 14(3): 254-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7614972
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Fatal septicaemia due to Listeria monocytogenes in a patient with systemic lupus erythematosus receiving cyclosporin and high prednisone doses. Author(s): Giunta G, Piazza I. Source: The Netherlands Journal of Medicine. 1992 April; 40(3-4): 197-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1603211
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Fate of Listeria monocytogenes in processed meat products during refrigerated storage. Author(s): Glass KA, Doyle MP. Source: Applied and Environmental Microbiology. 1989 June; 55(6): 1565-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2504110
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Fecal carriage of Listeria monocytogenes--observations during a community-wide, common-source outbreak. Author(s): Mascola L, Sorvillo F, Goulet V, Hall B, Weaver R, Linnan M. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1992 September; 15(3): 557-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1520812
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Fetal death in utero secondary to Listeria monocytogenes placental infection. Author(s): Plaza MC, Gilbert-Barness E. Source: Pediatric Pathology & Molecular Medicine. 2001 September-October; 20(5): 4337. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11552741
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First documented outbreak of Listeria monocytogenes in Quebec, 2002. Author(s): Gaulin C, Ramsay D, Ringuette L, Ismail J. Source: Can Commun Dis Rep. 2003 November 1; 29(21): 181-6. English, French. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14603730
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First-trimester maternal Listeria monocytogenes sepsis and chorioamnionitis with normal neonatal outcome. Author(s): Cruikshank DP, Warenski JC. Source: Obstetrics and Gynecology. 1989 March; 73(3 Pt 2): 469-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2783771
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Flt3 ligand pretreatment promotes protective immunity to Listeria monocytogenes. Author(s): Gregory SH, Sagnimeni AJ, Zurowski NB, Thomson AW. Source: Cytokine. 2001 February 21; 13(4): 202-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11237427
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Food-borne Listeria monocytogenes risk assessment. Author(s): Hitchins AD, Whiting RC. Source: Food Additives and Contaminants. 2001 December; 18(12): 1108-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11761122
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Formation of D-alanyl-lipoteichoic acid is required for adhesion and virulence of Listeria monocytogenes. Author(s): Abachin E, Poyart C, Pellegrini E, Milohanic E, Fiedler F, Berche P, TrieuCuot P. Source: Molecular Microbiology. 2002 January; 43(1): 1-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11849532
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Frequency of bacteriocin resistance development and associated fitness costs in Listeria monocytogenes. Author(s): Gravesen A, Jydegaard Axelsen AM, Mendes da Silva J, Hansen TB, Knochel S. Source: Applied and Environmental Microbiology. 2002 February; 68(2): 756-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11823216
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From hot dogs to CD8+ T cells: Listeria monocytogenes. Author(s): Wing EJ, Gregory SH. Source: Trans Am Clin Climatol Assoc. 2000; 111: 76-83; Discussion 84. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10881333
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Fulminant Listeria monocytogenes meningitis complicated with acute hydrocephalus in healthy children beyond the newborn period. Author(s): Ulloa-Gutierrez R, Avila-Aguero ML, Huertas E. Source: Pediatric Emergency Care. 2004 April; 20(4): 233-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15057178
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Functional assembly of two membrane-binding domains in listeriolysin O, the cytolysin of Listeria monocytogenes. Author(s): Dubail I, Autret N, Beretti JL, Kayal S, Berche P, Charbit A. Source: Microbiology (Reading, England). 2001 October; 147(Pt 10): 2679-88. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11577147
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Gamma interferon induces monocyte killing of Listeria monocytogenes by an oxygen-dependent pathway; alpha- or beta-interferons by oxygen-independent pathways. Author(s): Peck R. Source: Journal of Leukocyte Biology. 1989 November; 46(5): 434-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2509611
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Gastroenteritis caused by Listeria monocytogenes in a private day-care facility. Author(s): Heitmann M, Gerner-Smidt P, Heltberg O. Source: The Pediatric Infectious Disease Journal. 1997 August; 16(8): 827-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9271054
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Gastrointestinal carriage of Listeria monocytogenes in household contacts of patients with listeriosis. Author(s): Schuchat A, Deaver K, Hayes PS, Graves L, Mascola L, Wenger JD. Source: The Journal of Infectious Diseases. 1993 May; 167(5): 1261-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8486970
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gC1q-R/p32, a C1q-binding protein, is a receptor for the InlB invasion protein of Listeria monocytogenes. Author(s): Braun L, Ghebrehiwet B, Cossart P. Source: The Embo Journal. 2000 April 3; 19(7): 1458-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10747014
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Gelsolin, a protein that caps the barbed ends and severs actin filaments, enhances the actin-based motility of Listeria monocytogenes in host cells. Author(s): Laine RO, Phaneuf KL, Cunningham CC, Kwiatkowski D, Azuma T, Southwick FS. Source: Infection and Immunity. 1998 August; 66(8): 3775-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9673261
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Gene fragments distinguishing an epidemic-associated strain from a virulent prototype strain of Listeria monocytogenes belong to a distinct functional subset of genes and partially cross-hybridize with other Listeria species. Author(s): Herd M, Kocks C. Source: Infection and Immunity. 2001 June; 69(6): 3972-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11349066
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Generalized transduction of serotype 1/2 and serotype 4b strains of Listeria monocytogenes. Author(s): Hodgson DA. Source: Molecular Microbiology. 2000 January; 35(2): 312-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10652092
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Genetic basis of tetracycline resistance in clinical isolates of Listeria monocytogenes. Author(s): Poyart-Salmeron C, Trieu-Cuot P, Carlier C, MacGowan A, McLauchlin J, Courvalin P. Source: Antimicrobial Agents and Chemotherapy. 1992 February; 36(2): 463-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1605611
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Genetic characterisation of isolates of Listeria monocytogenes from man, animals and food. Author(s): Trott DJ, Robertson ID, Hampson DJ. Source: Journal of Medical Microbiology. 1993 February; 38(2): 122-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8429537
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Genetic characterization of plasmid-encoded multiple antibiotic resistance in a strain of Listeria monocytogenes causing endocarditis. Author(s): Hadorn K, Hachler H, Schaffner A, Kayser FH. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 1993 December; 12(12): 928-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8187788
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Genetic homogeneity among Listeria monocytogenes strains from infected patients and meat products from two geographic locations determined by phenotyping, ribotyping and PCR analysis of virulence genes. Author(s): Jaradat ZW, Schutze GE, Bhunia AK. Source: International Journal of Food Microbiology. 2002 June 5; 76(1-2): 1-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12038565
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Genetic typing of human and food isolates of Listeria monocytogenes from episodes of listeriosis. Author(s): Franciosa G, Pourshaban M, Gianfranceschi M, Aureli P. Source: European Journal of Epidemiology. 1998 February; 14(2): 205-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9556182
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Genetic variability among isolates of Listeria monocytogenes from food products, clinical samples and processing environments, estimated by RAPD typing. Author(s): Martinez I, Rorvik LM, Brox V, Lassen J, Seppola M, Gram L, FonnesbechVogel B. Source: International Journal of Food Microbiology. 2003 August 1; 84(3): 285-97. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12810292
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Genomic fingerprinting of 80 strains from the WHO multicenter international typing study of listeria monocytogenes via pulsed-field gel electrophoresis (PFGE). Author(s): Brosch R, Brett M, Catimel B, Luchansky JB, Ojeniyi B, Rocourt J. Source: International Journal of Food Microbiology. 1996 October; 32(3): 343-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8913805
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Glucose and nutrient concentrations affect the expression of a 104-kilodalton Listeria adhesion protein in Listeria monocytogenes. Author(s): Jaradat ZW, Bhunia AK. Source: Applied and Environmental Microbiology. 2002 October; 68(10): 4876-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12324334
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Good visual outcome after Listeria monocytogenes endogenous endophthalmitis. Author(s): Deramo VA, Shah GK, Garden M, Maguire JI. Source: Retina (Philadelphia, Pa.). 1999; 19(6): 566-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10606462
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Growth and thermal inactivation of Listeria monocytogenes in cabbage and cabbage juice. Author(s): Beuchat LR, Brackett RE, Hao DY, Conner DE. Source: Canadian Journal of Microbiology. 1986 October; 32(10): 791-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3098397
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Growth of Listeria monocytogenes at refrigeration temperatures. Author(s): Walker SJ, Archer P, Banks JG. Source: The Journal of Applied Bacteriology. 1990 February; 68(2): 157-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2108109
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Growth suppression of Listeria monocytogenes in a meat product. Author(s): Qvist S, Sehested K, Zeuthen P. Source: International Journal of Food Microbiology. 1994 December; 24(1-2): 283-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7703021
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Growth, morphology and surface properties of Listeria monocytogenes Scott A and LO28 under saline and acid environments. Author(s): Bereksi N, Gavini F, Benezech T, Faille C. Source: Journal of Applied Microbiology. 2002; 92(3): 556-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11872133
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H2-M3 restricted presentation of Listeria monocytogenes antigens. Author(s): Lenz LL, Bevan MJ. Source: Immunological Reviews. 1996 June; 151: 107-21. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8872487
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Health risk assessment of Listeria monocytogenes in Canada. Author(s): Farber JM, Ross WH, Harwig J. Source: International Journal of Food Microbiology. 1996 June; 30(1-2): 145-56. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8856380
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Hemolytic activity reevaluation of putative nonpathogenic Listeria monocytogenes strains. Author(s): Lachica RV. Source: Applied and Environmental Microbiology. 1996 November; 62(11): 4293-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8984907
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Heteroduplex mobility assay for the identification of Listeria sp and Listeria monocytogenes strains: application to characterisation of strains from sludge and food samples. Author(s): Garrec N, Marault M, Kerouanton A, Brisabois A, Pourcher AM, Sutra L. Source: Fems Immunology and Medical Microbiology. 2003 October 15; 38(3): 257-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14522461
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Heterogeneity of virulence-related properties in Listeria monocytogenes strains isolated from patients with haematological malignancies. Author(s): Longhi C, Penta M, Conte MP, Girmenia C, Seganti L. Source: Int J Immunopathol Pharmacol. 2003 May-August; 16(2): 119-27. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12797902
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High incidence of Listeria monocytogenes in European red smear cheese. Author(s): Rudol M, Scherer S. Source: International Journal of Food Microbiology. 2001 January 22; 63(1-2): 91-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11205958
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High-frequency endonuclease (REA) typing: results from the WHO collaborative study group on subtyping of Listeria monocytogenes. Author(s): Gerner-Smidt P, Boerlin P, Ischer F, Schmidt J. Source: International Journal of Food Microbiology. 1996 October; 32(3): 313-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8913803
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High-level expression of the Listeria monocytogenes listeriolysin O in Escherichia coli and preliminary characterization of the purified protein. Author(s): Giammarini C, Andreoni F, Amagliani G, Casiere A, Barocci S, Magnani M. Source: Protein Expression and Purification. 2003 March; 28(1): 78-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12651110
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High-pressure destruction kinetics of Listeria monocytogenes on pork. Author(s): Mussa DM, Ramaswamy HS, Smith JP. Source: J Food Prot. 1999 January; 62(1): 40-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9921827
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Host cell protein tyrosine kinases are activated during the entry of Listeria monocytogenes. Possible role of pp60c-src family protein kinases. Author(s): Van Langendonck N, Velge P, Bottreau E. Source: Fems Microbiology Letters. 1998 May 1; 162(1): 169-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9595679
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Host cell signal transduction during Listeria monocytogenes infection. Author(s): Kuhn M, Pfeuffer T, Greiffenberg L, Goebel W. Source: Archives of Biochemistry and Biophysics. 1999 December 1; 372(1): 166-72. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10562430
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Host cell signalling during Listeria monocytogenes infection. Author(s): Kuhn M, Goebel W. Source: Trends in Microbiology. 1998 January; 6(1): 11-5. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9481817
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Host-pathogen interactions during entry and actin-based movement of Listeria monocytogenes. Author(s): Ireton K, Cossart P. Source: Annual Review of Genetics. 1997; 31: 113-38. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9442892
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Human dendritic cells infected by Listeria monocytogenes: induction of maturation, requirements for phagolysosomal escape and antigen presentation capacity. Author(s): Paschen A, Dittmar KE, Grenningloh R, Rohde M, Schadendorf D, Domann E, Chakraborty T, Weiss S. Source: European Journal of Immunology. 2000 December; 30(12): 3447-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11093163
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Human endothelial cell activation and mediator release in response to Listeria monocytogenes virulence factors. Author(s): Rose F, Zeller SA, Chakraborty T, Domann E, Machleidt T, Kronke M, Seeger W, Grimminger F, Sibelius U. Source: Infection and Immunity. 2001 February; 69(2): 897-905. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11159983
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Human gamma/delta T-cell response to Listeria monocytogenes protein components in vitro. Author(s): Munk ME, Elser C, Kaufmann SH. Source: Immunology. 1996 February; 87(2): 230-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8698384
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Human HLA-B27 gene enhances susceptibility of rats to oral infection by Listeria monocytogenes. Author(s): Warner TF, Madsen J, Starling J, Wagner RD, Taurog JD, Balish E. Source: American Journal of Pathology. 1996 November; 149(5): 1737-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8909262
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Human T-cell recognition of Listeria monocytogenes: recognition of listeriolysin O by TcR alpha beta + and TcR gamma delta + T cells. Author(s): Guo Y, Ziegler HK, Safley SA, Niesel DW, Vaidya S, Klimpel GR. Source: Infection and Immunity. 1995 June; 63(6): 2288-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7768611
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Human toll-like receptor 2 mediates monocyte activation by Listeria monocytogenes, but not by group B streptococci or lipopolysaccharide. Author(s): Flo TH, Halaas O, Lien E, Ryan L, Teti G, Golenbock DT, Sundan A, Espevik T. Source: Journal of Immunology (Baltimore, Md. : 1950). 2000 February 15; 164(4): 2064-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10657659
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Hydrocephalus internus--first manifestation of chronic meningitis due to Listeria monocytogenes. Author(s): Grafe G, Handrik W, Geyer C. Source: European Journal of Pediatric Surgery : Official Journal of Austrian Association of Pediatric Surgery. [et Al] = Zeitschrift Fur Kinderchirurgie. 2001 December; 11 Suppl 1: S46-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11848049
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Identification of Listeria monocytogenes genes involved in salt and alkaline-pH tolerance. Author(s): Gardan R, Cossart P, Labadie J; European Listeria Genome Consortium. Source: Applied and Environmental Microbiology. 2003 June; 69(6): 3137-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12788708
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Identification of LpeA, a PsaA-like membrane protein that promotes cell entry by Listeria monocytogenes. Author(s): Reglier-Poupet H, Pellegrini E, Charbit A, Berche P. Source: Infection and Immunity. 2003 January; 71(1): 474-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12496198
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Identification of the agr locus of Listeria monocytogenes: role in bacterial virulence. Author(s): Autret N, Raynaud C, Dubail I, Berche P, Charbit A. Source: Infection and Immunity. 2003 August; 71(8): 4463-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12874326
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Impairment of growth of Listeria monocytogenes in THP-1 macrophages by granulocyte macrophage colony-stimulating factor: release of tumor necrosis factoralpha and nitric oxide. Author(s): Carryn S, Van de Velde S, Van Bambeke F, Mingeot-Leclercq MP, Tulkens PM. Source: The Journal of Infectious Diseases. 2004 June 1; 189(11): 2101-9. Epub 2004 May 12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15143479
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In vitro and in vivo invasiveness of different pulsed-field gel electrophoresis types of Listeria monocytogenes. Author(s): Larsen CN, Norrung B, Sommer HM, Jakobsen M. Source: Applied and Environmental Microbiology. 2002 November; 68(11): 5698-703. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12406767
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In vitro study of Listeria monocytogenes infection to murine primary and human transformed B cells. Author(s): Menon A, Shroyer ML, Wampler JL, Chawan CB, Bhunia AK. Source: Comparative Immunology, Microbiology and Infectious Diseases. 2003 May; 26(3): 157-74. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12581746
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Inactivation of Listeria monocytogenes Scott A 49594 in apple juice supplemented with cinnamon. Author(s): Yuste J, Fung DY. Source: J Food Prot. 2002 October; 65(10): 1663-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380758
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Incidence and susceptibility to antimicrobial agents of Listeria spp. and Listeria monocytogenes isolated from poultry carcasses in Porto, Portugal. Author(s): Antunes P, Reu C, Sousa JC, Pestana N, Peixe L. Source: J Food Prot. 2002 December; 65(12): 1888-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12495006
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Incidence of fecal carriage of Listeria monocytogenes in three healthy volunteers: a one-year prospective stool survey. Author(s): Grif K, Patscheider G, Dierich MP, Allerberger F. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2003 January; 22(1): 16-20. Epub 2003 January 18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12582739
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Incidence of Listeria monocytogenes in food and environmental samples in Italy between 1990 and 1999: serotype distribution in food, environmental and clinical samples. Author(s): Gianfranceschi M, Gattuso A, Tartaro S, Aureli P. Source: European Journal of Epidemiology. 2003; 18(10): 1001-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14598931
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Inducible costimulator protein controls the protective T cell response against Listeria monocytogenes. Author(s): Mittrucker HW, Kursar M, Kohler A, Yanagihara D, Yoshinaga SK, Kaufmann SH. Source: Journal of Immunology (Baltimore, Md. : 1950). 2002 November 15; 169(10): 5813-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12421962
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Infection with Listeria monocytogenes following orthotopic liver transplantation: case report and review of the literature. Author(s): Rettally CA, Speeg KV. Source: Transplantation Proceedings. 2003 June; 35(4): 1485-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12826201
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Listeria monocytogenes
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Influence of P-glycoprotein and MRP efflux pump inhibitors on the intracellular activity of azithromycin and ciprofloxacin in macrophages infected by Listeria monocytogenes or Staphylococcus aureus. Author(s): Seral C, Carryn S, Tulkens PM, Van Bambeke F. Source: The Journal of Antimicrobial Chemotherapy. 2003 May; 51(5): 1167-73. Epub 2003 April 14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12697643
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InlB, a surface protein of Listeria monocytogenes that behaves as an invasin and a growth factor. Author(s): Bierne H, Cossart P. Source: Journal of Cell Science. 2002 September 1; 115(Pt 17): 3357-67. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12154067
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Intestinal P glycoprotein acts as a natural defense mechanism against Listeria monocytogenes. Author(s): Neudeck BL, Loeb JM, Faith NG, Czuprynski CJ. Source: Infection and Immunity. 2004 July; 72(7): 3849-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15213126
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Intra-abdominal abscess caused by Listeria monocytogenes in a patient with acquired hemolytic anemia and thrombocytopenia. Author(s): Sile H, Norwood J. Source: Southern Medical Journal. 2002 November; 95(11): 1350-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12540008
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Intracellular activity of fosfomycin against two distinct enteropathogenic bacteria, Salmonella enterica and Listeria monocytogenes, alive inside host cells. Author(s): Okada N, Nishio M, Danbara H. Source: Chemotherapy. 2003 May; 49(1-2): 49-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12714811
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Invasion of mammalian cells by Listeria monocytogenes: functional mimicry to subvert cellular functions. Author(s): Cossart P, Pizarro-Cerda J, Lecuit M. Source: Trends in Cell Biology. 2003 January; 13(1): 23-31. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12480337
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Involvement of Listeria monocytogenes in the abortive disease. Author(s): Caplan DM. Source: Roum Arch Microbiol Immunol. 2001 October-December; 60(4): 329-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12561675
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Isolation of Listeria monocytogenes mutants with high-level in vitro expression of host cytosol-induced gene products. Author(s): Shetron-Rama LM, Mueller K, Bravo JM, Bouwer HG, Way SS, Freitag NE. Source: Molecular Microbiology. 2003 June; 48(6): 1537-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12791137
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Joint infections due to Listeria monocytogenes: case report and review. Author(s): Ellis LC, Segreti J, Gitelis S, Huber JF. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1995 June; 20(6): 1548-50. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7548508
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Killing of Listeria monocytogenes by human neutrophils and monocytes, but not by monocyte-derived macrophages. Author(s): Czuprynski CJ, Campbell PA, Henson PM. Source: J Reticuloendothel Soc. 1983 July; 34(1): 29-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6410063
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Lactoferricin influences early events of Listeria monocytogenes infection in THP-1 human macrophages. Author(s): Longhi C, Conte MP, Penta M, Cossu A, Antonini G, Superti F, Seganti L. Source: Journal of Medical Microbiology. 2004 February; 53(Pt 2): 87-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14729926
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Listeria monocytogenes and inflammatory bowel disease: detection of Listeria species in intestinal mucosal biopsies by real-time PCR. Author(s): Huijsdens XW, Linskens RK, Taspinar H, Meuwissen SG, VandenbrouckeGrauls CM, Savelkoul PH. Source: Scandinavian Journal of Gastroenterology. 2003 March; 38(3): 332-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12737451
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Listeria monocytogenes and listeriosis: a review of hazard characterisation for use in microbiological risk assessment of foods. Author(s): McLauchlin J, Mitchell RT, Smerdon WJ, Jewell K. Source: International Journal of Food Microbiology. 2004 April 1; 92(1): 15-33. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15033265
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Listeria monocytogenes contamination of finishing pigs: an exploratory epidemiological survey in France. Author(s): Beloeil PA, Chauvin C, Toquin MT, Fablet C, Le Notre Y, Salvat G, Madec F, Fravalo P. Source: Veterinary Research. 2003 November-December; 34(6): 737-48. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14746769
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Listeria monocytogenes
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Listeria monocytogenes encephalitis mimicking West Nile encephalitis. Author(s): Cunha BA, Filozov A, Reme P. Source: Heart & Lung : the Journal of Critical Care. 2004 January-February; 33(1): 61-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14983142
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Listeria monocytogenes infection as a complication of treatment with tumor necrosis factor alpha-neutralizing agents. Author(s): Slifman NR, Gershon SK, Lee JH, Edwards ET, Braun MM. Source: Arthritis and Rheumatism. 2003 February; 48(2): 319-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12571839
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Listeria monocytogenes infection in patients with cancer. Author(s): Rivero GA, Torres HA, Rolston KV, Kontoyiannis DP. Source: Diagnostic Microbiology and Infectious Disease. 2003 October; 47(2): 393-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14522512
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Listeria monocytogenes isolates from invasive infections: variation of sero- and genotypes during an 11-year period in Finland. Author(s): Lukinmaa S, Miettinen M, Nakari UM, Korkeala H, Siitonen A. Source: Journal of Clinical Microbiology. 2003 April; 41(4): 1694-700. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12682162
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Listeria monocytogenes meningitis in a patient with chronic hepatitis C infection, treated by interferon alfa and ribavirin. Author(s): Vander T, Medvedovsky M, Hallevy C, Golzman G, Herishanu Y. Source: The Journal of Infection. 2003 January; 46(1): 70-1. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12504615
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Listeria monocytogenes mutants that fail to compartmentalize listerolysin O activity are cytotoxic, avirulent, and unable to evade host extracellular defenses. Author(s): Glomski IJ, Decatur AL, Portnoy DA. Source: Infection and Immunity. 2003 December; 71(12): 6754-65. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14638761
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Listeria monocytogenes peritonitis complicated by septic shock in a patient on continuous ambulatory peritoneal dialysis. Author(s): Tse KC, Li FK, Chan TM, Lai KN. Source: Clinical Nephrology. 2003 July; 60(1): 61-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12872862
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Listeria monocytogenes sepsis in patients treated with anti-tumor necrosis factoralpha. Author(s): Tweezer-Zaks N, Shiloach E, Spivak A, Rapoport M, Novis B, Langevitz P. Source: Isr Med Assoc J. 2003 November; 5(11): 829-30. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14650115
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Listeria monocytogenes serotype identification by PCR. Author(s): Borucki MK, Call DR. Source: Journal of Clinical Microbiology. 2003 December; 41(12): 5537-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14662936
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Listeria monocytogenes sigma B regulates stress response and virulence functions. Author(s): Kazmierczak MJ, Mithoe SC, Boor KJ, Wiedmann M. Source: Journal of Bacteriology. 2003 October; 185(19): 5722-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13129943
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Listeria monocytogenes virulence and pathogenicity, a food safety perspective. Author(s): Kathariou S. Source: J Food Prot. 2002 November; 65(11): 1811-29. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12430709
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Listeria monocytogenes: diagnostic problems. Author(s): Beumer RR, Hazeleger WC. Source: Fems Immunology and Medical Microbiology. 2003 April 1; 35(3): 191-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12648836
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Listeria monocytogenes: low levels equal low risk. Author(s): Chen Y, Ross WH, Scott VN, Gombas DE. Source: J Food Prot. 2003 April; 66(4): 570-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12696678
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Listeria monocytogenes--host interaction. Author(s): Zlei M, Ailiesei O, Carasevici E. Source: Roum Arch Microbiol Immunol. 2002 October-December; 61(4): 275-83. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15055261
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Listeria monocytogenes-induced endogenous endophthalmitis: bioultrasonic findings. Author(s): Mendez-Hernandez C, Garcia-Feijoo J, Garcia-Sanchez J. Source: American Journal of Ophthalmology. 2004 March; 137(3): 579-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15013893
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Listeriolysin O-mediated calcium influx potentiates entry of Listeria monocytogenes into the human Hep-2 epithelial cell line. Author(s): Dramsi S, Cossart P. Source: Infection and Immunity. 2003 June; 71(6): 3614-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12761148
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Meropenem therapy failure in Listeria monocytogenes infection. Author(s): Stepanovic S, Lazarevic G, Jesic M, Kos R. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 2004 June; 23(6): 484-6. Epub 2004 May 13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15141335
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Met, the HGF-SF receptor: another receptor for Listeria monocytogenes. Author(s): Cossart P. Source: Trends in Microbiology. 2001 March; 9(3): 105-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11239771
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Mixed-genome microarrays reveal multiple serotype and lineage-specific differences among strains of Listeria monocytogenes. Author(s): Call DR, Borucki MK, Besser TE. Source: Journal of Clinical Microbiology. 2003 February; 41(2): 632-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12574259
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Modeling the growth of Listeria monocytogenes in cured ready-to-eat processed meat products by manipulation of sodium chloride, sodium diacetate, potassium lactate, and product moisture content. Author(s): Seman DL, Borger AC, Meyer JD, Hall PA, Milkowski AL. Source: J Food Prot. 2002 April; 65(4): 651-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11952214
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Modelling and predicting the simultaneous growth of Listeria monocytogenes and spoilage micro-organisms in cold-smoked salmon. Author(s): Gimenez B, Dalgaard P. Source: Journal of Applied Microbiology. 2004; 96(1): 96-109. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14678163
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Modification of the signal sequence cleavage site of listeriolysin O does not affect protein secretion but impairs the virulence of Listeria monocytogenes. Author(s): Lety MA, Frehel C, Beretti JL, Berche P, Charbit A. Source: Microbiology (Reading, England). 2003 May; 149(Pt 5): 1249-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12724386
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Modulation of actA gene expression in Listeria monocytogenes by iron. Author(s): Conte MP, Longhi C, Petrone G, Polidoro M, Valenti P, Seganti L. Source: Journal of Medical Microbiology. 2000 August; 49(8): 681-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10933250
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Modulation of the immune system by Listeria monocytogenes-mediated gene transfer into mammalian cells. Author(s): Shen H, Kanoh M, Liu F, Maruyama S, Asano Y. Source: Microbiology and Immunology. 2004; 48(4): 329-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15107544
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Molecular and cellular basis of the infection by Listeria monocytogenes: an overview. Author(s): Cossart P. Source: International Journal of Medical Microbiology : Ijmm. 2002 February; 291(6-7): 401-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11890537
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Molecular epidemiological survey of Listeria monocytogenes in broilers and poultry products. Author(s): Rorvik LM, Aase B, Alvestad T, Caugant DA. Source: Journal of Applied Microbiology. 2003; 94(4): 633-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12631199
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Molecular subtyping methods for Listeria monocytogenes. Author(s): Wiedmann M. Source: J Aoac Int. 2002 March-April; 85(2): 524-31. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11990041
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Molecular typing by pulsed-field gel electrophoresis of Spanish animal and human Listeria monocytogenes isolates. Author(s): Vela AI, Fernandez-Garayzabal JF, Vazquez JA, Latre MV, Blanco MM, Moreno MA, de La Fuente L, Marco J, Franco C, Cepeda A, Rodriguez Moure AA, Suarez G, Dominguez L. Source: Applied and Environmental Microbiology. 2001 December; 67(12): 5840-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11722943
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Molecular typing of Listeria monocytogenes isolated in Japan by pulsed-field gel electrophoresis. Author(s): Nakama A, Matsuda M, Itoh T, Kaneuchi C. Source: The Journal of Veterinary Medical Science / the Japanese Society of Veterinary Science. 1998 June; 60(6): 749-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9673950
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Molecular typing of Listeria monocytogenes. Author(s): Jersek B. Source: Acta Microbiol Immunol Hung. 2002; 49(1): 81-92. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12073828
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MRI findings in mesenrhombencephalitis due to Listeria monocytogenes. Author(s): Mrowka M, Graf LP, Odin P. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 2002 December; 73(6): 775. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12438491
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Multiple cerebral abscesses because of Listeria monocytogenes: three case reports and a literature review of supratentorial listerial brain abscess(es). Author(s): Cone LA, Leung MM, Byrd RG, Annunziata GM, Lam RY, Herman BK. Source: Surgical Neurology. 2003 April; 59(4): 320-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12748019
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Multi-virulence-locus sequence typing of Listeria monocytogenes. Author(s): Zhang W, Jayarao BM, Knabel SJ. Source: Applied and Environmental Microbiology. 2004 February; 70(2): 913-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14766571
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Nationwide survey of human Listeria monocytogenes infection in Japan. Author(s): Okutani A, Okada Y, Yamamoto S, Igimi S. Source: Epidemiology and Infection. 2004 August; 132(4): 769-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15310181
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Natural milk fatty acids affect survival and invasiveness of Listeria monocytogenes. Author(s): Petrone G, Conte MP, Longhi C, di Santo S, Superti F, Ammendolia MG, Valenti P, Seganti L. Source: Letters in Applied Microbiology. 1998 December; 27(6): 362-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9871355
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Naturally occurring virulence-attenuated isolates of Listeria monocytogenes capable of inducing long term protection against infection by virulent strains of homologous and heterologous serotypes. Author(s): Chakraborty T, Ebel F, Wehland J, Dufrenne J, Notermans S. Source: Fems Immunology and Medical Microbiology. 1994 November; 10(1): 1-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7874073
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Negative regulation of PrfA, the key activator of Listeria monocytogenes virulence gene expression, is dispensable for bacterial pathogenesis. Author(s): Greene SL, Freitag NE. Source: Microbiology (Reading, England). 2003 January; 149(Pt 1): 111-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12576585
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Neonatal lead exposure potentiates sickness behavior induced by Listeria monocytogenes infection of mice. Author(s): Dyatlov VA, Lawrence DA. Source: Brain, Behavior, and Immunity. 2002 August; 16(4): 477-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12096892
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Neonatal meningitis due to multi-resistant Listeria monocytogenes. Author(s): Tsakris A, Papa A, Douboyas J, Antoniadis A. Source: The Journal of Antimicrobial Chemotherapy. 1997 April; 39(4): 553-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9145834
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Nonneonatal relapsing meningitis caused by Listeria monocytogenes. Author(s): Hervas JA, Fiol M, Cuesta M. Source: Pediatr Infect Dis. 1986 November-December; 5(6): 721. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3797313
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Nonspecific phospholipase C of Listeria monocytogenes: activity on phospholipids in Triton X-100-mixed micelles and in biological membranes. Author(s): Goldfine H, Johnston NC, Knob C. Source: Journal of Bacteriology. 1993 July; 175(14): 4298-306. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8331063
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Nosocomial infections by Listeria monocytogenes: analysis of a cluster of septicemias in immunocompromised patients. Author(s): Elsner HA, Tenschert W, Fischer L, Kaulfers PM. Source: Infection. 1997 May-June; 25(3): 135-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9181378
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Occurrence of Listeria monocytogenes in feces of pregnant women with and without direct animal contact. Author(s): Kampelmacher EH, Maas DE, van Noorle Jansen LM. Source: Zentralbl Bakteriol [orig A]. 1976 March; 234(2): 238-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=818853
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Occurrence of Listeria monocytogenes in sewage sludge. Author(s): De Luca G, Zanetti F, Fateh-Moghadm P, Stampi S. Source: Zentralbl Hyg Umweltmed. 1998 September; 201(3): 269-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9789361
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Ondine's curse in listeria monocytogenes brain stem encephalitis. Author(s): Jensen TH, Hansen PB, Brodersen P. Source: Acta Neurologica Scandinavica. 1988 June; 77(6): 505-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3407390
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Opsonization of Listeria monocytogenes type 4b by human adult and newborn sera. Author(s): Bortolussi R, Issekutz A, Faulkner G. Source: Infection and Immunity. 1986 May; 52(2): 493-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3084384
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Oral pretreatment of mice with CpG DNA reduces susceptibility to oral or intraperitoneal challenge with virulent Listeria monocytogenes. Author(s): Ray NB, Krieg AM. Source: Infection and Immunity. 2003 August; 71(8): 4398-404. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12874318
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Oral trimethoprim as follow-up treatment of meningitis caused by Listeria monocytogenes. Author(s): Gunther G, Philipson A. Source: Reviews of Infectious Diseases. 1988 January-February; 10(1): 53-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3258438
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Osmoprotectants and cryoprotectants for Listeria monocytogenes. Author(s): Bayles DO, Wilkinson BJ. Source: Letters in Applied Microbiology. 2000 January; 30(1): 23-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10728555
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Outcome of Listeria monocytogenes infection in compromised and non-compromised adults; a comparative study of seventy-two cases. Author(s): Iwarson S, Larsson S. Source: Infection. 1979; 7(2): 54-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=437892
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Overview of Listeria monocytogenes contamination in Japan. Author(s): Okutani A, Okada Y, Yamamoto S, Igimi S. Source: International Journal of Food Microbiology. 2004 June 1; 93(2): 131-40. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15135952
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Perinephric abscess (presenting as abdominal pain) due to Listeria monocytogenes. Author(s): Gomber S, Revathi G, Krishna A, Gupta A. Source: Annals of Tropical Paediatrics. 1998 March; 18(1): 61-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9692004
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Pneumonia involving Legionella pneumophila and Listeria monocytogenes in an immunocompromised patient: an unusual coinfection. Author(s): Lerolle N, Zahar JR, Duboc V, Tissier F, Rabbat A. Source: Respiration; International Review of Thoracic Diseases. 2002; 69(4): 359-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12169753
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Predictive model for the combined effect of temperature, sodium lactate, and sodium diacetate on the heat resistance of Listeria monocytogenes in beef. Author(s): Juneja VK. Source: J Food Prot. 2003 May; 66(5): 804-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12747689
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Prevalence and characterization of Listeria monocytogenes in the feces of healthy Austrians. Author(s): Grif K, Hein I, Wagner M, Brandl E, Mpamugo O, McLauchlin J, Dierich MP, Allerberger F. Source: Wiener Klinische Wochenschrift. 2001 October 15; 113(19): 737-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11715752
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Prevalence of Listeria monocytogenes in, and microbiological and sensory quality of, rainbow trout, whitefish, and vendace roes from Finnish retail markets. Author(s): Miettinen H, Arvola A, Luoma T, Wirtanen G. Source: J Food Prot. 2003 October; 66(10): 1832-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14572220
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Production of antibacterial substances by bifidobacterial isolates from infant stool active against Listeria monocytogenes. Author(s): Toure R, Kheadr E, Lacroix C, Moroni O, Fliss I. Source: Journal of Applied Microbiology. 2003; 95(5): 1058-69. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14633035
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Production of IL-12 and IL-18 in human dendritic cells upon infection by Listeria monocytogenes. Author(s): Kolb-Maurer A, Kammerer U, Maurer M, Gentschev I, Brocker EB, Rieckmann P, Kampgen E. Source: Fems Immunology and Medical Microbiology. 2003 April 1; 35(3): 255-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12648844
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Prosthetic valve endocarditis due to Listeria monocytogenes. Report of two cases and reviews. Author(s): Fernandez Guerrero ML, Rivas P, Rabago R, Nunez A, de Gorgolas M, Martinell J. Source: International Journal of Infectious Diseases : Ijid : Official Publication of the International Society for Infectious Diseases. 2004 March; 8(2): 97-102. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14732327
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Pulsed-field gel electrophoresis for the analysis of Listeria monocytogenes infection clusters after kidney transplantation. Author(s): Reek C, Tenschert W, Elsner HA, Kaulfers PM, Huland H. Source: Urological Research. 2000 April; 28(2): 93-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10850630
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Pyrosequencing as a method for grouping of Listeria monocytogenes strains on the basis of single-nucleotide polymorphisms in the inlB gene. Author(s): Unnerstad H, Ericsson H, Alderborn A, Tham W, Danielsson-Tham ML, Mattsson JG. Source: Applied and Environmental Microbiology. 2001 November; 67(11): 5339-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11679367
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Quantitative risk assessment for Listeria monocytogenes in smoked or gravad salmon and rainbow trout in Sweden. Author(s): Lindqvist R, Westoo A. Source: International Journal of Food Microbiology. 2000 July 15; 58(3): 181-96. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10939268
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Quantitative risk assessment of Listeria monocytogenes in ready-to-eat foods: the FAO/WHO approach. Author(s): Rocourt J, BenEmbarek P, Toyofuku H, Schlundt J. Source: Fems Immunology and Medical Microbiology. 2003 April 1; 35(3): 263-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12648845
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Rapidly enlarging iliac aneurysm secondary to listeria monocytogenes infection: a case report. Author(s): Clouse WD, DeWitt CC, Hagino RT, DeCaprio J, Kashyap VS. Source: Vascular and Endovascular Surgery. 2003 March-April; 37(2): 145-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12669148
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Rational design of DNA sequence-based strategies for subtyping Listeria monocytogenes. Author(s): Cai S, Kabuki DY, Kuaye AY, Cargioli TG, Chung MS, Nielsen R, Wiedmann M. Source: Journal of Clinical Microbiology. 2002 September; 40(9): 3319-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12202573
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Recurrent Listeria monocytogenes aortic graft infection: confirmation of relapse by molecular subtyping. Author(s): Rohde H, Horstkotte MA, Loeper S, Aberle J, Jenicke L, Lampidis R, Mack D. Source: Diagnostic Microbiology and Infectious Disease. 2004 January; 48(1): 63-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14761724
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Report of an additional case of anti-tumor necrosis factor therapy and Listeria monocytogenes infection: comment on the letter by Gluck et al. Author(s): Aparicio AG, Munoz-Fernandez S, Bonilla G, Miralles A, Cerdeno V, MartinMola E. Source: Arthritis and Rheumatism. 2003 June; 48(6): 1764-5; Author Reply 1765-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12794847
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Requirement of the Listeria monocytogenes broad-range phospholipase PC-PLC during infection of human epithelial cells. Author(s): Grundling A, Gonzalez MD, Higgins DE. Source: Journal of Bacteriology. 2003 November; 185(21): 6295-307. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14563864
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Restriction fragment length polymorphisms detected with novel DNA probes differentiate among diverse lineages of serogroup 4 Listeria monocytogenes and identify four distinct lineages in serotype 4b. Author(s): Tran HL, Kathariou S. Source: Applied and Environmental Microbiology. 2002 January; 68(1): 59-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11772609
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Role of ctc from Listeria monocytogenes in osmotolerance. Author(s): Gardan R, Duche O, Leroy-Setrin S, Labadie J; European Listeria Genome Consortium. Source: Applied and Environmental Microbiology. 2003 January; 69(1): 154-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12513990
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Role of flagellin and the two-component CheA/CheY system of Listeria monocytogenes in host cell invasion and virulence. Author(s): Dons L, Eriksson E, Jin Y, Rottenberg ME, Kristensson K, Larsen CN, Bresciani J, Olsen JE. Source: Infection and Immunity. 2004 June; 72(6): 3237-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15155625
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Role of heparan sulfate in interactions of Listeria monocytogenes with enterocytes. Author(s): Henry-Stanley MJ, Hess DJ, Erickson EA, Garni RM, Wells CL. Source: Medical Microbiology and Immunology. 2003 May; 192(2): 107-15. Epub 2003 March 05. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12684756
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Role of Listeria monocytogenes sigma(B) in survival of lethal acidic conditions and in the acquired acid tolerance response. Author(s): Ferreira A, Sue D, O'Byrne CP, Boor KJ. Source: Applied and Environmental Microbiology. 2003 May; 69(5): 2692-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12732538
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Sequence and binding activity of the autolysin-adhesin Ami from epidemic Listeria monocytogenes 4b. Author(s): Milohanic E, Jonquieres R, Glaser P, Dehoux P, Jacquet C, Berche P, Cossart P, Gaillard JL. Source: Infection and Immunity. 2004 August; 72(8): 4401-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15271896
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Series of incidents of Listeria monocytogenes non-invasive febrile gastroenteritis involving ready-to-eat meats. Author(s): Sim J, Hood D, Finnie L, Wilson M, Graham C, Brett M, Hudson JA. Source: Letters in Applied Microbiology. 2002; 35(5): 409-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12390491
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Serotyping of Listeria monocytogenes by enzyme-linked immunosorbent assay and identification of mixed-serotype cultures by colony immunoblotting. Author(s): Palumbo JD, Borucki MK, Mandrell RE, Gorski L. Source: Journal of Clinical Microbiology. 2003 February; 41(2): 564-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12574247
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Sodium pentobarbital anesthesia transiently enhances the severity of infection following intragastric, but not intravenous, inoculation of Listeria monocytogenes in mice. Author(s): Czuprynski CJ, Faith NG, Steinberg H, Neudeck B. Source: Microbial Pathogenesis. 2003 August; 35(2): 81-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12901847
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Structural aspects of adhesion to and invasion of host cells by the human pathogen Listeria monocytogenes. Author(s): Schubert WD, Heinz DW. Source: Chembiochem : a European Journal of Chemical Biology. 2003 December 5; 4(12): 1285-91. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14661268
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Structure of internalin, a major invasion protein of Listeria monocytogenes, in complex with its human receptor E-cadherin. Author(s): Schubert WD, Urbanke C, Ziehm T, Beier V, Machner MP, Domann E, Wehland J, Chakraborty T, Heinz DW. Source: Cell. 2002 December 13; 111(6): 825-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12526809
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Subtyping Listeria monocytogenes through the combined analyses of genotype and expression of the hlyA virulence determinant. Author(s): Rudi K, Nogva HK, Naterstad K, Dromtorp SM, Bredholt S, Holck A. Source: Journal of Applied Microbiology. 2003; 94(4): 720-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12631208
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Surface proteins and the pathogenic potential of Listeria monocytogenes. Author(s): Cabanes D, Dehoux P, Dussurget O, Frangeul L, Cossart P. Source: Trends in Microbiology. 2002 May; 10(5): 238-45. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11973158
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Survey of Listeria monocytogenes in ready-to-eat foods. Author(s): Gombas DE, Chen Y, Clavero RS, Scott VN. Source: J Food Prot. 2003 April; 66(4): 559-69. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12696677
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Survival of Escherichia coli O157:H7, Listeria monocytogenes 4b and Yersinia enterocolitica O3 in different yogurt and kefir combinations as prefermentation contaminant. Author(s): Gulmez M, Guven A. Source: Journal of Applied Microbiology. 2003; 95(3): 631-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12911712
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T cell responses to Listeria monocytogenes. Author(s): Lara-Tejero M, Pamer EG. Source: Current Opinion in Microbiology. 2004 February; 7(1): 45-50. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15036139
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Targeting and crossing of the human maternofetal barrier by Listeria monocytogenes: role of internalin interaction with trophoblast E-cadherin. Author(s): Lecuit M, Nelson DM, Smith SD, Khun H, Huerre M, Vacher-Lavenu MC, Gordon JI, Cossart P. Source: Proceedings of the National Academy of Sciences of the United States of America. 2004 April 20; 101(16): 6152-7. Epub 2004 Apr 08. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15073336
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The cell biology of Listeria monocytogenes infection: the intersection of bacterial pathogenesis and cell-mediated immunity. Author(s): Portnoy DA, Auerbuch V, Glomski IJ. Source: The Journal of Cell Biology. 2002 August 5; 158(3): 409-14. Epub 2002 Aug 05. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12163465
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The contribution of both oxygen and nitrogen intermediates to the intracellular killing mechanisms of C1q-opsonized Listeria monocytogenes by the macrophagelike IC-21 cell line. Author(s): Alvarez-Dominguez C, Carrasco-Marin E, Lopez-Mato P, Leyva-Cobian F. Source: Immunology. 2000 September; 101(1): 83-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11012757
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The interplay between classical and alternative isoprenoid biosynthesis controls gammadelta T cell bioactivity of Listeria monocytogenes. Author(s): Begley M, Gahan CG, Kollas AK, Hintz M, Hill C, Jomaa H, Eberl M. Source: Febs Letters. 2004 March 12; 561(1-3): 99-104. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15013758
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The possible effect of a sanitization program on intraspecies differentiation of Listeria monocytogenes strains isolated from a fish processing plant. Author(s): Medrala D, Dabrowski W, Czekajlo-Kolodziej U, Daczkowska-Kozon E, Koronkiewicz A, Augustynowicz E, Manzano M. Source: International Journal of Hygiene and Environmental Health. 2003 October; 206(6): 583-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14626905
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The role of the sigB gene in the general stress response of Listeria monocytogenes varies between a strain of serotype 1/2a and a strain of serotype 4c. Author(s): Moorhead SM, Dykes GA. Source: Current Microbiology. 2003 June; 46(6): 461-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12732955
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Two Listeria monocytogenes vaccine vectors that express different molecular forms of human papilloma virus-16 (HPV-16) E7 induce qualitatively different T cell immunity that correlates with their ability to induce regression of established tumors immortalized by HPV-16. Author(s): Gunn GR, Zubair A, Peters C, Pan ZK, Wu TC, Paterson Y. Source: Journal of Immunology (Baltimore, Md. : 1950). 2001 December 1; 167(11): 64719. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11714814
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Typing of food-borne Listeria monocytogenes by the optimized repetitive extragenic palindrome-based polymerase chain reaction. Author(s): Pangallo D, Karpiskova R, Turna J, Kuchta T. Source: New Microbiol. 2002 October; 25(4): 449-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12437224
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Typing of Listeria monocytogenes isolates by random amplification of polymorphic DNA. Author(s): Dhanashree B, Otta SK, Karunasagar I, Karunasagar I. Source: The Indian Journal of Medical Research. 2003 January; 117: 19-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12866822
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Ultrastructural study of Listeria monocytogenes entry into cultured human colonic epithelial cells. Author(s): Karunasagar I, Senghaas B, Krohne G, Goebel W. Source: Infection and Immunity. 1994 August; 62(8): 3554-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8039928
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Unusual food-borne pathogens. Listeria monocytogenes, Aeromonas, Plesiomonas, and Edwardsiella species. Author(s): Janda JM, Abbott SL. Source: Clin Lab Med. 1999 September; 19(3): 553-82. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10549426
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Update on Listeria monocytogenes infection. Author(s): Crum NF. Source: Current Gastroenterology Reports. 2002 August; 4(4): 287-96. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12149174
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Uptake and killing of Listeria monocytogenes by normal human peripheral blood granulocytes and monocytes as measured by flow cytometry and cell sorting. Author(s): Raybourne RB, Roth G, Deuster PA, Sternberg EM, Singh A. Source: Fems Immunology and Medical Microbiology. 2001 October; 31(3): 219-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11720818
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Use of a fluorogenic probe in a PCR-based assay for the detection of Listeria monocytogenes. Author(s): Bassler HA, Flood SJ, Livak KJ, Marmaro J, Knorr R, Batt CA. Source: Applied and Environmental Microbiology. 1995 October; 61(10): 3724-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7487008
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Use of automated ribotyping of Austrian Listeria monocytogenes isolates to support epidemiological typing. Author(s): Allerberger F, Fritschel SJ. Source: Journal of Microbiological Methods. 1999 April; 35(3): 237-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10333075
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Use of capillary tubes and plate heat exchanger to validate U.S. Department of Agriculture pasteurization protocols for elimination of Listeria monocytogenes in liquid egg products. Author(s): Michalski CB, Brackett RE, Hung YC, Ezeike GO. Source: J Food Prot. 2000 July; 63(7): 921-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10914661
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Use of molecular typing methods to trace the dissemination of Listeria monocytogenes in a shrimp processing plant. Author(s): Destro MT, Leitao MF, Farber JM. Source: Applied and Environmental Microbiology. 1996 February; 62(2): 705-11. Erratum In: Appl Environ Microbiol 1996 May; 62(5): 1852-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8593073
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Use of PFGE to characterize clonal relationships among Belgian clinical isolates of Listeria monocytogenes. Author(s): Yde M, Genicot A. Source: Journal of Medical Microbiology. 2004 May; 53(Pt 5): 399-402. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15096548
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Utilization of exogenous siderophores and natural catechols by Listeria monocytogenes. Author(s): Simon N, Coulanges V, Andre P, Vidon DJ. Source: Applied and Environmental Microbiology. 1995 April; 61(4): 1643-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7747980
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Vancomycin therapy failure in Listeria monocytogenes peritonitis in a patient on continuous ambulatory peritoneal dialysis. Author(s): Dryden MS, Jones NF, Phillips I. Source: The Journal of Infectious Diseases. 1991 December; 164(6): 1239. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1955728
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Variation in biofilm formation among strains of Listeria monocytogenes. Author(s): Borucki MK, Peppin JD, White D, Loge F, Call DR. Source: Applied and Environmental Microbiology. 2003 December; 69(12): 7336-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14660383
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Variations in tolerance of Listeria monocytogenes to nisin, pediocin PA-1 and bavaricin A. Author(s): Rasch M, Knochel S. Source: Letters in Applied Microbiology. 1998 November; 27(5): 275-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9830144
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Variations in virulence between different electrophoretic types of Listeria monocytogenes. Author(s): Norrung B, Andersen JK. Source: Letters in Applied Microbiology. 2000 March; 30(3): 228-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10747256
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Ventriculoperitoneal shunt infection due to Listeria monocytogenes. Author(s): Winslow DL, Steele-Moore L. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1995 May; 20(5): 1437. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7677902
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Ventriculoperitoneal shunt infection due to Listeria monocytogenes. Author(s): Dominguez EA, Patil AA, Johnson WM. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 1994 July; 19(1): 223-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7677812
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Verification of causal relationships between Listeria monocytogenes isolates implicated in food-borne outbreaks of listeriosis by randomly amplified polymorphic DNA patterns. Author(s): Czajka J, Batt CA. Source: Journal of Clinical Microbiology. 1994 May; 32(5): 1280-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8051257
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Viability of Salmonella, Escherichia coli O157:H7, and Listeria monocytogenes in yellow fat spreads as affected by storage temperature. Author(s): Holliday SL, Beuchat LR. Source: J Food Prot. 2003 April; 66(4): 549-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12696676
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Virulence testing of Listeria monocytogenes. Author(s): Raybourne RB. Source: J Aoac Int. 2002 March-April; 85(2): 516-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11990040
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Virulent rough filaments of Listeria monocytogenes from clinical and food samples secreting wild-type levels of cell-free p60 protein. Author(s): Rowan NJ, Candlish AA, Bubert A, Anderson JG, Kramer K, McLauchlin J. Source: Journal of Clinical Microbiology. 2000 July; 38(7): 2643-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10878057
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Western blot analysis of the antibody response in patients with Listeria monocytogenes meningitis and septicemia. Author(s): Renneberg J, Persson K, Christensen P. Source: European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology. 1990 September; 9(9): 65963. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2121484
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WHO International Multicenter Listeria monocytogenes Subtyping Study--rationale and set-up of the study. Author(s): Bille J, Rocourt J. Source: International Journal of Food Microbiology. 1996 October; 32(3): 251-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8913798
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Why is Listeria monocytogenes not a pathogen in the acquired immunodeficiency syndrome? Author(s): Jacobs JL, Murray HW. Source: Archives of Internal Medicine. 1986 July; 146(7): 1299-300. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2940988
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CHAPTER 2. NUTRITION AND LISTERIA MONOCYTOGENES Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and Listeria monocytogenes.
Finding Nutrition Studies on Listeria monocytogenes 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 “Listeria monocytogenes” (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 “Listeria monocytogenes” (or a synonym): •
Antimicrobial activity of essential oils of some Abies (fir) species from Turkey. Author(s): Biology Department, Faculty of Arts and Science, Firat University, 23169Elazig (Turkey) Source: Bagci, E. Digrak, M. Flavour-and-Fragrance-Journal (United Kingdom). (1996). volume 11(4) page 251-256.
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Comparative study between Yemeni and Egyptian types of honey by means of antibacterial activity. Author(s): Mansoura Univ. (Egypt). Faculty of Agriculture Source: El Fadaly, H. Abdilla, F.S. El Badrawy, E.E.Y. Pakistan-Journal-of-BiologicalSciences (Pakistan). (January 1999). volume 2(1) page 1-6.
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Freeze-dried spinach powder inhibits growth of Listeria species and strains in tryptic soy broth. Author(s): ARS, USDA, Beltsville, MD. Source: Babic, I. Watada, A.E. HortScience-:-a-publication-of-the-American-Society-forHorticultural-Science (USA). (August 1998). volume 33(5) page 884-886.
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Inhibitory effects of probiotic bacteria against selected food-borne pathogens. Author(s): University Putra Malaysia, Selangor (Malaysia). Dept. of Food Technology Source: Yazid, A.M. Salina, A.B. Shuhaimi, M. Osman, H. Normah, J. Pakistan-Journalof-Biological-Sciences (Pakistan). (July 1999). volume 2(3) page 660-663.
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Isolation and partial characterization of an antibacterial substance produced by Enterococcus faecium. Author(s): University of Sofia (Bulgaria). Dept. of Microbiology Source: Pantev, A. Kabadjova, P. Ivanova, I. Dalgalarrondo, M. Haertle, T. Dousset, X. Prevost, H. Chobert, J. M. Folia-Microbiologica (Czech Republic). (August 2002). volume 47(4) page 391-400.
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Recombinant interleukin-12 enhances resistance of mice to Listeria monocytogenes infection. Author(s): Department of Pathobiological Sciences, University of Wisconsin School of Veterinary Medicine, 2015 Linden Drive West, Madison, WI 53706 (USA) Source: Wagner, R.D. Steinberg, H. Brown, J.F. Czuprynski, C.J. Microbial-Pathogenesis (United Kingdom). (1994). volume 17(3) page 175-186.
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Response Surface Methodology, an approach to predict the effects of a lactoperoxidase system, nisin, alone or in combination, on Listeria monocytogenes in skim milk. Author(s): Laboratoire de Fermentations et Bioconversions Industrielles, ENSAIA-INPL, Vandoeuvre-les-Nancy (France) Source: Boussouel, N. Mathieu, F. Benoit, V. Linder, M. Revol Junelles, A.M. Milliere, J.B. Journal-of-Applied-Microbiology (United Kingdom). (1999). volume 86(4) page 642652.
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Synergist effect of sucrose fatty acid esters on nisin inhibition of Gram-positive bacteria. Author(s): Cardiff School of Biosciences, Cardiff University, Cardiff (United Kingdom) Source: Thomas, L.V. Davies, E.A. Delves Broughton, J. Wimpenny, J.W.T. Journal-ofApplied-Microbiology (United Kingdom). (1998). volume 85(6) page 1013-1022.
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Additional physician-oriented references include: •
A comparison of quantitative structure-activity relationships for the effect of benzoic and cinnamic acids on Listeria monocytogenes using multiple linear regression, artificial neural network and fuzzy systems. Author(s): Food Safety Group, School of Biological Sciences, University of Surrey, Guildford, Surrey, UK. Source: Ramos Nino, M E Ramirez Rodriguez, C A Clifford, M N Adams, M R J-ApplMicrobiol. 1997 February; 82(2): 168-76 1364-5072
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Calcinated calcium killing of Escherichia coli O157:H7, Salmonella, and Listeria monocytogenes on the surface of tomatoes. Author(s): National Food Research Institute, Research Planning and Coordination Division, Tsukuba, Japan. Source: Bari, M L Inatsu, Y Kawasaki, S Nazuka, E Isshiki, K J-Food-Prot. 2002 November; 65(11): 1706-11 0362-028X
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Control of Listeria monocytogenes on turkey frankfurters by generally-recognized-assafe preservatives. Author(s): Center for Food Safety, University of Georgia, Griffin 30223-1797, USA.
[email protected] Source: Islam, M Chen, J Doyle, M P Chinnan, M J-Food-Prot. 2002 September; 65(9): 1411-6 0362-028X
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Death of Salmonella, Escherichia coli O157:H7, and Listeria monocytogenes in garlic butter as affected by storage temperature. Author(s): Center for Food Safety and Department of Food Science and Technology, University of Georgia, 1109 Experiment Street, Griffin, Georgia 30223-1797, USA. Source: Adler, B B Beuchat, L R J-Food-Prot. 2002 December; 65(12): 1976-80 0362-028X
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Effect of free or liposome-encapsulated muramyl dipeptide on uptake and intracellular survival of Listeria monocytogenes in mouse peritoneal macrophages in vitro. Author(s): Department of Clinical Microbiology, Erasmus University Rotterdam, the Netherlands. Source: Bakker Woudenberg, I A Lokerse, A F Vink van den Berg, J C Roerdink, F H Eur-J-Clin-Microbiol-Infect-Dis. 1989 July; 8(7): 603-9 0934-9723
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Effect of lauric acid and nisin-impregnated soy-based films on the growth of Listeria monocytogenes on turkey bologna. Author(s): Department of Food Science and Human Nutrition, Clemson University, South Carolina 29634-0371, USA.
[email protected] Source: Dawson, P L Carl, G D Acton, J C Han, I Y Poult-Sci. 2002 May; 81(5): 721-6 0032-5791
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Efficacy of plant extracts in inhibiting Aeromonas hydrophila and Listeria monocytogenes in refrigerated, cooked poultry. Source: Hao, Y.Y. Brackett, R.E. Doyle, M.P. Food-microbiol. London; Orlando : Academic Press, c1984-. August 1998. volume 15 (4) page 367-378. 0740-0020
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Freezing and frozen storage on the survival of Listeria monocytogenes in different foods. Source: Gianfranceschi, M. Aureli, P. Ital-j-food-sci. Pinerolo, Italy : Chiriotti Editori, 1989-. 1996. volume 8 (4) page 303-309. 1120-1770
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Gbu glycine betaine porter and carnitine uptake in osmotically stressed Listeria monocytogenes cells. Author(s): Department of Agronomy and Range Science, University of California, Davis, California 95616, USA.
[email protected] Source: Mendum, M L Smith, L T Appl-Environ-Microbiol. 2002 November; 68(11): 5647-55 0099-2240
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Growth of Listeria monocytogenes in Camembert and other soft cheeses at refrigeration temperatures. Author(s): AFRC Institute of Food Research, Reading, UK. Source: Back, J P Langford, S A Kroll, R G J-Dairy-Res. 1993 August; 60(3): 421-9 00220299
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Inhibition of Listeria monocytogenes and Salmonella enteriditis by combinations of plant oils and derivatives of benzoic acid: the development of synergistic antimicrobial combinations. Author(s): Department of Dietetics and Nutrition, Queen Margaret College, Edinburgh, UK. Source: Fyfe, L Armstrong, F Stewart, J Int-J-Antimicrob-Agents. 1997 January; 9(3): 1959 0924-8579
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Involvement of inflammatory cytokines and nitric oxide in the expression of nonspecific resistance to Listeria monocytogenes in mice induced by viable but not killed Mycobacterium bovis BCG. Author(s): Department of Bacteriology, Niigata University School of Medicine, Japan. Source: Yang, J Kawamura, I Mitsuyama, M Microb-Pathog. 1997 February; 22(2): 79-88 0882-4010
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Isolation, purification and partial characterization of a new extracellular cytotoxin from a virulent clinical strain of Listeria monocytogenes serotype 4b, and an avirulent, nonhemolytic variant ATCC 15313 serotype 1/2a. Source: Van der Kelen, D. Lindsay, J.A. J-Food-Saf. Trumbull, Conn. : Food & Nutrition Press. 1991. volume 11 (2) page 81-98. 0149-6085
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Membranes of class IIa bacteriocin-resistant Listeria monocytogenes cells contain increased levels of desaturated and short-acyl-chain phosphatidylglycerols. Author(s): Department of Biochemistry. Electrospray Mass Spectrometry Unit, Central Analytical Facility, University of Stellenbosch, Matieland 7602, Republic of South Africa. Source: Vadyvaloo, V Hastings, J W van der Merwe, M J Rautenbach, M Appl-EnvironMicrobiol. 2002 November; 68(11): 5223-30 0099-2240
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Modulation of delayed-type hypersensitivity and acquired cellular resistance by orally administered viable indigenous lactobacilli in Listeria monocytogenes infected Wistar rats. Author(s): Department of the Science of Food of Animal Origin, Utrecht University, PO Box 80175, 3508 TD Utrecht, the Netherlands.
[email protected] Source: de Waard, R Garssen, J Vos, J G Claassen, E Lett-Appl-Microbiol. 2002; 35(3): 256-60 0266-8254
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Multiple deletions of the osmolyte transporters BetL, Gbu, and OpuC of Listeria monocytogenes affect virulence and growth at high osmolarity. Author(s): Laboratory of Food Microbiology, Wageningen University, The Netherlands. Source: Wemekamp Kamphuis, H H Wouters, J A Sleator, R D Gahan, C G Hill, C Abee, T Appl-Environ-Microbiol. 2002 October; 68(10): 4710-6 0099-2240
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Nitric oxide mediates immunosuppression induced by Listeria monocytogenes infection: quantitative studies. Author(s): Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA, 19140, USA. Source: MacFarlane, A S Huang, D Schwacha, M G Meissler, J J Gaughan, J P Eisenstein, T K Microb-Pathog. 1998 November; 25(5): 267-77 0882-4010
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Osmoprotection by carnitine in a Listeria monocytogenes mutant lacking the OpuC transporter: evidence for a low affinity carnitine uptake system. Author(s): Department of Molecular and Cell Biology, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, Scotland, UK. Source: Fraser, K R O'Byrne, C P FEMS-Microbiol-Lett. 2002 June 4; 211(2): 189-94 03781097
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Potential use of microbiological reference materials for the evaluation of detection methods for Listeria monocytogenes and the effect of competitors: a collaborative study. Source: Veld, P.H. in't Notermans, S.H.W. Berg, M. van de. Food-microbiol. London; Orlando : Academic Press, c1984-. April 1995. volume 12 (2) page 125-134. 0740-0020
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Prevalence of Listeria monocytogenes in foods: incidence in dairy products. Source: Kozak, J. Balmer, T. Byrne, R. Fisher, K. Food-control. Oxford, UK : Elsevier Science Ltd. Aug/October 1996. volume 7 (4/5) page 215-221. 0956-7135
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Protective effect of a traditional Japanese medicine Hochu-ekki-to (Chinese name: Bu-zhong-yi-qi-tang), on the susceptibility against Listeria monocytogenes in infant mice. Author(s): Kampo (Traditional Japanese Medicine) and Healthcare Research Laboratories, Kanebo Co. Ltd, Takaoka, Japan. Source: Yamaoka, Y Kawakita, T Nomoto, K Int-Immunopharmacol. 2001 September; 1(9-10): 1669-77 1567-5769
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Specific binding of the Listeria monocytogenes transcriptional regulator PrfA to target sequences requires additional factor(s) and is influenced by iron. Author(s): Theodor-Boveri-Institut fur Biowissenschaften der Universitat Wurzburg, Germany. Source: Bockmann, R Dickneite, C Middendorf, B Goebel, W Sokolovic, Z MolMicrobiol. 1996 November; 22(4): 643-53 0950-382X
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The antibacterial efficacy of trovafloxacin against an experimental infection with Listeria monocytogenes in hydrocortisone-treated mice. Author(s): Department of Medical Microbiology, Leiden University Medical Centre, The Netherlands. Source: van Ogtrop, M L J-Antimicrob-Chemother. 1999 August; 44(2): 229-34 0305-7453
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The Canadian position on Listeria monocytogenes in ready-to-eat foods. Source: Farber, J.M. Harwig, J. Food-control. Oxford, UK : Elsevier Science Ltd. Aug/October 1996. volume 7 (4/5) page 253-258. 0956-7135
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The Danish government position on the control of Listeria monocytogenes in foods. Source: Qvist, S. Food-control. Oxford, UK : Elsevier Science Ltd. Aug/October 1996. volume 7 (4/5) page 249-252. 0956-7135
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The role of hepatic lectins and the activity of the mononuclear phagocyte system in systemic Listeria monocytogenes infection in Balb/c mice. Author(s): Hygiene-Institut der Universitat, Koln, Federal Republic of Germany.
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Source: Beuth, J Ko, H L Pulverer, G Med-Microbiol-Immunol-(Berl). 1988; 177(1): 47-9 0300-8584 •
The virulence regulator protein of Listeria ivanovii is highly homologous to PrfA from Listeria monocytogenes and both belong to the Crp-Fnr family of transcription regulators. Source: Lampidis, R. Gross, R. Sokolovic, Z. Goebel, W. Kreft, J. Mol-microbiol. Oxford : Blackwell Scientific Publications,. July 1994. volume 13 (1) page 141-151. 0950-382X
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US position on Listeria monocytogenes in foods. Source: Shank, F.R. Elliot, E.L. Wachsmuth, I.K. Losikoff, M.E. Food-control. Oxford, UK : Elsevier Science Ltd. Aug/October 1996. volume 7 (4/5) page 229-234. 0956-7135
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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CHAPTER 3. ALTERNATIVE MEDICINE AND LISTERIA MONOCYTOGENES Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to Listeria monocytogenes. 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 Listeria monocytogenes 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 “Listeria monocytogenes” (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 Listeria monocytogenes: •
2-deoxy-D-glucose-induced metabolic stress enhances resistance to Listeria monocytogenes infection in mice. Author(s): Miller ES, Bates RA, Koebel DA, Fuchs BB, Sonnenfeld G. Source: Physiology & Behavior. 1998 December 1; 65(3): 535-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9877421
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Antagonistic activity of Lactobacillus casei strain shirota against gastrointestinal Listeria monocytogenes infection in rats. Author(s): de Waard R, Garssen J, Bokken GC, Vos JG. Source: International Journal of Food Microbiology. 2002 February 25; 73(1): 93-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11885574
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Antibacterial activity of hen egg white lysozyme against Listeria monocytogenes Scott A in foods. Author(s): Hughey VL, Wilger PA, Johnson EA. Source: Applied and Environmental Microbiology. 1989 March; 55(3): 631-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2494938
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Antimicrobial effect of herb extracts against Escherichia coli O157:H7, Listeria monocytogenes, and Salmonella typhimurium associated with beef. Author(s): Cutter CN. Source: J Food Prot. 2000 May; 63(5): 601-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10826716
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Antimicrobial effects of garlic, clove and red hot chilli on Listeria monocytogenes in broth model systems and soft cheese. Author(s): Leuschner RG, Ielsch V. Source: International Journal of Food Sciences and Nutrition. 2003 March; 54(2): 127-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12701369
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Anti-oxidant properties of N-acetyl-L-cysteine do not improve the immune resistance of mice fed dietary lipids to Listeria monocytogenes infection. Author(s): Puertollano MA, de Pablo MA, Alvarez de Cienfuegos G. Source: Clinical Nutrition (Edinburgh, Lothian). 2003 June; 22(3): 313-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12765672
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Application of purified polysaccharides from cell cultures of the plant Echinacea purpurea to mice mediates protection against systemic infections with Listeria monocytogenes and Candida albicans. Author(s): Roesler J, Steinmuller C, Kiderlen A, Emmendorffer A, Wagner H, LohmannMatthes ML. Source: International Journal of Immunopharmacology. 1991; 13(1): 27-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2026472
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Assurance polyclonal enzyme immunoassay for detection of Listeria monocytogenes and related Listeria species in selected foods: collaborative study. Author(s): Feldsine PT, Lienau AH, Forgey RL, Calhoon RD. Source: J Aoac Int. 1997 July-August; 80(4): 775-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9241842
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Augmentation of host resistance to Listeria monocytogenes infection by a traditional Chinese medicine, ren-shen-yang-rong-tang (Japanese name: ninjin-youei-to). Author(s): Yonekura K, Kawakita T, Saito Y, Suzuki A, Nomoto K.
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Source: Immunopharmacology and Immunotoxicology. 1992; 14(1-2): 165-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1597654 •
Bactericidal activities of plant essential oils and some of their isolated constituents against Campylobacter jejuni, Escherichia coli, Listeria monocytogenes, and Salmonella enterica. Author(s): Friedman M, Henika PR, Mandrell RE. Source: J Food Prot. 2002 October; 65(10): 1545-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12380738
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Biopreservation in modified atmosphere stored mungbean sprouts: the use of vegetable-associated bacteriocinogenic lactic acid bacteria to control the growth of Listeria monocytogenes. Author(s): Bennik MH, van Overbeek W, Smid EJ, Gorris LG. Source: Letters in Applied Microbiology. 1999 March; 28(3): 226-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10196774
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Changes in the immune functions and susceptibility to Listeria monocytogenes infection in mice fed dietary lipids. Author(s): Puertollano MA, Puertollano E, Ruiz-Bravo A, Jimenez-Valera M, De Pablo MA, Alvarez De Cienfuegos G. Source: Immunology and Cell Biology. 2004 August; 82(4): 370-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15283846
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Combined action of S-carvone and mild heat treatment on Listeria monocytogenes Scott A. Author(s): Karatzas AK, Bennik MH, Smid EJ, Kets EP. Source: Journal of Applied Microbiology. 2000 August; 89(2): 296-301. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10971762
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Combined PCR and slot blot assay for detection of Salmonella and Listeria monocytogenes. Author(s): Li X, Boudjellab N, Zhao X. Source: International Journal of Food Microbiology. 2000 June 1; 56(2-3): 167-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10857543
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Comparative evaluation of culture- and BAX polymerase chain reaction-based detection methods for Listeria spp. and Listeria monocytogenes in environmental and raw fish samples. Author(s): Hoffman AD, Wiedmann M. Source: J Food Prot. 2001 October; 64(10): 1521-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11601700
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Contribution of cytokines to time-dependent augmentation of resistance against Listeria monocytogenes after administration of a traditional Chinese medicine, xiaochai-hu-tang (Japanese name: shosaiko-to). Author(s): Kawakita T, Mitsuyama M, Kumazawa Y, Miura O, Yumioka E, Nomoto K. Source: Immunopharmacology and Immunotoxicology. 1989; 11(2-3): 233-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2516094
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Control of Listeria monocytogenes with combined antimicrobials after postprocess contamination and extended storage of frankfurters at 4 degrees C in vacuum packages. Author(s): Samelis J, Bedie GK, Sofos JN, Belk KE, Scanga JA, Smith GC. Source: J Food Prot. 2002 February; 65(2): 299-307. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11848561
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Cytokine profile and natural killer cell activity in Listeria monocytogenes infected mice treated orally with Petiveria alliacea extract. Author(s): Queiroz ML, Quadros MR, Santos LM. Source: Immunopharmacology and Immunotoxicology. 2000 August; 22(3): 501-18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10946828
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Death of Salmonella, Escherichia coli O157:H7, and Listeria monocytogenes in garlic butter as affected by storage temperature. Author(s): Adler BB, Beuchat LR. Source: J Food Prot. 2002 December; 65(12): 1976-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12495019
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Detection of Listeria monocytogenes in salmon using the Probelia polymerase chain reaction system. Author(s): Wan J, King K, Forsyth S, Coventry MJ. Source: J Food Prot. 2003 March; 66(3): 436-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12636297
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Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes. Author(s): de Pablo MA, Puertollano MA, Galvez A, Ortega E, Gaforio JJ, Alvarez de Cienfuegos G. Source: Fems Immunology and Medical Microbiology. 2000 February; 27(2): 127-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10640607
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Development of a polymerase chain reaction assay for the detection of Listeria monocytogenes in foods. Author(s): Bansal NS.
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Dietary fish oil impairs primary host resistance against Listeria monocytogenes more than the immunological memory response. Author(s): Irons R, Anderson MJ, Zhang M, Fritsche KL. Source: The Journal of Nutrition. 2003 April; 133(4): 1163-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12672937
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Dietary fish oil reduces survival and impairs bacterial clearance in C3H/Hen mice challenged with Listeria monocytogenes. Author(s): Fritsche KL, Shahbazian LM, Feng C, Berg JN. Source: Clinical Science (London, England : 1979). 1997 January; 92(1): 95-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9038598
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Dietary supplementation with conjugated linoleic acid does not alter the resistance of mice to Listeria monocytogenes infection. Author(s): Turnock L, Cook M, Steinberg H, Czuprynski C. Source: Lipids. 2001 February; 36(2): 135-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11269693
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Differential role of cytosolic phospholipase A2 in the invasion of brain microvascular endothelial cells by Escherichia coli and Listeria monocytogenes. Author(s): Das A, Asatryan L, Reddy MA, Wass CA, Stins MF, Joshi S, Bonventre JV, Kim KS. Source: The Journal of Infectious Diseases. 2001 September 15; 184(6): 732-7. Epub 2001 August 13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11517434
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Docosahexaenoic acid, a constituent of fetal and neonatal serum, inhibits nitric oxide production by murine macrophages stimulated by IFN gamma plus LPS, or by IFN gamma plus Listeria monocytogenes. Author(s): Lu CY, Penfield JG, Khair-el-Din TA, Sicher SC, Kielar ML, Vazquez MA, Che L. Source: Journal of Reproductive Immunology. 1998 April; 38(1): 31-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9616876
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Effect of “siljo” fermentation on growth of Staphylococcus aureus, Bacillus cereus and Listeria monocytogenes. Author(s): Dessie G, Abegaz K, Ashenafi M. Source: Ethiop Med J. 1997 October; 35(4): 215-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10214435
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Effect of a traditional Chinese medicine, bu-zhong-yi-qi-tang (Japanese name: Hochuekki-to) on the protection against Listeria monocytogenes infection in mice. Author(s): Li XY, Takimoto H, Miura S, Yoshikai Y, Matsuzaki G, Nomoto K. Source: Immunopharmacology and Immunotoxicology. 1992; 14(3): 383-402. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1517527
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Effect of a traditional Chinese medicine, Bu-zhong-yi-qi-tang on the protection against an oral infection with Listeria monocytogenes. Author(s): Yamaoka Y, Kawakita T, Kishihara K, Nomoto K. Source: Immunopharmacology. 1998 June; 39(3): 215-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9754907
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Effects of gamma irradiation on the survival of Listeria monocytogenes and on its growth at refrigeration temperature in poultry and red meat. Author(s): Gursel B, Gurakan GC. Source: Poultry Science. 1997 December; 76(12): 1661-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9438279
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Endogenous tumor necrosis factor alpha is required for enhanced antimicrobial activity against Toxoplasma gondii and Listeria monocytogenes in recombinant gamma interferon-treated mice. Author(s): Langermans JA, van der Hulst ME, Nibbering PH, van Furth R. Source: Infection and Immunity. 1992 December; 60(12): 5107-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1452344
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Evaluation of the BAX system for detection of Listeria monocytogenes in foods: collaborative study. Author(s): Silbernagel K, Jechorek R, Barbour WM, Mrozinski P, Alejo W, Aleo V, Andaloro B, Beacorn F, Benzinger J, Bogar S, Brayman C, Broom J, Carson M, Carver C, Cheng C, Centrella B, Clayborn J, Collins C, Deibel C, Divine M, Eliasberg S, Farmer D, Frye S, Gatesy T, Goodstein E, Halker C, Hall G, Hanson P, Hartman G, Heddaeus K, Hembree J, Hutchins J, Istafanos P, Jechorek R, Jenkins J, Kerdahi K, Kremer S, Lal A, Leighton S, Lester D, Lewis J, Lin J, Martin J, Maselli M, McCarthy P, McGovern B, Mills M, Mohnke F, Moon B, Moss D, Plaza M, Robeson S, Romero H, Rubalcaba D, Schultz A, Seehusen J, Shaw C, Siem K, Sloan E, Stanerson J, Stepanova N, Van K, Van Enkenvoort K, Vialpando M, Warren W, Watts K, Wilson K, Woodruff T. Source: J Aoac Int. 2004 March-April; 87(2): 395-410. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15164834
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Evaluation of two commercial methods for the detection of Listeria sp. and Listeria monocytogenes in a chicken nugget processing plant. Author(s): Rodrigues D, Landgraf M, Destro MT. Source: Canadian Journal of Microbiology. 2002 March; 48(3): 275-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11989773
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Growth inhibition of selected food-borne bacteria, particularly Listeria monocytogenes, by plant extracts. Author(s): Chung KT, Thomasson WR, Wu-Yuan CD. Source: The Journal of Applied Bacteriology. 1990 October; 69(4): 498-503. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2127264
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Growth kinetics and cell morphology of Listeria monocytogenes Scott A as affected by temperature, NaCl, and EDTA. Author(s): Zaika LL, Fanelli JS. Source: J Food Prot. 2003 July; 66(7): 1208-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12870754
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Growth of Listeria monocytogenes in Camembert and other soft cheeses at refrigeration temperatures. Author(s): Back JP, Langford SA, Kroll RG. Source: The Journal of Dairy Research. 1993 August; 60(3): 421-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8376636
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Hot water extracts of Chlorella vulgaris reduce opportunistic infection with Listeria monocytogenes in C57BL/6 mice infected with LP-BM5 murine leukemia viruses. Author(s): Hasegawa T, Okuda M, Makino M, Hiromatsu K, Nomoto K, Yoshikai Y. Source: International Journal of Immunopharmacology. 1995 June; 17(6): 505-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7499027
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Identification of the gene encoding the alternative sigma factor sigmaB from Listeria monocytogenes and its role in osmotolerance. Author(s): Becker LA, Cetin MS, Hutkins RW, Benson AK. Source: Journal of Bacteriology. 1998 September; 180(17): 4547-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9721294
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Immunomodulatory effects of dietary lipids alter host natural resistance of mice to Listeria monocytogenes infection. Author(s): Puertollano MA, de Pablo MA, Alvarez de Cienfuegos G. Source: Fems Immunology and Medical Microbiology. 2001 December; 32(1): 47-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11750222
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Inhibition of Listeria monocytogenes and Salmonella enteriditis by combinations of plant oils and derivatives of benzoic acid: the development of synergistic antimicrobial combinations. Author(s): Fyfe L, Armstrong F, Stewart J. Source: International Journal of Antimicrobial Agents. 1997 January; 9(3): 195-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9552716
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Inhibitory effects of sucrose monolaurate, alone and in combination with organic acids, on Listeria monocytogenes and Staphylococcus aureus. Author(s): Monk JD, Beuchat LR, Hathcox AK. Source: The Journal of Applied Bacteriology. 1996 July; 81(1): 7-18. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8675484
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Involvement of MAP-kinases and -phosphatases in uptake and intracellular replication of Listeria monocytogenes in J774 macrophage cells. Author(s): Kugler S, Schuller S, Goebel W. Source: Fems Microbiology Letters. 1997 December 1; 157(1): 131-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9418248
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Iron acquisition systems of Listeria monocytogenes. Author(s): Adams TJ, Vartivarian S, Cowart RE. Source: Infection and Immunity. 1990 August; 58(8): 2715-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2115028
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Lack of apoptosis in Listeria monocytogenes-infected thymocytes from mice fed with dietary lipids. Author(s): Puertollano MA, Puertollano E, Jimenez-Valera M, Ruiz-Bravo A, De Pablo MA, Cienfuegos GA. Source: Current Microbiology. 2004 May; 48(5): 373-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=15060735
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Listeria monocytogenes infection and activation of human brain microvascular endothelial cells. Author(s): Wilson SL, Drevets DA. Source: The Journal of Infectious Diseases. 1998 December; 178(6): 1658-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9815218
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Listeria monocytogenes invasion of epithelial cells requires the MEK-1/ERK-2 mitogen-activated protein kinase pathway. Author(s): Tang P, Sutherland CL, Gold MR, Finlay BB. Source: Infection and Immunity. 1998 March; 66(3): 1106-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9488402
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Listeria monocytogenes, an invasive bacterium, stimulates MAP kinase upon attachment to epithelial cells. Author(s): Tang P, Rosenshine I, Finlay BB. Source: Molecular Biology of the Cell. 1994 April; 5(4): 455-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8054686
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Mechanism for nonspecific immunity of Listeria monocytogenes in rats mediated by platelets and the clotting system. Author(s): Davies WA, Ackerman VP, Nelson DS. Source: Infection and Immunity. 1981 August; 33(2): 477-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6792078
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Microbiological quality of fresh leafy vegetables, salad components and ready-to-eat salads: an evidence of inhibition of Listeria monocytogenes in tomatoes. Author(s): Pingulkar K, Kamat A, Bongirwar D. Source: International Journal of Food Sciences and Nutrition. 2001 January; 52(1): 15-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11225173
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Modulation of delayed-type hypersensitivity and acquired cellular resistance by orally administered viable indigenous lactobacilli in Listeria monocytogenes infected Wistar rats. Author(s): de Waard R, Garssen J, Vos JG, Claassen E. Source: Letters in Applied Microbiology. 2002; 35(3): 256-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12180952
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N-terminal E-cadherin peptides act as decoy receptors for Listeria monocytogenes. Author(s): da Silva Tatley F, Aldwell FE, Dunbier AK, Guilford PJ. Source: Infection and Immunity. 2003 March; 71(3): 1580-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12595481
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Optimized, one-step, recovery-enrichment broth for enhanced detection of Listeria monocytogenes in pasteurized milk and hot dogs. Author(s): Knabel SJ. Source: J Aoac Int. 2002 March-April; 85(2): 501-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11990038
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Organic acids and their salts as dipping solutions to control listeria monocytogenes inoculated following processing of sliced pork bologna stored at 4 degrees C in vacuum packages. Author(s): Samelis J, Sofos JN, Kain ML, Scanga JA, Belk KE, Smith GC. Source: J Food Prot. 2001 November; 64(11): 1722-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726150
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Petiveria alliacea L. extract protects mice against Listeria monocytogenes infection-effects on bone marrow progenitor cells. Author(s): Quadros MR, Souza Brito AR, Queiroz ML. Source: Immunopharmacology and Immunotoxicology. 1999 February; 21(1): 109-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10084333
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Polysaccharides isolated from plant cell cultures of Echinacea purpurea enhance the resistance of immunosuppressed mice against systemic infections with Candida albicans and Listeria monocytogenes. Author(s): Steinmuller C, Roesler J, Grottrup E, Franke G, Wagner H, Lohmann-Matthes ML. Source: International Journal of Immunopharmacology. 1993 July; 15(5): 605-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8375943
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Protective effect of a traditional Chinese medicine, xiao-chai-hu-tang (Japanese name: shosaiko-to), on Listeria monocytogenes infection in mice. Author(s): Kawakita T, Yamada A, Mitsuyama M, Kumazawa Y, Nomoto K. Source: Immunopharmacology and Immunotoxicology. 1988; 10(3): 345-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3264299
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Protective effect of a traditional Japanese medicine Hochu-ekki-to (Chinese name: Bu-zhong-yi-qi-tang), on the susceptibility against Listeria monocytogenes in infant mice. Author(s): Yamaoka Y, Kawakita T, Nomoto K. Source: International Immunopharmacology. 2001 September; 1(9-10): 1669-77. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11562059
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Protective effect of a traditional Japanese medicine, Bu-zhong-yi-qi-tang (Japanese name: Hochu-ekki-to), on the restraint stress-induced susceptibility against Listeria monocytogenes. Author(s): Yamaoka Y, Kawakita T, Nomoto K. Source: Immunopharmacology. 2000 June; 48(1): 35-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10822087
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Protein tyrosine kinase inhibitors block the entries of Listeria monocytogenes and Listeria ivanovii into epithelial cells. Author(s): Velge P, Bottreau E, Kaeffer B, Yurdusev N, Pardon P, Van Langendonck N. Source: Microbial Pathogenesis. 1994 July; 17(1): 37-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7861952
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Purification and characterization of Listeria monocytogenes phosphatidylinositolspecific phospholipase C. Author(s): Goldfine H, Knob C. Source: Infection and Immunity. 1992 October; 60(10): 4059-67. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1398918
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Rapid determination of Listeria monocytogenes by automated enzyme-linked immunoassay and nonradioactive DNA probe. Author(s): Kerdahi KF, Istafanos PF.
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Source: J Aoac Int. 2000 January-February; 83(1): 86-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10693007 •
Reduction of Listeria monocytogenes and Escherichia coli O157:H7 numbers on vacuum-packaged fresh beef treated with nisin or nisin combined with EDTA. Author(s): Zhang S, Mustapha A. Source: J Food Prot. 1999 October; 62(10): 1123-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10528714
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Reduction of listeria monocytogenes on green peppers (Capsicum annuum L.) by gaseous and aqueous chlorine dioxide and water washing and its growth at 7 degrees C. Author(s): Han Y, Linton RH, Nielsen SS, Nelson PE. Source: J Food Prot. 2001 November; 64(11): 1730-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11726151
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Relevance of dietary lipids as modulators of immune functions in cells infected with Listeria monocytogenes. Author(s): Puertollano MA, de Pablo MA, Alvarez de Cienfuegos G. Source: Clinical and Diagnostic Laboratory Immunology. 2002 March; 9(2): 352-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11874877
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Respiratory activity in Listeria monocytogenes. Author(s): Patchett RA, Kelly AF, Kroll RG. Source: Fems Microbiology Letters. 1991 February; 62(1): 95-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1903352
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Sensitization of heat-treated Listeria monocytogenes to added lysozyme in milk. Author(s): Kihm DJ, Leyer GJ, An GH, Johnson EA. Source: Applied and Environmental Microbiology. 1994 October; 60(10): 3854-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7986052
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Surface Listeria monocytogenes carbohydrate-binding components revealed by agglutination with neoglycoproteins. Author(s): Cottin J, Loiseau O, Robert R, Mahaza C, Carbonnelle B, Senet JM. Source: Fems Microbiology Letters. 1990 March 15; 56(3): 301-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2111260
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Symposium on microbiology update: old friends and new enemies. Listeria monocytogenes. Author(s): Farber JM.
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Source: J Assoc Off Anal Chem. 1991 July-August; 74(4): 701-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1917819 •
The combined effect of nisin, leucocin F10, pH, NaCl and EDTA on the survival of Listeria monocytogenes in broth. Author(s): Parente E, Giglio MA, Ricciardi A, Clementi F. Source: International Journal of Food Microbiology. 1998 March 3; 40(1-2): 65-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9600612
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The development of a combined surface adhesion and polymerase chain reaction technique in the rapid detection of Listeria monocytogenes in meat and poultry. Author(s): Duffy G, Cloak OM, Sheridan JJ, Blair IS, McDowell DA. Source: International Journal of Food Microbiology. 1999 August 15; 49(3): 151-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10490225
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The effect of cytotoxic agents on the primary immune response to Listeria monocytogenes. Author(s): Tripathy SP, Mackaness GB. Source: The Journal of Experimental Medicine. 1969 July 1; 130(1): 1-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4978231
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The microtubule depolymerizing drugs nocodazole and colchicine inhibit the uptake of Listeria monocytogenes by P388D1 macrophages. Author(s): Kuhn M. Source: Fems Microbiology Letters. 1998 March 1; 160(1): 87-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9495017
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The VIT technology for rapid detection of Listeria monocytogenes and other Listeria spp. Author(s): Stephan R, Schumacher S, Zychowska MA. Source: International Journal of Food Microbiology. 2003 December 31; 89(2-3): 287-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14623395
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Visual immunoprecipitate assay (VIP) for Listeria monocytogenes and related Listeria species detection in selected foods: collaborative study. Author(s): Feldsine PT, Lienau AH, Forgey RL, Calhoon RD. Source: J Aoac Int. 1997 July-August; 80(4): 791-805. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9241843
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Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to Listeria monocytogenes; 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 Food Poisoning Source: Integrative Medicine Communications; www.drkoop.com Immune Function Source: Healthnotes, Inc.; www.healthnotes.com Meningitis Source: Integrative Medicine Communications; www.drkoop.com
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Herbs and Supplements Aesculus Alternative names: Horse Chestnut; Aesculus hippocastanum L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Eugenia Clove Alternative names: Cloves; Eugenia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Foeniculum Alternative names: Fennel; Foeniculum vulgare Mill Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Ocimum Alternative names: Basil, Albahaca; Ocimum basilicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Pimpinella Alternative names: Anise; Pimpinella anisum (L) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON LISTERIA MONOCYTOGENES Overview In this chapter, we will give you a bibliography on recent dissertations relating to Listeria monocytogenes. 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 “Listeria monocytogenes” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on Listeria monocytogenes, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Listeria monocytogenes 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 Listeria monocytogenes. 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: •
Biocontrol of Listeria monocytogenes in minimally processed brined refrigerated cucumbers by Reina, Laura D., PhD from NORTH CAROLINA STATE UNIVERSITY, 2003, 245 pages http://wwwlib.umi.com/dissertations/fullcit/3099014
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Catabolite repression and virulence gene expression in Listeria monocytogenes 10403S by Evans-Gilbreth, Stefanie N., PhD from THE UNIVERSITY OF NEBRASKA LINCOLN, 2003, 109 pages http://wwwlib.umi.com/dissertations/fullcit/3078608
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CD4 and CD8 T cell proliferation and differentiation in response to Listeria monocytogenes infection by Foulds, Kathryn Elizabeth, PhD from UNIVERSITY OF PENNSYLVANIA, 2003, 140 pages http://wwwlib.umi.com/dissertations/fullcit/3087402
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Characteristics of Listeria monocytogenes important for pulsed electric field process optimization by Lado, Beatrice H., PhD from THE OHIO STATE UNIVERSITY, 2003, 274 pages http://wwwlib.umi.com/dissertations/fullcit/3119242
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Development and characterization of monoclonal antibody probes with high affinity and specificity for Listeria monocytogenes (heat-killed) or Campylobacter jejuni by Heo, Seok Andy, PhD from UNIVERSITY OF ARKANSAS, 2003, 128 pages http://wwwlib.umi.com/dissertations/fullcit/3122378
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Differential sensitivity of Listeria monocytogenes to nisin and diacetyl with a starvation period in sodium phosphate buffered saline by Sostrin, Michael Lane, PhD from UNIVERSITY OF ARKANSAS, 2003, 163 pages http://wwwlib.umi.com/dissertations/fullcit/3122387
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Effect of acid adaptation on the thermal inactivation of Listeria monocytogenes in heating menstrua having various combinations of pH and water activities by EdelsonMammel, Sharon G., MS from UNIVERSITY OF MARYLAND COLLEGE PARK, 2004, 133 pages http://wwwlib.umi.com/dissertations/fullcit/1417629
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Enhanced inhibition of Listeria monocytogenes and Salmonella enterica serovar Enteritidis in ready-to-eat meat by lactate and diacetate by Mbandi, Evelyne, PhD from WAYNE STATE UNIVERSITY, 2003, 124 pages http://wwwlib.umi.com/dissertations/fullcit/3086451
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Food safety: Inhibition of Listeria monocytogenes by lactic acid bacteria and their bacteriocins by Katla, Tone, DrScient from NORGES LANDBRUKSHOGSKOLE (NORWAY), 2003, 80 pages http://wwwlib.umi.com/dissertations/fullcit/f186017
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Influence of cold, surfactant or carbon dioxide adaptation on the sensitivity of Listeria monocytogenes to nisin: A mechanistic study of the membrane composition and physical properties by Li, Jie, PhD from RUTGERS THE STATE UNIVERSITY OF NEW JERSEY - NEW BRUNSWICK, 2003, 209 pages http://wwwlib.umi.com/dissertations/fullcit/3105471
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Inhibition of Listeria monocytogenes on a processed meat product with a lactic acid bacterium by Rivard, Denise Rachel, MSc from UNIVERSITY OF ALBERTA (CANADA), 2003, 94 pages http://wwwlib.umi.com/dissertations/fullcit/MQ82338
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Ozone inactivation and attachment of Listeria monocytogenes to abiotic surfaces by Fisher, Christopher William, PhD from UNIVERSITY OF ILLINOIS AT URBANACHAMPAIGN, 2003, 182 pages http://wwwlib.umi.com/dissertations/fullcit/3101837
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Primary and secondary CD8+ T cell responses after Listeria monocytogenes infection or peptide-coated dendritic cell immunization by Hamilton, Sara Elizabeth, PhD from THE UNIVERSITY OF IOWA, 2003, 176 pages http://wwwlib.umi.com/dissertations/fullcit/3088250
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Recombinant Listeria monocytogenes as a live oral delivery vector of SIV Gag protein by Johnson, Ross Stephen, PhD from UNIVERSITY OF PENNSYLVANIA, 2003, 120 pages http://wwwlib.umi.com/dissertations/fullcit/3095894
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Salmonella enterica, Listeria monocytogenes and Clostridium perfringens: Diversity of human isolates studied by phenotypic and molecular methods by Lukinmaa, Susanna, PhD from HELSINGIN YLIOPISTO (FINLAND), 2003, 139 pages http://wwwlib.umi.com/dissertations/fullcit/f186001
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Structure and function of Listeria monocytogenes internalin B by Marino, Michael Ernest, PhD from UNIVERSITY OF CALIFORNIA, SAN DIEGO, 2003, 179 pages http://wwwlib.umi.com/dissertations/fullcit/3083463
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Synergistic effect of ozone and Microgard (MG300) to inactivate Listeria monocytogenes in ready to eat cooked and cured ham by Jhala, Ravirajsinh P., MS from SOUTH DAKOTA STATE UNIVERSITY, 2003, 143 pages http://wwwlib.umi.com/dissertations/fullcit/1417444
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The ecology of Listeria monocytogenes in ready-to-eat (RTE) meats by Foong, Chi Ching Sally, PhD from IOWA STATE UNIVERSITY, 2003, 145 pages http://wwwlib.umi.com/dissertations/fullcit/3085906
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Use of pediocin with other barriers for control of Listeria monocytogenes on ready-toeat (RTE) processed meats by Chen, Chih-Ming, PhD from IOWA STATE UNIVERSITY, 2003, 123 pages http://wwwlib.umi.com/dissertations/fullcit/3085893
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 LISTERIA MONOCYTOGENES 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 “Listeria monocytogenes” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on Listeria monocytogenes, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Listeria monocytogenes By performing a patent search focusing on Listeria monocytogenes, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. 8Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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The following is an example of the type of information that you can expect to obtain from a patent search on Listeria monocytogenes: •
Genetic markers and methods for the detection of Listeria monocytogenes and Listeria spp Inventor(s): Hazel; James William (Conowingo, MD), Jensen; Mark Anton (West Chester, PA) Assignee(s): E.I. du Pont de Nemours and Company (Wilmington, DE) Patent Number: 5,922,538 Date filed: December 12, 1996 Abstract: A method, diagnostic sequences and primers are provided that are useful in identifying the Listeria monocytogenes and Listeria spp. The method involves identifying a RAPD-amplified DNA fragment common to Listeria monocytogenes, then identifying the most conserved regions of that DNA fragment, and the preparing specific primers useful for detecting the presence of a marker within the fragment whereby that set of primers is then useful in the identification of all Listeria monocytogenes. Markers within the same fragment that are specific to the Listeria genus are also identified and are useful for the identification of all Listeria spp. Excerpt(s): The invention relates to the field of molecular biology and the use of randomly amplified nucleic acid fragments (RAPD) for the selection of genetic markers useful in the identification of bacteria. More specifically, the invention relates to specific DNA marker sequences useful for the detection of Listeria monocytogenes and Listeria spp. and use of those diagnostic markers to determine if an unknown bacterium is a member of either Listeria monocytogenes or Listeria spp. Central to the field of microbiology is the ability to positively identify microorganisms at the level of genus, species or serotype. Correct identification is not only an essential tool in the laboratory, but it plays a significant role in the control of microbial contamination in the processing of food stuffs, the production of agricultural products, and the monitoring of environmental media such as ground water. Increasing stringency in regulations that apply to microbial contamination have resulted in a corresponding increase in industry resources which must be dedicated to contamination monitoring. Of greatest concern is the detection and control of pathogenic microorganisms. Although a broad range of microorganisms have been classified as pathogenic, attention has primarily focused on a few bacterial groupings such as Escherichia, Salmonella, Listeria and Clostridia. Typically, pathogen identification has relied on methods for distinguishing phenotypic aspects such as growth or motility characteristics, and for immunological and serological characteristics. Selective growth procedures and immunological methods are the traditional methods of choice for bacterial identification and these can be effective for the presumptive detection of a large number of species within a particular genus. However, these methods are time consuming and are subject to error. Selective growth methods require culturing and subculturing in selective media, followed by subjective analysis by an experienced investigator. Immunological detection (e.g., ELISA) is more rapid and specific, however, it still requires growth of a significant population of organisms and isolation of the relevant antigens. For these reasons interest has turned to detection of bacterial pathogens on the basis of nucleic acid sequence. Web site: http://www.delphion.com/details?pn=US05922538__
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Immunostimulant agent from Salmonella typhimurium or Listeria monocytogenes bacterial cells and pharmaceutical composition Inventor(s): Fauve; Robert (Sevres, FR) Assignee(s): Institut Pasteur (Paris, FR) Patent Number: 4,180,563 Date filed: February 23, 1978 Abstract: An immunostimulant from bacterial cells of Salmonella typhimurium or Listeria monocytogenes; it promotes non-specific resistance to pathogens which has no antigenic relationship to the immunostimulant. Excerpt(s): The invention, produced at the Pasteur Institute, relates to an agent capable of stimulating the non-specific resistance of the human or animal organism, with respect to various pathogenic agents (virus, bacteria, parasites, etc.), in the absence of antigenic relationship between the stimulant product and the infectious agent. Agents possessing this action will be denoted below, for convenience of language, by the expression "immunostimulant agents". There are already known a certain number of substances or compositions which constitute such non-specific immunostimulant agents. Their application in human or veterinary therapeutics, has however been scarcely contemplated, by reason of their toxicity being too great and also of their action being too much delayed. The invention rests on the discovery that a very active immunostimulant agent, with short time for taking effect and, at the same time, practically devoid of toxicity, could be easily isolated from splenic cells of animal origin, from Ehrlich ascites cells and from bacterial strains, or of Bacillus subtili cells and of Saccharomyces cerevisiae, this immunostimulant agent beng of such a nature as to constitute a valuable active principle for the constitution of medicaments, for example for stimulating in non-specific manner the resistance of the organism against numerous infectious agents, of the type which have been cited above. Web site: http://www.delphion.com/details?pn=US04180563__
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Inhibition of food pathogens by hop acids Inventor(s): Millis; James R. (Kohler, WI), Schendel; Mark J. (Manitowoc, WI) Assignee(s): Bio-Technical Resources (Manitowoc, WI) Patent Number: 5,286,506 Date filed: October 29, 1992 Abstract: The protection of food products from contamination by food pathogens, particularly Listeria monocytogenes, by incorporation of 6 to 50 ppm and preferably 6 to 15 ppm of beta-acids, as extracted from hops, into such food products. Excerpt(s): The present invention relates to the use of beta-acids as extracted from hops for controlling Listeria and other food pathogens in food products intended for human consumption. Recent studies have revealed that listeriosis in humans as caused by Listeria species and particularly Listeria monocytogenes is associated with the consumption of various types of foods, particularly soft cheese and pate as well as hams and other prepacked meat and poultry products. "Listeria monocytogenes in Prepacked Ready-To-Eat Sliced Meats", a survey by the 16 public health laboratories in the PHLS food chain, by S. Velani and R. J. Gilbert, PHLS Microbiology Digest Vol. 7 (1990). Hops and their associated acids have long been recognized as bacteriological inhibitors. More
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specifically, hop acids and resins have been shown to be primarily active against gram positive bacteria, e.g., Bacilli, Corynebacteria, Diplococci, Mycobacteria, Streptococci, Lactobacilli and Streptomyces. Most of the publications have focused on Lactobacilli, since this organism is a major contaminant in beer fermentation. Activity against gram negative bacteria is far less pronounced. Teuber and Schmalrek (Arch. Mikrobiol. 94, pp. 159-171, 1973) and Simpson and Hammond (European Brewery Convention, 1991) have suggested that the effect was due to induced permeability of the cell membrane in gram positive bacteria, but was inactivated by serumphosphatides in gram negative bacteria. Web site: http://www.delphion.com/details?pn=US05286506__ •
Listeria monocytogenes specific proteins, and uses thereof Inventor(s): Chakraborty; Trinad (Wurzburg, DE), Goebel; Werner (Veitshochheim, DE), Notermans; Servatius Hubertus Wilhelmus (Bilthoven, NL) Assignee(s): Boehringer Amnnheim GmbH (Mannheim, DE) Patent Number: 5,696,232 Date filed: June 2, 1995 Abstract: The present invention is directed to Listeria monocytogenes specific protein that is encoded by nucleotide sequence of FIG. 1, the complementary sequence of which hybridizes to the nucleotide sequence of FIG. 1 at 5-6x SSC and 42.degree.-60.degree. C. A Listeria monocytogenes specific protein is also described having an amino aicd sequence as set forth in FIGS. 1A-1D. The proteins are suitable for the production of antibodies against Listeria monocytogenes. Excerpt(s): The invention concerns a method for the determination of pathogenic Listeria bacteria, a nucleic acid probe, as well as a protein which is suitable for the production of antibodies against pathogenic Listeria bacteria. Listeria are a heterogeneous group of gram-positive bacteria and consist essentially of the species Listeria monocytogenes, L. innocua, L. welshimeri, L. seeligeri, L. ivanovii, L. grayi and L. murrayi. Only two of these species are pathogenic, namely L. monocytogenes for humans and animals and L. ivanovii for animals. Listeriosis usually manifests itself in humans as a bacterial meningitis and septicaemia as well as miscarriages and stillbirths in pregnant women. In sheep and cattle listeriosis manifests itself as miscarriage, encephalitis, septicaemia and mastitis. (N. Engl. J. Med. 308 (1983), 203-206, J. Infec. 15 (1987), 165-168, Linnan, M. J. et al., An investigation of listeriosis in Southern California 1985, in Courtieu, A. L. et al., (eds) Listeriose, Listeria, Listeriosis 1985-1986, University of Nantes). Recently an increasing number of listeriosis diseases have been observed in humans, the cause of which is regarded to be due to the contamination of milk and cheese, above all soft cheese varieties, by Listeria bacteria. Therefore an examination of food for Listeria contamination is important and is obligatory for cheese in the USA. Web site: http://www.delphion.com/details?pn=US05696232__
Patents 167
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Live, recombinant listeria monocytogenes and production of cytotoxic T-cell response Inventor(s): Paterson; Yvonne (Philadelphia, PA), Portnoy; Daniel A. (Philadelphia, PA) Assignee(s): The Trustees of the University of Pennsylvania (Philadelphia, PA) Patent Number: 5,830,702 Date filed: December 30, 1994 Abstract: Vaccines comprising an attenuated strain of Listeria spp. expressing a selected foreign antigen and methods of eliciting protective immunity by administering an effective amount of the vaccine are provided. The vaccines of the present invention are designed specifically to elicit strong cell-mediated immunity, and are particularly useful for protection in infections which can apparently persist and spread in the presence of neutralizing antibodies invoked by humoral immunity. Excerpt(s): Listeria monocytogenes is a Gram-positive, food-borne human and animal pathogen responsible for serious infections in immunocompromised individuals and pregnant women. Severe L. monocytogenes infections in humans are characterized by meningitis, meningoencephalitis, septicemia, and fetal death. L. monocytogenes is ubiquitous in nature and, in addition, can be isolated from a wide variety of warm blooded animals. L. monocytogenes enters the host cytoplasm and uses a host system of actin-based motility to mediate movement both within a cell and from cell-to-cell without leaving the cytoplasm. The intracellular parasitism of L. monocytogenes can be broadly divided into five stages, including (i) internalization, (ii) escape from a host vacuole, (iii) intracellular growth, (iv) intracellular movement and pseudopod formation using host actin filaments, and (v) cell-to-cell spread which proceeds through an intermediate double-membraned vacuole. More specifically, subsequent to internalization, L. monocytogenes escapes from a host vacuole, an event mediated, at least in part, by the action of a pore-forming hemolysin, Listeriolysin O. Next, rapid cell division ensues and the bacteria become encapsulated by short actin filaments and other actin binding proteins. The actin based structure is rearranged to form a long tail behind the bacteria which appears to mediate movement of the bacteria through the cytoplasm to the cell periphery. Next, some of the bacteria are presented in pseudopod-like structures which are apparently recognized and internalized by neighboring cells. Thus, within the cytoplasm of the second cell, the bacteria are found surrounded by a double membrane. Both membranes are solubilized and the cycle is repeated. In this way, the bacteria spread from one cell to another without ever leaving the cytoplasm thereby providing an explanation for the absolute requirement of cell mediated immunity and the observation that antibodies are not protective. Thus, once inside a host cell, infecting Listeria monocytogenes and their progeny can spread from cell to cell by remaining intracellular, bypassing the humoral immune system of the host organism. Further, data suggest that actin filaments are essential for the spread of L. monocytogenes from cell to cell. Tilney and Portnoy, J. Cell. Biol. 1989, 109, 1597-1608. Web site: http://www.delphion.com/details?pn=US05830702__
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Method for detecting Listeria monocytogenes Inventor(s): Baquero; Fernando (Madrid, ES), Cossart; Pascale (Paris, FR) Assignee(s): Institut Pasteur (Paris, FR) Patent Number: 5,389,513 Date filed: April 22, 1991
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Abstract: A DNA probe is disclosed which is capable of hybridizing to a portion of the genome of pathogenic Listeria monocytogenes but which does not hybridize to portions of the genomes of other Listeria species and other humilytic bacteria. This probe is useful to identify food sources infected with Listeria monocytogenes and to distinguish these food services from those infected nearly with non-pathogenic Listeria species. In addition, methods for the detection of pathogenic Listeria in samples using the disclosed probes are provided. Excerpt(s): Listeria monocytogenes is a facultative intracellular gram positive bacterium. In the genus Listeria, only L. monocytogenes and L. ivanovii are pathogens for human and animals. L. monocytogenes is increasingly recognized as responsible for severe infections in both animals and humans. Pregnant women, new-born and immunocompromised patients are especially susceptible to infection. To avoid human infection, food sources have, routinely been screened for the presence of Listeria organisms. Potential food sources infected with any species of Listeria have routinely been discarded to avoid infecting the consumer because of the time and expense involved in determining whether the infecting organisms are or are not pathogenic. Thus, there is a need for a means identifying and distinguishing pathogenic Listeria. In addition, another need has arisen for means to distinguish readily and efficiently between pathogenic and non-pathogenic Listeria species. This information is necessary to determine the course of treatment of suspected listeria infections and for the development of data for epidemiological studies. Web site: http://www.delphion.com/details?pn=US05389513__ •
Method for detecting Listeria monocytogenes via esculin hydrolysis and nucleic acid hybridization Inventor(s): Fraser; Judy A. (Apple Valley, MN) Assignee(s): The Pillsbury Company (Minneapolis, MN) Patent Number: 6,001,559 Date filed: July 13, 1992 Abstract: A method for rapidly detecting non-viral organisms disclosed. The method involves pelleting an enrichment culture of a sample, optionally washing the pellet, resuspending the pellet in an appropriate reagent before performing a nucleic acid hybridization confirmation test on the sample. Excerpt(s): The present invention deals with detecting non-viral organisms. Specifically, the invention is a method of rapidly obtaining a culture suitable for detecting pathogens via a DNA probe. The method of the invention saves both time and money as compared to currently used DNA probe detection methods and more conventional procedures used by the FDA and the USDA such as biochemical and physiological methods. The method of the invention may be used to obtain a culture to detect the presence of pathogens or any non-viral organism in areas such as medical, veterinary, and agricultural diagnostics; industrial and pharmaceutical quality control. Bacterial pathogens can cause severe illness and even death if they are ingested by animals or humans. Detecting pathogens is critical in the food industry because foodborne pathogens infect unsuspecting consumers. Quality assurance tests must be done before food is shipped to ensure that pathogens are not present. Quality assurance tests, including environmental tests, must also be performed on an ongoing basis during production to ensure that the food is not contaminated during processing. Traditional
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techniques for identifying pathogens are complicated and are time and labor intensive. Recently developed identification techniques utilize DNA probes and rely on the ability of complimentary nucleic acid strands to specifically align and associate to form stable double-stranded complexes. Although nucleic acid hybridization techniques greatly reduce the time required to identify pathogens as compared to physiological and biochemical methods; hybridization methods still require a culture suitable for testing. The process for obtaining a suitable culture is lengthy. It is the object of the present invention to reduce the amount of time and money required to obtain a suitable culture for detecting pathogens via nucleic acid hybridization techniques. Web site: http://www.delphion.com/details?pn=US06001559__ •
Method for inhibiting Listeria monocytogenes using a bacteriocin Inventor(s): Kunka; Blair S. (Bradenton, FL), Pucci; Michael J. (Sarasota, FL), Vandenbergh; Peter A. (Sarasota, FL), Vedamuthu; Ebenezer R. (Bradenton, FL) Assignee(s): Microlife Technics, Inc. (Sarasota, FL) Patent Number: 4,929,445 Date filed: January 25, 1988 Abstract: A method for inhibiting Listeria monocytogenes in a food or other material which can be contaminated with this pathogen using a bacteriocin produced by DNA in Pediococcus acidilactici is described. The bacteriocin is particularly produced by Pediococcus acidilactici containing a 6.2 Mdal (9.4 Kilobase pairs) plasmid encoding for the bacteriocin. Excerpt(s): The present invention relates to a method for inhibiting Listeria monocytogenes, a foodborne pathogen, in a food or other materials which can be contaminated by this pathogen using a bacteriocin. In particular the present invention relates to the use of a bacteriocin derived from Pediococcus acidilactici to inhibit the Listeria monocytogenes in the food or other materials which can be contaminated by this pathogen. The term "bacteriocin" refers to a protein of the colicin type, characterized by lethal biosynthesis by the producing bacterium, intraspecific activity in related species of bacteria, and adsorption to specific receptors on the sensitive bacteria (Tagg, J. R., A. S. Dajani, and L. W. Wannamaker, Bacteriol. Rev. 40:722-756 (1976)). Bacteriocins have been described as being produced by many bacteria, however the bacterial strains inhibited by the bacteriocin are usually related to the strain which produces the bacteriocin (Gonzalez, C. F., and B. S. Kunka, Appl. Environ. Microbiol. 53:2534-2538 (1987)). In U.S. Pat. No. 4,883,673, filed Feb. 9, 1987 by Carlos Gonzalez, which is assigned to a common assignee, the preparation and use of a bacteriocin derived from Pediococcus acidilactici, particularly Pediococcus acidilactici NRRL-B-18050, to inhibit spoilage bacteria, particularly Lactobacillus fermentum and Lactobacillus bifermentum, is described. These spoilage bacteria are lactic acid producing strains of the genus Lactobacillus and Pediococcus. No activity was found against Lactococcus lactis, Lactococcus lactis subsp. diacetylactis, Lactococcus cremoris (previously in the genus "Streptococcus") or Streptococcus thermophilus, Staphylococcus aureus, Micrococcus varians, Micrococcus sodonensis, Staphylococcus xylosus, Staphylococcus epidermidis, Staphylococcus carnosus, Lactobacillus acidophilus, Lactobacillus lactis and Lactobacillus bulgaricus. It was concluded that the bacteriocin had a limited range of inhibitory activity related to gram positive, lactic acid bacteria. Web site: http://www.delphion.com/details?pn=US04929445__
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Monoclonal antibody assay for Listeria monocytogenes Inventor(s): Batt; Carl A. (Groton, NY) Assignee(s): Cornell Research Foundation, Inc. (Ithaca, NY) Patent Number: 5,294,537 Date filed: September 23, 1991 Abstract: Mouse monoclonal antibodies which will specifically recognize the pathogen Listeria monocytogenes were produced by fusion of spleen cells from an animal immunized with live L. monocytogenes to an NS-1 myeloma partner, and three hybridomas were identified upon subsequent subcloning, Mab 20-10-2, Mab 36-6-12 and Mab 56-9-16 which were preferentially reactive with L. monocytogenes in a direct binding ELISA assay. An indirect "sandwich" assay was developed and used to further confirm the reactivity of these hybridomas using four serotypes of L. monocytogenes and other common cross reacting bacteria. Excerpt(s): Listeria monocytogenes is a gram-positive non spore forming, motile bacillus first described in 1926. This organism is ubiquitous and has been isolated from milk and milk products, vegetables, raw meats, poultry, shellfish and other food products. The presence of Listeria monocytogenes in food products represents an ever increasing food safety problem particularly in infants and immunocompromised persons. Fatalities in symptomatic infected individuals within these groups may be as great as 40%. Although there clearly exists a need for a reliable diagnostic procedure to identify this microorganism in contaminated food products, the techniques currently available for the detection and enumeration of L. monocytogenes are not sufficiently rapid to assure the safety of the products prior to their consumption. These techniques are presently only useful in diagnosing the probable etiological agent following a suspected food illness outbreak. Current methodology for the detection and enumeration of Listeria involves enrichment in selective media including, in certain cases, incubation for a minimum of seven days at refrigeration temperatures. This is usually followed by a series of biochemical tests to confirm the micro-organism's identification as Listeria. The time required for final confirmation may exceed several weeks depending upon the initial population, the type of food and the co-contaminating microflora (Listeria species have been reported as cross-reactive to a wide number of other grampositive organisms). This protracted analysis time precludes the prescreening of a number of perishable, yet suspect products such as ready-to-eat foods and dairy products. Since there is an antigenic cross reactivity between Listeria species and other gram-positive bacteria, any acceptable method for confirming the presence of these micro-organisms will require very specific antibodies if an immunodiagnostic approach is to be taken. To this end, it is believed any approach will require the use of homogenous (that is monoclonal) antibodies. Web site: http://www.delphion.com/details?pn=US05294537__
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Mutant strain of Listeria monocytogenes and its use in production of IgM antibodies and as an immunotherapeutic agent Inventor(s): Likhite; Vilas V. (229 White St., Belmont, MA 02178) Assignee(s): none reported Patent Number: 4,567,041 Date filed: August 2, 1983 Abstract: A novel mutant strain of Listeria monocytogenes has been discovered which functions as a killed strain not only as an antigen resulting in the production of relatively large titers of IgM antibodies in host animals but also as an immunopotentiating agent when conjugated to a sensitising antigen, for example, living tumor cells and herpes simplex virus. The high molecular weight IgM antibodies are readily separated from serum and recovered without loss of appreciable activity. The IgM antibodies can be divided into five subunits of IgG antibodies, of lesser molecular weight, having the same specificity as the IgM immunoglobulins. When the sensitizing antigens conjugated with the Listeria monocytogenes strain of this invention are tumor cells, the conjugate acts as an immunotherapeutic agent effective in cancer immunotherapy. Excerpt(s): This invention relates to a novel mutant strain of Listeria monocytogenes, to its use in the production of high titers of IgM antibodies specific thereto, to its use and functioning as an immunopotentiating agent (or immunostimulant adjuvant) when conjugated to a sensitizing antigen, to the antibodies responsive to the mutant strain or conjugate, and to such conjugates used as immunotherapeutic agents for use in the treatment of various diseases. Immunity is an everyday word applied to a special category of defenses possessed by the body, i.e., the reticuloendothelial and lymphoproliferation systems, by means of which infectious agents, e.g., antigens, may be checked or destroyed even after they have entered the body tissues. The immunity is largely due to the development within the body of substances known as antibodies (or immune bodies) which interact specifically with the antigen destroying or inactivating the disease causing agent. Immunity may be natural or acquired, and in the latter case may be acquired naturally or artificially. Artificial immunity, as is well known, can be either passive, i.e., by injection of an antiserum (prophylactic, therapeutic), or active, as by vaccination with, for example, live or dead organisms. (6) nucleic acides, such as ribonucleic acid and deoxyribonucleic acid. Web site: http://www.delphion.com/details?pn=US04567041__
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Nucleic acid probes to Listeria monocytogenes Inventor(s): Hogan; James J. (Coronado, CA) Assignee(s): Gen-Probe Incorporated (San Diego, CA) Patent Number: 6,028,187 Date filed: June 7, 1995 Abstract: Hybridization assay probes specific for Listeria monocytogenes and no other Listeria species. Excerpt(s): The inventions described and claimed herein relate to the design and construction of nucleic acid probes to Listeria monocytogenes which are capable of detecting the organism in test samples of, e.g., sputum, urine, blood and tissue sections,
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food, soil and water. Two single strands of deoxyribo- ("DNA") or ribo- ("RNA") nucleic acid, formed from nucleotides (including the bases adenine (A), cytosine (C), thymidine (T), guanine (G), uracil (U), or inosine (I)), may associate ("hybridize") to form a double stranded structure in which the two strands are held together by hydrogen bonds between pairs of complementary bases. Generally, A is hydrogen bonded to T or U, while G is hydrogen bonded to C. At any point along the chain, therefore, one may find the classical base pairs AT or AU, TA or UA, GC, or CG. One may also find AG, GU and other "wobble" or mismatched base pairs. When a first single strand of nucleic acid contains sufficient contiguous complementary bases to a second, and those two strands are brought together under conditions which will promote their hybridization, double stranded nucleic acid will result. Under appropriate conditions, DNA/DNA, RNA/DNA, or RNA/RNA hybrids may be formed. Web site: http://www.delphion.com/details?pn=US06028187__ •
Process and medium for identification of bacteria of the listeria genus Inventor(s): Monget; Daniel (Saint-Sorlin en Bugey, FR) Assignee(s): Bio Merieux (FR) Patent Number: 5,330,889 Date filed: January 13, 1992 Abstract: The invention relates to a process of bacteriological analysis for differentiating the pathogenic monocytogenes species in a sample which may contain bacteria of the listeria genus, a medium for its implementation and a device for identifying Listeria monocytogenes. The process consists in bringing the sample to be analyzed into contact with an identification medium comprising a chromogenic or fluorigenic substrate capable of being hydrolyzed by glycine aminopeptidase. Excerpt(s): The subject of the present invention is a process and a medium for bacteriological identification enabling the various species of the Listeria genus to be differentiated and/or identified. More specifically, the main subject of the invention is the differentiation of the pathogenic monocytogenes species from the other nonpathogenic species of the Listeria genus. The Listeria genus today comprises seven species of which only Listeria monocytogenes is pathogenic for man. Microorganisms are the cause of severe epidemics in man following contaminations caused by food. Two species of Listeria are mainly isolated from foodstuffs (mainly milk and milk products): Listeria innocua, non-pathogenic and Listeria monocytogenes, pathogenic. These two species have numerous biochemical characteristics in common and it is therefore difficult to differentiate between them. The tests currently used are as follows. Web site: http://www.delphion.com/details?pn=US05330889__
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Selective and differential medium for isolation of Listeria monocytogenes Inventor(s): Eklund; Mel W. (Seattle, WA), Lashbrook; Laura C. (Seattle, WA), Paranjpye; Rohinee N. (Seattle, WA), Pelroy; Gretchen A. (Seattle, WA), Peterson; Mark E. (Seattle, WA), Poysky; Frank T. (Seattle, WA) Assignee(s): The United States of America as represented by the Secretary of Commerce (Washington, DC) Patent Number: 6,165,776 Date filed: March 30, 1994 Abstract: Esculin-free hemolytic Ceftazidime lithium chloride agar (HCLA) as a selective and differential medium specific for the isolation of Listeria monocytogenes. The medium also contains red blood cells. Excerpt(s): The present invention relates to a plating medium as a selective and differential medium for the isolation of Listeria monocytogenes. Listeria monocytogenes is a gram positive, motile, aerobic and facultatively anaerobic bacterium which is ubiquitous in nature. It can cause various diseases in man including meningoencephalitis, low-grade septicemia, infectious mononucleosis-like syndrome, pneumonia, endocarditis, bacterial aortic aneurysm, localized abscesses, papular or pustular cutaneous lesions, conjunctivitis and urethritis. In the past decade, Listeria monocytogenes have been recognized as a major foodborne pathogen. Outbreaks of listeriosis have been linked to a number of contaminated foods such as coleslaw, Mexican-style soft cheese, pasteurized milk and turkey franks. It has been isolated from fresh produce, dairy products, processed meats and seafood products. About 500 people die each year in the United States from Listerial food poisoning; the victims are usually the immunocompromised, pregnant women and neonates. Because of the pernicious effects of this pathogen and its increasing presence in human foods, there is a need for a quick and reliable method for selectively determining the presence of the subject bacterium in a food sample. Web site: http://www.delphion.com/details?pn=US06165776__
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Synthetically derived peptide Inventor(s): Henderson; James T. (Bradenton, FL), Vandenbergh; Peter A. (Sarasota, FL) Assignee(s): Quest International Flavors & Food Ingredients Company, division of (Bridgewater, NJ) Patent Number: 5,861,376 Date filed: March 15, 1993 Abstract: A peptide (QSP-9124) was synthesized corresponding to the 34 residue sequence of a peptide precursor to the bacteriocin LL-2 produced by Lactococcus lactis LLA-2.0. The precursor to native bacteriocin LL-2 is extensively modified by posttranslational mechanisms. Serine and threonine residues are dehydrated and lanthionine and methyl-lanthionine sulfur bridges are formed between cysteine and several of the dehydrated serine and threonine residues. The synthesized peptide has greater anti-bacterial action against Listeria monocytogenes, than did the native, posttranslationally modified protein LL-2. Antibacterial activity against several beneficial food lactobacterial strains was absent, so that the peptide is of value as a food preservative against L. monocytogenes.
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Excerpt(s): The present invention relates to a synthetically derived peptide which is believed to be structurally related to a precursor peptide to a bacteriocin, preferably bacteriocin LL-2 produced by Lactococcus lactis subspecies lactis NRRL-B-18809. The peptide is referred to hereinafter as a "precursor peptide". In particular the present invention relates to a precursor peptide which is active against Listeria monocytogenes and inactive against Lactococcal food fermenting strains so that the precursor peptide is useful in fermented foods. Nisin and LL-2 are bacteriocins which differ from each other by a single amino acid in position 27. Nisin has a histidine (His) residue and LL-2 has an asparagine (Asn) residue. The compounds are characterized by a lanthionine bridge between residues 3 and 7. In the preparation of precursor peptides, one approach is to chemically or thermally inactivate the pathway in the bacterium responsible for protein modification and then hope that the immunity genes also recognize the unmodified "immature" form of the peptide. The precursor peptide gene product would be selflethal to the bacterium unless there is such immunity. This approach is time consuming to complete and may result in the intended modification but without a method for production due to lack of immunity. The applicability of this strategy is also less than certain, since the inactivation of a multi-enzyme pathway would be required, which might be difficult to obtain without losing viability of the bacterium due to a high level of mutations throughout the genome. Also, one or more of the enzymes responsible for post-translational modification of the precursor peptide to produce the bacteriocin might also be essential to cell viability. Further a lack of information exists regarding the generality of side chain dehydration and lanthionine formation in cellular proteins. Also, the bacterial strain might have developed specialized transport mechanisms which serve to keep unmodified bacteriocin inside and modified bacteriocin outside of the cell. To maintain a system of modification enzymes and then allow unmodified bacteriocin precursor peptide to escape the confines of the cell is contradictory. Web site: http://www.delphion.com/details?pn=US05861376__ •
Viral products Inventor(s): Gasson; Michael John (Dereham, GB) Assignee(s): Agricultural & Food Research Council (Norwich, GB) Patent Number: 5,763,251 Date filed: April 20, 1992 Abstract: Bacteriophages of food-contaminating or pathogenic bacteria or the lysins thereof are used to kill such bacteria. Examples include lysins from bacteriophages of Listeria monocytogenes and Clostridium tyrobutyricum.Tests for bacterial contamination can be made specific for specific bacteria by using the appropriate bacteriophage or lysin thereof and determining whether cells are lysed thereby. Excerpt(s): This invention relates to the use of bacterial viruses (bacteriophages) which use bacteria as hosts and produce a bacteriophage lysin responsible for cell-wall degradation and lysis of the host cells. Attempts to use a bacteriophage as an antimicrobial agent have failed to be effective. We have previously used the lysin of the bacteriophage.phi.vML3 of Lactococcus lactis ML3, which is active against all strains of all subspecies of Lactococcus lactis, very weakly affects group D enterococci, but does not have any action on a wide variety of other species tested (Shearman et al (1989) Molecular and General Genetics 218: 214-221), to lyse cheese starter cultures (WO90/00599). WO90/00599 also discloses the use of micro-organisms, transformed to express the.phi.vML3 lysin, to suppress populations of bacteria susceptible to the lysin,
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i.e. the Lactococcus lactis cheese starter culture strains. It is also known to use cheese starter culture bacteria to produce the simple peptide nisin in order to destroy harmful bacteria. Web site: http://www.delphion.com/details?pn=US05763251__
Patent Applications on Listeria monocytogenes 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 Listeria monocytogenes: •
Detection of microbial metabolites Inventor(s): Frampton, Elon W.; (Us-DeKalb, IL), Restaino, Lawrence; (Chicago, IL), Schabert, Gunter; (Goldach, CH) Correspondence: Blank Rome Comisky & Mccauley, Llp; 900 17th Street, N.W., Suite 1000; Washington; DC; 20006; US Patent Application Number: 20020151725 Date filed: December 19, 2001 Abstract: Chromogenic 3-Indoxyl choline phosphate compounds of formula (I): 1wherein R is selected from the group consisting of hydrogen and C.sub.1-4 alkyl, such as methyl, ethyl, propyl and butyl while R.sup.1, R.sup.2, R.sup.3, and R.sup.4 are independently selected from the group consisting of hydrogen, halogen, cyano, nitro, carboxy, amino, amino substituted with one or two C.sub.1-4 alkyl groups, aminomethyl, hydroxy, C.sub.1-4 alkoxy, carboxyalkyl, and sulphonyl. These compounds are capable of being cleaved by lecithinase C leading to products which are calorimetrically detectable. The invention provides safe and sensitive detection of potentially pathogenic bacterial activity of such microbes as Clostridium perfringens, Bacillus cereus, Bacillus anthracis, Pseudomonas aeruginosa, Listeria monocytogenes, Heliobacter pylori, Legionella pneumophila, and others in material which may contain such activity typically including physiological samples, goods for consumption, such as food and beverages, and any other potentially infected objects or articles. Excerpt(s): The present invention relates to novel compounds and substrates having utility for detection of microbial metabolites, i.e. substances secreted or otherwise produced by such microorganisms, by color formation upon contact with such metabolites, as well as to methods of producing such compounds and substrates and of using them for detection and identification of various microorganisms including bacteria. Phospholipase C enzymes are found in a variety of microbes. These enzymes have been associated with the pathogenicity of the microbes to its host. More specifically, it is known that an enzyme named "phosphatidylcholine-specific phospholipase C (also known as phosphatidylcholine cholinephosphohydrolase, or lecithinase C, termed PC-PLC herein for short; enzyme classification EC 3.1.4.3) can be found in a variety of microbes including Clostridium perfringens, Clostridium novyi, Bacillus cereus, Bacillus thuringiensis, Pseudomonas aeruginosa and Staphylococcus aureus (cf. J. G. Songer; Trends in Microbiology 5 (1997), 156) as well as Bacillus
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This has been a common practice outside the United States prior to December 2000.
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anthracis (cf D. M. Guttmann, D. J. Ellar, FEMS Microbiology Letters 188 (2000) 7), Helicobacter pylori (cf. J.-H. Weitkamp et al.; Zentralblatt fur Bakteriologie 280 (1993), 11), Legionella pneumophila (cf. W. B. Baine; Journal of General Microbiology 134 (1988), 489), and Listeria monocytogenes (cf. A. Coffey et al.; Applied and Environmental Microbiology 62 (1996), 1252). Furthermore, PC-PLC has been found in yeasts, e.g. Candida albicans, and in molds, e.g. Aspergillus fumigatus (cf. M. Birch et al.; Infect. Immun. 64 (1996), 751). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Device for detecting bacterial contamination and method of use Inventor(s): Sanders, Mitchell C.; (West Boylston, MA) Correspondence: Hamilton, Brook, Smith & Reynolds, P.C.; 530 Virginia Road; P.O. Box 9133; Concord; MA; 01742-9133; US Patent Application Number: 20030096315 Date filed: May 3, 2001 Abstract: A device and method for detecting the presence or absence of a prokaryotic microorganism are provided, comprising the steps of identifying a protein, such as a microbial-specific protease that characterizes the presence of a specific prokaryotic microbe and thereby provides a marker for that microbe; detecting the protease that is a marker for the presence of a specific prokaryotic microbe by cleaving a substrate when the protease is present; and signaling the presence of that protease when cleavage has occurred. More specifically, the method comprises identifying at least one outer membrane protein or a secreted protein that is unique to a particular microbial pathogen such as for example Listeria monocytogenes and that is substrate specific. Excerpt(s): This application claims priority to U.S. Provisional Application Serial No. 60/201,405, filed May 3, 2000. The present invention relates to the detection of prokaryotic microorganisms. In particular, the present invention relates to a method and a device for detecting the presence or absence of a prokaryotic microorganism or pathogen that contaminants food and food related work areas. Presently, the United States Department of Food Safety and Inspection Services (FSIS) spend over half a billion dollars annually on meat, poultry, and fish inspections for bacterial contaminants. Broadly, the inspections are used to determine the cleanliness of the work area and to detect pathogenic microbes in foodstuffs. Ingestion of pathogenic microbes can result in food poisoning when the microbes are inadvertently packaged into supermarket goods. One example of a pathogenic microbe is Salmonella. Salmonella is a genus of gram-negative bacterium that is a major source of human foodborne illness worldwide. Up to 4 million cases of salmonellosis are reported each year in the United States alone. A number of different serotypes of pathogenic Salmonella are known, the most common of which are S. typhimurium and S. enteriditis. Typically, salmonellosis is treated with antibiotics. However, antibiotic resistant strains of Salmonella are emerging. Listeria and E. coli are also commonly occurring microbial contaminants. Listeria monocytogenes is a gram-positive bacterium that is a common cause of gastroenteritis. Tests for E. coli are performed as an indication of fecal contamination of food and work areas. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Listeria inocua, genome and applications Inventor(s): Glaser, Philippe; (Paris, FR), Kunst, Frederik; (Ivry Sur Seine, FR) Correspondence: Finnegan, Henderson, Farabow, Garrett & Dunner; Llp; 1300 I Street, NW; Washington; DC; 20005; US Patent Application Number: 20040018514 Date filed: July 10, 2003 Abstract: The invention concerns a nucleotide sequence derived from Listeria inocua corresponding to a sequence selected among SEQ ID NO: 1 to SEQ ID NO: 11 and the comparative analysis of said genome with that of Listeria monocytogenes. Excerpt(s): The invention relates to a method for demonstrating the nucleotide sequences specific for the genome of a strain of bacterium of the genus Listeria, in particular of a strain of L. innocua or L. monocytogenes. The present invention also relates to the genomic sequence and to nucleotide sequences encoding polypeptides of Listeria innocua, such as cell envelope polypeptides secreted polypeptides or specific polypeptides or polypeptides involved in metabolism and in the replication process, and also to vectors including said sequences and to cells or animals transformed with these vectors. The invention also relates to the comparison of these nucleotide sequences with those encoding the polypeptides of Listeria monocytogenes, strain EGDe or L. monocytogenes 4b, and also the nucleotide sequences specific to these strains of Listeria. The invention also relates to methods for detecting these nucleic acids or polypeptides and kits for diagnosing contamination with bacteria of the genus Listeria and kits for typing contaminating strains. The invention is also directed toward a method for selecting compounds capable of modulating the bacterial infection engendered by other Listeria, and a method of biosynthesis or biodegradation of molecules of interest using said nucleotide sequences or said polypeptides. Finally, the invention comprises pharmaceutical, in particular vaccine, compositions for preventing and/or treating bacterial infections, in particular infections with Listeria, in particular monocytogenes, and compositions containing antibodies directed against polypeptides specific for L. innocua or for L. monocytogenes, strain EGDe or L. monocytogenes 4b. In Listeria infections, Listeria monocytogenes is the most common and the most dangerous. Listeria monocytogenes is a facultative intracellular pathogen. It is the etiological agent of listeriosis, a food-related infection which poses increasingly great public health problems, with a considerable economic impact for the food industry. Listeriosis is the most lethal food-related infection (approximately 30% mortality). Listeria monocytogenes has the unusual property of being able to cross three barriers: the intestinal barrier, the blood-brain barrier and the placental barrier. Clinical manifestations of listeriosis include meningitis, meningoencephalitis, abortions and septicemia. This infection is opportunistic and affects mainly pregnant women, babies, elderly individuals and immunodepressed individuals, in particular individuals suffering from AIDS. This disease also affects healthy individuals and is responsible for a considerable amount of epidemics due to contaminated food products. Listeria monocytogenes is also important in veterinary terms, with a main risk for members of the sheep family and bovines. Listeria monocytogenes is particularly resistant to stress or to extreme conditions and it is important to search for its presence with care, not only for food safety problems but also for environmental safety problems. Following the discovery of a contamination, it is necessary to type the strain(s) isolated in order to identify the origin of the contamination. Moreover, when the same installation is contaminated by two successive events, it is important to show with certainty whether these are two independent contaminations or whether the same strain is responsible for
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these two events. The most effective method currently used, the pulsed field gel electrophoresis (PFGE) profile after digestion of the chromosomal DNA, is a very laborious method which cannot be carried out systematically. An alternative method, less effective but automated, ribotyping, is very expensive per analysis, which limits its use. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods and compositions for immunotherapy of cancer Inventor(s): Paterson, Yvonne; (Philadelphia, PA) Correspondence: Morgan, Lewis & Bockius Llp; 1701 Market Street; Philadelphia; PA; 19103-2921; US Patent Application Number: 20030202985 Date filed: May 20, 2003 Abstract: Methods and vaccines for inducing an immune response to a tumor associated antigen in a host are provided wherein the vaccine contains either a fusion protein of the tumor associated antigen fused to a truncated form of listeriolysin or a recombinant form of Listeria monocytogenes which grows and spreads and is capable of expressing the tumor associated antigen alone or as a listeriolysin fusion protein. Methods of suppressing formation of tumors and inhibiting growth of tumors in a host via administration of these vaccines are also provided. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 08/336,372, filed Nov. 8, 1994. The invention was made in the course of work supported by the National Cancer Institute. The U.S. Government may have certain rights in this invention. Stimulation of an immune response is dependent upon the presence of antigens recognized as foreign by the host immune system. The discovery of the existence of tumor associated antigens has now raised the possibility of using a host's immune system to intervene in tumor growth. Various mechanisms of harnessing both the humoral and cellular arms of the immune system are currently being explored for cancer immunotherapy. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods and oligonucleotides for the detection of Salmonella sp., E. coli O157:H7, and Listeria monocytogenes Inventor(s): Ellingson, Jay L.E.; (Marshfield, WI), Vevea, Dirk N.; (Hewitt, WI) Correspondence: Zhibin Ren; Quarles & Brady Llp; 1 South Pinckney Street; P O Box 2113; Madison; WI; 53701-2113; US Patent Application Number: 20030022214 Date filed: June 21, 2002 Abstract: A method for detecting a Salmonella species, E. coli O157:H7, or Listeria monocytogenes is disclosed. The method involves amplifying a genomic nucleotide sequence of a corresponding species and detecting the amplification product. Various primers and probes that can be used in the method are also disclosed. In one embodiment, the amplification step of the method is accomplished by real-time PCR
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and the amplification product is detected by fluorescence resonance energy transfer using a pair of labeled polynucleotides. Excerpt(s): This application claims the benefit of U.S. application Serial No. 60/300,199, filed on Jun. 22, 2001, U.S. application Serial No. 60/373,588, filed on Apr. 18, 2002, and U.S. application Serial No. 60/373,589, filed on Apr. 18, 2002. None. Federal and state health and safety standards mandate that industrial food service companies and manufacturing facilities perform routine testing for common bacteria, such as Salmonella species, E. coli O157:H7, and Listeria monocytogenes, that cause food-borne illnesses. As a safety precaution, companies are required to perform testing on each batch or lot of food prior to the food reaching the public. Several methods are currently available for industrial testing of bacteria in the food service industry. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
SEROTYPE-SPECIFIC PROBES FOR LISTERIA MONOCYTOGENES Inventor(s): KATHARIOU, SOPHIA; (HONOLULU, HI), LEI, XIANG-HEI; (SAN FRANCISCO, CA) Correspondence: Flehr Hohbach Test; Albrittton & Herbert; Four Embarcadero Center; Suite 3400; San Francisco; CA; 94111 Patent Application Number: 20010055759 Date filed: July 14, 1998 Abstract: Recombinant nucleic acids comprising region(s) of Listeria monocytogenes genome that are unique to an individual serotype and genomic cluster are provided. Also provided are oligonucleotide probes and primers derived from the recombinant nucleic acid sequences and methods for their use in the detection and identification serovar 4 and genomic cluster IIB strains. Excerpt(s): The present invention relates to the identification and characterization of novel DNA sequences that are specific to Listeria monocytogenes strains that are commonly associated with human disease and provides improved oligonucleotides and methods for their use in the detection and typing of these strains. Listeria monocytogenes, a bacterium, is the causative agent of listeriosis, a serious disease of humans and animals that can be transmitted by means of contaminated food. Newborns, the elderly, and immunocompromised individuals are especially prone to infection. Listeria are commonly found in the environment and, unlike most other human pathogens, are capable of growth at refrigeration temperatures, often leading to problematic contamination of cold-stored foods. Such foods, especially dairy products, have been implicated in numerous cases of sporadic listeriosis as well as several common-source epidemics of the disease. Even though numerous serotypes of L. monocytogenes have been identified with the antigenic scheme of Seeliger and Hohne (Methods Microbiol. 13:31-49 (1979)), three serotypes (1/2a, 1/2b, and 4b) account for the vast majority of clinical isolates. Furthermore, strains of serotype 4b have been implicated in a large fraction (ca. 40%) of sporadic listeriosis cases and virtually all common-source outbreaks reported in Europe and North America during the past 20 years (Schuchat et al. 1991. Clin. Microbiol. Rev. 4:169-183). Pulsed-field fingerprinting of chromosomal DNA has revealed that serotypes 4b, 4d, and 4e strains constitute one genomic subdivision (cluster IIB) (Brosh et al. 1994. Appl. Environ. Microbiol. 60:25842592). From the perspective of human disease, serotype 4b strains are the major component of this genomic cluster because serotype 4d and 4e strains are isolated only
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rarely from foods and virtually never from patients (Farber et al., 1991. Microbiol. Rev. 55:476-511). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with Listeria monocytogenes, 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 “Listeria monocytogenes” (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 Listeria monocytogenes. You can also use this procedure to view pending patent applications concerning Listeria monocytogenes. 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 LISTERIA MONOCYTOGENES Overview This chapter provides bibliographic book references relating to Listeria monocytogenes. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on Listeria monocytogenes 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: 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 “Listeria monocytogenes” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “Listeria monocytogenes” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “Listeria monocytogenes” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Risk Assessment of Listeria monocytogenes in Ready-to-Eat Foods: Technical Report by World Health Organization; ISBN: 9241562625; http://www.amazon.com/exec/obidos/ASIN/9241562625/icongroupinterna
Chapters on Listeria monocytogenes In order to find chapters that specifically relate to Listeria monocytogenes, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and Listeria monocytogenes 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.”
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Type “Listeria monocytogenes” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on Listeria monocytogenes: •
Food-Related Illnesses and Allergies Source: in Townsend, C.E. and Roth, R.A. Nutrition and Diet Therapy. 7th ed. Albany, NY: Delmar Publishers. 1999. 171-187 p. Contact: Available from Delmar Publishers. 3 Columbia Circle, Albany, NY 12212. (800) 865-5840. E-mail:
[email protected]. PRICE: $44.95 plus shipping and handling. ISBN: 0766802965. Summary: This chapter on food related illnesses and allergies is from an undergraduate textbook on nutrition and diet therapy. The chapter identifies the diseases caused by contaminated food, along with their signs and the means by which they are spread; lists the signs of food contamination; reviews precautions for protecting food from contamination; and covers allergies and elimination diets and their uses. Foodborne illnesses covered include Campylobacter jejuni, Clostridium botulinum, Clostridium perfringens, Cyclospora, Escherichia coli (O157:H7), Listeria monocytogenes, Salmonella, Shigella, and Staphylococcus aureas. The authors stress that infection or poisoning traced to food is usually caused by human ignorance or carelessness. Food should not be prepared by anyone who has or carries a contagious disease. All fresh fruits and vegetables should be washed before being eaten. Meats, poultry, fish, eggs, and dairy products should be refrigerated. Food should be covered to prevent contamination by dust, insects, or animals. Food allergies can cause many different and unpleasant symptoms, and elimination diets are used to determine their causes. Some of the most common food allergens are milk, chocolate, eggs, tomatoes, fish, citrus fruit, legumes, strawberries, and wheat. The chapter includes lists of key terms to learn, recommended discussion topics, and suggested supplemental activities, and a section of review questions so readers can test their comprehension of the material. Two illustrative case studies are appended. 1 figure. 4 tables.
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Safe Kitchen Source: in Duyff, R.L. American Dietetic Association's Complete Food and Nutrition Guide. Minneapolis, MN: Chronimed Publishing. 1996. p. 299-322. Contact: Available from Chronimed Publishing. P.O. Box 59032, Minneapolis, MN 55459. (800) 848-2793 or (612) 541-0239. Fax (800) 395-3344 or (612) 541-0210. PRICE: $29.95; bulk orders available. ISBN: 1565610989. Summary: This chapter on food safety is from a food and nutrition guide that focuses on a healthful diet for all stages of life. Foodborne illness, sometimes called food poisoning, comes from eating contaminated food. Because symptoms vary, from fatigue, chills, a mild fever, dizziness, headaches, an upset stomach, and diarrhea to dehydration, severe cramps, vision problems, and even death, diagnosing foodborne illness is difficult. While many reported cases are caused by food prepared outside the home, small outbreaks in home settings are considered to be far more common. Also, different people react differently to the same contaminated food. The reaction depends on the type of bacteria or toxin, how extensively the food was contaminated, how much food was eaten, and the person's susceptibility to the bacteria. Topics include bacteria that cause foodborne illness, including salmonella, staph, clostridium perfringens, clostridium botulinum, E. coli, and listeria monocytogenes; illnesses related to parasites and viruses, including trichinosis, toxoplasmosis, and hepatitis A; when to consult with a health care provider regarding a possible foodborne illness; common food safety
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mistakes; storage tips for cupboards, refrigerator, and freezer storage; safe food preparation and serving; microwave safety tips; picnicking and safety; and preventing injuries in the kitchen. The chapter concludes with a self assessment questionnaire with which readers can determine their level of food safety knowledge. The chapter includes numerous charts and sidebars with fun facts, meat and fish target temperatures, strategies for how to avoid choking and how to help someone who is choking, and recommended storage temperatures. •
Small Intestine: Infections with Common Bacterial and Viral Pathogens Source: in Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 1530-1560. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-6423. Fax: (301) 223-2400. Website: www.lww.com. PRICE: $289.00. ISBN: 781728614. Summary: This chapter on infections of the small intestine is from a lengthy, twovolume textbook that integrates the various demands of science, technology, expanding information, good judgment, and common sense into the diagnosis and management of gastrointestinal patients. In this chapter, the authors focus on the major bacterial and viral pathogens that infect the small intestine. Whether by toxin-mediated effects or direct destruction of intestinal epithelial cells, these microbial pathogens have devised ways to disrupt the normal fluid handling capabilities of the intestinal tract and cause diarrhea. In general, the diarrhea caused by infection with a small bowel pathogen is characterized by high-volume, less frequent bowel movements, whereas lower-volume and more frequent bowel movements are associated with colonic diarrhea. Topics covered include food poisoning and common source outbreaks, traveler's diarrhea, bacterial infection, viral pathogens, and therapeutic considerations. Specific organisms discussed include Clostridium perfringens, Listeria monocytogenes, Escherichia coli, Salmonella, Yersinia, Vibrio (including Vibrio cholera), Aeromonas, Plesiomonas, Edwardsiella, rotavirus, Norwalk and Norwalk-like caliciviruses, astrovirus, and enteric adenovirus. Treatment options discussed include oral rehydration therapy (ORT), antimicrobial therapy, antidiarrheal drugs, and enteric vaccines. 5 tables. 368 references.
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CHAPTER 7. PERIODICALS AND NEWS ON LISTERIA MONOCYTOGENES Overview In this chapter, we suggest a number of news sources and present various periodicals that cover Listeria monocytogenes.
News Services and Press Releases One of the simplest ways of tracking press releases on Listeria monocytogenes 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 “Listeria monocytogenes” (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 Listeria monocytogenes. 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 “Listeria monocytogenes” (or synonyms). The following was recently listed in this archive for Listeria monocytogenes: •
Hyperattenuated Listeria monocytogenes effectively presents HIV antigens Source: Reuters Industry Breifing Date: November 02, 2000
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The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “Listeria monocytogenes” (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 “Listeria monocytogenes” (or synonyms). If you know the name of a company that is relevant to Listeria monocytogenes, 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 “Listeria monocytogenes” (or synonyms).
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Academic Periodicals covering Listeria monocytogenes Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to Listeria monocytogenes. In addition to these sources, you can search for articles covering Listeria monocytogenes 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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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
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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
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
10
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.11 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:12 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
11
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 12 See http://www.nlm.nih.gov/databases/databases.html.
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Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway13 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “Listeria monocytogenes” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 9865 22 10 37 41 9975
HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.17 Simply search by “Listeria monocytogenes” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
13
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
14
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17
The HSTAT URL is http://hstat.nlm.nih.gov/.
Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.
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Coffee Break: Tutorials for Biologists18 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.19 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.20 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
18 Adapted 19
from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 20 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on Listeria monocytogenes 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 Listeria monocytogenes. 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 Listeria monocytogenes. 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 “Listeria monocytogenes”:
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E. Coli Infections http://www.nlm.nih.gov/medlineplus/ecoliinfections.html Food Contamination and Poisoning http://www.nlm.nih.gov/medlineplus/foodcontaminationandpoisoning.html Food Safety http://www.nlm.nih.gov/medlineplus/foodsafety.html Gastroenteritis http://www.nlm.nih.gov/medlineplus/gastroenteritis.html Listeria Infections http://www.nlm.nih.gov/medlineplus/listeriainfections.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 Listeria monocytogenes. 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: •
Safe Eating: A Guide to Preventing Foodborne Illness Source: Chicago, IL: American Dietetic Association. 1997. 12 p. Contact: Available from American Dietetic Association. 216 West Jackson Boulevard, Chicago, IL 60606-6995. (312) 899-0040. Fax (312) 899-4899. PRICE: $5.00 for members, $6.25 for nonmembers for pack of 25. Summary: Foodborne illness, sometimes called food poisoning, results from eating contaminated foods. When food is not handled properly during shopping, storage, preparation, or serving, microorganisms that cause foodborne illness can contaminate it. These microorganisms include bacteria, viruses, parasites, and molds. This brochure summarizes food safety and storage advice to help consumers maintain the freshness and quality of foods that they purchase. Topics include bacteria that cause foodborne illness, including salmonella, escherichia coli, listeria monocytogenes, and clostridium botulinum; tips for safe shopping; refrigerator, freezer, and pantry storage; safe food preparation; recommendations for how long to keep various foods; strategies for safe cooking and serving of meat, poultry, seafood, eggs, and hot foods; when to consult a health care provider regarding a foodborne illness; and the role of registered dietitians in preventing foodborne illness and supporting food safety. One chart illustrates the safe and dangerous temperatures for handling food. 1 figure. 2 tables. (AA-M).
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The NIH Search Utility The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to Listeria monocytogenes. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMDHealth: http://my.webmd.com/health_topics
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to Listeria monocytogenes. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with Listeria monocytogenes. 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 Listeria monocytogenes. 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.
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The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “Listeria monocytogenes” (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 “Listeria monocytogenes”. 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 “Listeria monocytogenes” (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 “Listeria monocytogenes” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.21
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
21
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)22: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
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California: Gateway Health Library (Sutter Gould Medical Foundation)
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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
22
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
•
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/
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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
•
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
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Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
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Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
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Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
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Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
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Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
Finding Medical Libraries
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
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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
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On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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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).
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
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MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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LISTERIA MONOCYTOGENES DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 1-phosphate: A drug that halts cell suicide in human white blood cells. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Cramps: Abdominal pain due to spasmodic contractions of the bowel. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Ablate: In surgery, is to remove. [NIH] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Abscess: A localized, circumscribed collection of pus. [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] Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acetylgalactosamine: The N-acetyl derivative of galactosamine. [NIH] Acetylglucosamine: The N-acetyl derivative of glucosamine. [NIH] Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH]
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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] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] 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] 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] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [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. [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
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preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]
Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allografts: A graft of tissue obtained from the body of another animal of the same species but with genotype differing from that of the recipient; tissue graft from a donor of one genotype to a host of another genotype with host and donor being members of the same species. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric
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acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amnion: The extraembryonic membrane which contains the embryo and amniotic fluid. [NIH]
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] Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Anaemia: A reduction below normal in the number of erythrocytes per cu. mm., in the quantity of haemoglobin, or in the volume of packed red cells per 100 ml. of blood which 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] 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] 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] Anaplasia: Loss of structural differentiation and useful function of neoplastic cells. [NIH] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans.
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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] 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] Anthrax: An acute bacterial infection caused by ingestion of bacillus organisms. Carnivores may become infected from ingestion of infected carcasses. It is transmitted to humans by contact with infected animals or contaminated animal products. The most common form in humans is cutaneous anthrax. [NIH] Anthropogenic: Of human origin or influence. [NIH] Antiallergic: Counteracting allergy or allergic conditions. [EU] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody-Dependent Cell Cytotoxicity: The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IgG whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [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
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immune system. This is an important part of an immune response. [NIH] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aortic Aneurysm: Aneurysm of the aorta. [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] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Aqueous: Having to do with water. [NIH] Archaea: One of the three domains of life (the others being bacteria and Eucarya), formerly called Archaebacteria under the taxon Bacteria, but now considered separate and distinct. They are characterized by: 1) the presence of characteristic tRNAs and ribosomal RNAs; 2) the absence of peptidoglycan cell walls; 3) the presence of ether-linked lipids built from branched-chain subunits; and 4) their occurrence in unusual habitats. While archaea resemble bacteria in morphology and genomic organization, they resemble eukarya in their method of genomic replication. The domain contains at least three kingdoms: crenarchaeota, euryarchaeota, and korarchaeota. [NIH] Arenavirus: The only genus in the family Arenaviridae. It contains two groups LCM-Lassa complex viruses and Tacaribe complex viruses, which are distinguished by antigenic relationships and geographic distribution. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU]
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Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ascites: Accumulation or retention of free fluid within the peritoneal cavity. [NIH] Aseptic: Free from infection or septic material; sterile. [EU] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] 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] 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] Atresia: Lack of a normal opening from the esophagus, intestines, or anus. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Azithromycin: A semi-synthetic macrolide antibiotic structurally related to erythromycin. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis. [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] Bacteraemia: The presence of bacteria in the blood. [EU] 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]
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Bacterial Proteins: Proteins found in any species of bacterium. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriocins: Substances elaborated by specific strains of bacteria that are lethal against other strains of the same or related species. They are protein or lipopolysaccharide-protein complexes used in taxonomy studies of bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriophage lambda: A temperate inducible phage and type species of the genus lambdalike Phages, in the family Siphoviridae. Its natural host is E. coli K12. Its virion contains linear double-stranded DNA, except for 12 complementary bases at the 5'-termini of the polynucleotide chains. The DNA circularizes on infection. [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] 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] Beer: An alcoholic beverage usually made from malted cereal grain (as barley), flavored with hops, and brewed by slow fermentation. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Benzene: Toxic, volatile, flammable liquid hydrocarbon biproduct of coal distillation. It is used as an industrial solvent in paints, varnishes, lacquer thinners, gasoline, etc. Benzene causes central nervous system damage acutely and bone marrow damage chronically and is carcinogenic. It was formerly used as parasiticide. [NIH] Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to glycine in the liver and excreted as hippuric acid. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [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] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU]
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Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biodegradation: The series of processes by which living organisms degrade pollutant chemicals, organic wastes, pesticides, and implantable materials. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biological Warfare: Warfare involving the use of living organisms or their products as disease etiologic agents against people, animals, or plants. [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] Bioterrorism: The use of biological agents in terrorism. This includes the malevolent use of bacteria, viruses, or toxins against people, animals, or plants. [NIH] Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blotting and transferred to strips of nitrocellulose paper. The blots are then detected by radiolabeled antibody probes. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and
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is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] 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] Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Broad-spectrum: Effective against a wide range of microorganisms; said of an antibiotic. [EU] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Cancer vaccine: A vaccine designed to prevent or treat cancer. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capping: A 7-methyl guanosine cap attached to the 5'-end of eucaryotic mRNAs by a phosphodiester linkage. The cap is believed to increase the stability of the message, since most nucleases require a 5'-3'or 3'-5'bond in order to cleave the RNA. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the
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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] Carboxy: Cannabinoid. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogens: Substances that increase the risk of neoplasms in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. [NIH] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovirus: A genus of the family Picornaviridae causing encephalitis and myocarditis in rodents. Encephalomyocarditis virus is the type species. [NIH] Carnitine: Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] 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] Catechols: A group of 1,2-benzenediols that contain the general formula R-C6H5O2. [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] 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]
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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 Movement: The movement of cells from one location to another. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [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] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] 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] 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
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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] Chimeras: Organism that contains a mixture of genetically different cells. [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] 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] Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. [NIH] Chorioamnionitis: An inflammatory process involving the chorion, its fetal blood vessels, the umbilical cord, and the amnion by extension of the inflammation, as the amnion itself has no blood supply. This inflammatory process is potentially fatal to mother and fetus. [NIH]
Chorion: The outermost extraembryonic membrane. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Ciprofloxacin: A carboxyfluoroquinoline antimicrobial agent that is effective against a wide range of microorganisms. It has been successfully and safely used in the treatment of resistant respiratory, skin, bone, joint, gastrointestinal, urinary, and genital infections. [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] Citric Acid: A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability. [NIH] Citric Acid Cycle: A series of reactions involving oxidation of a two-carbon acetyl unit to carbon dioxide and water with the production of high-energy phosphate bonds by means of
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tricarboxylic acid intermediate. [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] Cleave: A double-stranded cut in DNA with a restriction endonuclease. [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] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Clostridium: A genus of motile or nonmotile gram-positive bacteria of the family Bacillaceae. Many species have been identified with some being pathogenic. They occur in water, soil, and in the intestinal tract of humans and lower animals. [NIH] Clostridium botulinum: The etiologic agent of botulism in man, wild ducks, and other waterfowl. It is also responsible for certain forms of forage poisoning in horses and cattle. The bacterium produces a powerful exotoxin that is resistant to proteolytic digestion. [NIH] Clostridium perfringens: The most common etiologic agent of gas gangrene. It is differentiable into several distinct types based on the distribution of twelve different toxins. [NIH]
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] Codon: A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (codon, terminator). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Colchicine: A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (periodic disease). [NIH] Coliphages: Viruses whose host is Escherichia coli. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH]
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Collagen disease: A term previously used to describe chronic diseases of the connective tissue (e.g., rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis), but now is thought to be more appropriate for diseases associated with defects in collagen, which is a component of the connective tissue. [NIH] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] 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
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formation of a viable zygote. [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] Conjunctivitis: Inflammation of the conjunctiva, generally consisting of conjunctival hyperaemia associated with a discharge. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [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 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] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Corticosteroid: Any of the steroids elaborated by the adrenal cortex (excluding the sex hormones of adrenal origin) in response to the release of corticotrophin (adrenocorticotropic hormone) by the pituitary gland, to any of the synthetic equivalents of these steroids, or to angiotensin II. They are divided, according to their predominant biological activity, into
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three major groups: glucocorticoids, chiefly influencing carbohydrate, fat, and protein metabolism; mineralocorticoids, affecting the regulation of electrolyte and water balance; and C19 androgens. Some corticosteroids exhibit both types of activity in varying degrees, and others exert only one type of effect. The corticosteroids are used clinically for hormonal replacement therapy, for suppression of ACTH secretion by the anterior pituitary, as antineoplastic, antiallergic, and anti-inflammatory agents, and to suppress the immune response. Called also adrenocortical hormone and corticoid. [EU] 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] Co-trimoxazole: A combination of two anti-infection drugs, sulfamethoxazole and trimethoprim. It is used to fight bacterial and protozoal infections. [NIH] Cowpox: A mild, eruptive skin disease of milk cows caused by cowpox virus, with lesions occurring principally on the udder and teats. Human infection may occur while milking an infected animal. [NIH] Cowpox Virus: A species of orthopoxvirus that is the etiologic agent of cowpox. It is closely related to but antigenically different from vaccina virus. [NIH] 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] Cryptosporidiosis: Parasitic intestinal infection with severe diarrhea caused by a protozoan, Cryptosporidium. It occurs in both animals and humans. [NIH] Cues: Signals for an action; that specific portion of a perceptual field or pattern of stimuli to which a subject has learned to respond. [NIH] Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as agar or gelatin. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cutaneous: Having to do with the skin. [NIH] 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] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
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]
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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] Cytoplasmic Vesicles: Membrane-limited structures derived from the plasma membrane or various intracellular membranes which function in storage, transport or metabolism. [NIH] Cytosine: A pyrimidine base that is a fundamental unit of nucleic acids. [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] 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] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] 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] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [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]
Dengue Virus: A species of the genus Flavivirus which causes an acute febrile and sometimes hemorrhagic disease in man. Dengue is mosquito-borne and four serotypes are known. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Deoxyribonucleic: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [NIH] Deoxyribonucleotides: A purine or pyrimidine base bonded to a deoxyribose containing a bond to a phosphate group. [NIH] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss
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of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Desensitization: The prevention or reduction of immediate hypersensitivity reactions by administration of graded doses of allergen; called also hyposensitization and immunotherapy. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Diacetyl: Carrier of aroma of butter, vinegar, coffee, and other foods. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diarrhoea: Abnormal frequency and liquidity of faecal discharges. [EU] Diathesis: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the person more than usually susceptible to certain diseases. [EU] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Digoxigenin: 3 beta,12 beta,14-Trihydroxy-5 beta-card-20(22)-enolide. A cardenolide which is the aglycon of digoxin. Can be obtained by hydrolysis of digoxin or from Digitalis orientalis L. and Digitalis lanata Ehrh. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disaccharides: Sugars composed of two monosaccharides linked by glycoside bonds. [NIH] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of
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the environment, or lightheadedness. [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 Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] 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] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] 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]
Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Elastin: The protein that gives flexibility to tissues. [NIH] 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]
Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH]
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Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalitis: Inflammation of the brain due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see encephalitis, viral) are a relatively frequent cause of this condition. [NIH] 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] Encephalomyelitis: A general term indicating inflammation of the brain and spinal cord, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and encephalitis in the literature. [NIH] Encephalomyocarditis Virus: The type species of cardiovirus causing encephalomyelitis and myocarditis in rodents, pigs, and monkeys. Infection in man has been reported with CNS involvement but without myocarditis. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endocrine 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] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endometrium: The layer of tissue that lines the uterus. [NIH] Endophthalmitis: Suppurative inflammation of the tissues of the internal structures of the eye; not all layers of the uvea are affected. Fungi, necrosis of intraocular tumors, and retained intraocular foreign bodies often cause a purulent endophthalmitis. [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-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxins: Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. [NIH] Enterocytes: Terminally differentiated cells comprising the majority of the external surface of the intestinal epithelium (see intestinal mucosa). Unlike goblet cells, they do not produce or secrete mucins, nor do they secrete cryptdins as do the paneth cells. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed. [NIH] Eosinophils: Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidermoid carcinoma: A type of cancer in which the cells are flat and look like fish scales. Also called squamous cell carcinoma. [NIH] 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]
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Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
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] 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]
Esophagitis: Inflammation, acute or chronic, of the esophagus caused by bacteria, chemicals, or trauma. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exotoxin: Toxic substance excreted by living bacterial cells. [NIH] External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an
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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] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
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] Fetal Blood: Blood of the fetus. Exchange of nutrients and waste between the fetal and maternal blood occurs via the placenta. The cord blood is blood contained in the umbilical vessels at the time of delivery. [NIH] Fetal Death: Death of the young developing in utero. [NIH] 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] Fibronectin: An adhesive glycoprotein. One form circulates in plasma, acting as an opsonin; another is a cell-surface protein which mediates cellular adhesive interactions. [NIH] Filtration: The passage of a liquid through a filter, accomplished by gravity, pressure, or vacuum (suction). [EU] Fish Products: Food products manufactured from fish (e.g., fish flour, fish meal). [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so
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that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [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] 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] Fold: A plication or doubling of various parts of the body. [NIH] Food and Beverages: Edible or potable substances. [NIH] Food Chain: The sequence of transfers of matter and energy from organism to organism in the form of food. Food chains intertwine locally into a food web because most organisms consume more than one type of animal or plant. Plants, which convert solar energy to food by photosynthesis, are the primary food source. In a predator chain, a plant-eating animal is eaten by a larger animal. In a parasite chain, a smaller organism consumes part of a larger host and may itself be parasitized by smaller organisms. In a saprophytic chain, microorganisms live on dead organic matter. [NIH] Food Contamination: The presence in food of harmful, unpalatable, or otherwise objectionable foreign substances, e.g. chemicals, microorganisms or diluents, before, during, or after processing or storage. [NIH] Food Handling: Any aspect of the operations in the preparation, transport, storage, packaging, wrapping, exposure for sale, service, or delivery of food. [NIH] Food Services: Functions, equipment, and facilities concerned with the preparation and distribution of ready-to-eat food. [NIH] Foodborne Illness: An acute gastrointestinal infection caused by food that contains harmful bacteria. Symptoms include diarrhea, abdominal pain, fever, and chills. Also called food poisoning. [NIH] Fosfomycin: An antibiotic produced by Streptomyces fradiae. [NIH] Fovea: The central part of the macula that provides the sharpest vision. [NIH] 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]
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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] 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] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma irradiation: A type of radiation therapy that uses gamma radiation. Gamma radiation is a type of high-energy radiation that is different from x-rays. [NIH] Gangrenous: A circumscribed, deep-seated, suppurative inflammation of the subcutaneous tissue of the eyelid discharging pus from several points. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas Gangrene: A severe condition resulting from bacteria invading healthy muscle from adjacent traumatized muscle or soft tissue. The infection originates in a wound contaminated with bacteria of the genus Clostridium. C. perfringens accounts for the majority of cases (over eighty percent), while C. noyvi, C. septicum, and C. histolyticum cause most of the other cases. [NIH] Gastric: Having to do with the stomach. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]
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] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gelsolin: A 90-kD protein produced by macrophages that severs actin filaments and forms a cap on the newly exposed filament end. Gelsolin is activated by calcium ions and participates in the assembly and disassembly of actin, thereby increasing the motility of some cells. [NIH] Gemfibrozil: A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol. These decreases occur primarily in the VLDL fraction and less frequently in the LDL fraction. Gemfibrozil increases HDL subfractions HDL2 and HDL3 as well as apolipoproteins A-I and A-II. Its mechanism of action has not been definitely established. [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]
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Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Expression Profiling: The determination of the pattern of genes expressed i.e., transcribed, under specific circumstances or in a specific cell. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic 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 Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [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] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Geographic Locations: All of the continents and every country situated within, the United States and each of the constituent states arranged by region, Canada and each of its provinces, Australia and each of its states, the major bodies of water and major islands on both hemispheres, and selected major cities. Although the geographic locations are not printed in index medicus as main headings, in indexing they are significant in epidemiologic studies and historical articles and for locating administrative units in education and the delivery of health care. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] 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] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used
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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] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]
Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] 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] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [NIH] Gonadal: Pertaining to a gonad. [EU] 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] Gp120: 120-kD HIV envelope glycoprotein which is involved in the binding of the virus to its membrane receptor, the CD4 molecule, found on the surface of certain cells in the body. [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]
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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-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-Negative Bacteria: Bacteria which lose crystal violet stain but are stained pink when treated by Gram's method. [NIH] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Gram-Positive Bacteria: Bacteria which retain the crystal violet stain when treated by Gram's method. [NIH] Granule: A small pill made from sucrose. [EU] Granulocyte: A type of white blood cell that fights bacterial infection. Neutrophils, eosinophils, and basophils are granulocytes. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanine: One of the four DNA bases. [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] Guinea Pigs: A common name used for the family Caviidae. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research. [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] Haematological: Relating to haematology, that is that branch of medical science which treats of the morphology of the blood and blood-forming tissues. [EU] Haematology: The science of the blood, its nature, functions, and diseases. [NIH] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH]
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Heart attack: A seizure of weak or abnormal functioning of the heart. [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] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemolysins: Substances, usually of biological origin, that destroy blood cells; they may be antibodies or other immunologic factors, toxins, enzymes, etc.; hemotoxins are toxic to blood in general, including the clotting mechanism; hematotoxins may refer to the hematopoietic system. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] 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 clotting in vivo and vitro, in the form of many different salts. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocyte: A liver cell. [NIH] Hepatomegaly: Enlargement of the liver. [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] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic
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decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histocompatibility: The degree of antigenic similarity between the tissues of different individuals, which determines the acceptance or rejection of allografts. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Horseradish Peroxidase: An enzyme isolated from horseradish which is able to act as an antigen. It is frequently used as a histochemical tracer for light and electron microscopy. Its antigenicity has permitted its use as a combined antigen and marker in experimental immunology. [NIH] Host-cell: A cell whose metabolism is used for the growth and reproduction of a virus. [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] Hybridomas: Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure or "monoclonal" antibodies or T-cell products, identical to those produced by the immunologically competent parent, and continually grow and divide as the neoplastic parent. [NIH] Hydration: Combining with water. [NIH] Hydrocephalus: Excessive accumulation of cerebrospinal fluid within the cranium which may be associated with dilation of cerebral ventricles, intracranial hypertension; headache; lethargy; urinary incontinence; and ataxia (and in infants macrocephaly). This condition may be caused by obstruction of cerebrospinal fluid pathways due to neurologic abnormalities, intracranial hemorrhages; central nervous system infections; brain neoplasms; craniocerebral trauma; and other conditions. Impaired resorption of cerebrospinal fluid from the arachnoid villi results in a communicating form of hydrocephalus. Hydrocephalus ex-vacuo refers to ventricular dilation that occurs as a result of brain substance loss from cerebral infarction and other conditions. [NIH] Hydrocortisone: The main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless,
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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 Bonding: A low-energy attractive force between hydrogen and another element. It plays a major role in determining the properties of water, proteins, and other compounds. [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] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hyperaemia: An excess of blood in a part; engorgement. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Iliac Aneurysm: An aneurysm of the common, internal, or external iliac arteries. [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] 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] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunoblotting: Immunologic methods for isolating and quantitatively measuring immunoreactive substances. When used with immune reagents such as monoclonal antibodies, the process is known generically as western blot analysis (blotting, western).
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[NIH]
Immunocompetence: The ability of lymphoid cells to mount a humoral or cellular immune response when challenged by antigen. [NIH] 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] Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction. [NIH]
Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunologic Factors: Biologically active substances whose activities affect or play a role in the functioning of the immune system. [NIH] Immunology: The study of the body's immune system. [NIH] Immunomodulator: New type of drugs mainly using biotechnological methods. Treatment of cancer. [NIH] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive Agents: Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of suppressor T-cell populations or by inhibiting the activation of helper cells. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of interleukins and other cytokines are emerging. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] 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] 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] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH]
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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] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] 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] 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] 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] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inoculum: The spores or tissues of a pathogen that serve to initiate disease in a plant. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH]
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Integrase: An enzyme that inserts DNA into the host genome. It is encoded by the pol gene of retroviruses and also by temperate bacteriophages, the best known being bacteriophage lambda. EC 2.7.7.-. [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] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-12: A heterodimeric cytokine that stimulates the production of interferon gamma from T-cells and natural killer cells, and also induces differentiation of Th1 helper cells. It is an initiator of cell-mediated immunity. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] 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] Intervention Studies: Epidemiologic investigations designed to test a hypothesized causeeffect relation by modifying the supposed causal factor(s) in the study population. [NIH] Intestinal: Having to do with the intestines. [NIH] Intestinal Mucosa: The surface lining of the intestines where the cells absorb nutrients. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracellular Membranes: Membranes of subcellular structures. [NIH]
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Intracranial Hemorrhages: Bleeding within the intracranial cavity, including hemorrhages in the brain and within the cranial epidural, subdural, and subarachnoid spaces. [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] Intraocular: Within the eye. [EU] Intraperitoneal: IP. Within the peritoneal cavity (the area that contains the abdominal organs). [NIH] Intraspecific: Occurring among members of a single species. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Ionophores: Chemical agents that increase the permeability of biological or artificial lipid membranes to specific ions. Most ionophores are relatively small organic molecules that act as mobile carriers within membranes or coalesce to form ion permeable channels across membranes. Many are antibiotics, and many act as uncoupling agents by short-circuiting the proton gradient across mitochondrial membranes. [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 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] 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] Isoprenoid: Molecule that might anchor G protein to the cell membrane as it is hydrophobic. [NIH]
Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Kidney Transplantation: The transference of a kidney from one human or animal to another. [NIH] Killer Cells: Lymphocyte-like effector cells which mediate antibody-dependent cell cytotoxicity. They kill antibody-coated target cells which they bind with their Fc receptors. [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]
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Lactoperoxidase: An enzyme derived from cow's milk. It catalyzes the radioiodination of tyrosine and its derivatives and of peptides containing tyrosine. [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] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]
Lectins: Protein or glycoprotein substances, usually of plant origin, that bind to sugar moieties in cell walls or membranes and thereby change the physiology of the membrane to cause agglutination, mitosis, or other biochemical changes in the cell. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] 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] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligase: An enzyme that repairs single stranded discontinuities in double-stranded DNA molecules in the cell. Purified DNA ligase is used in gene cloning to join DNA molecules together. [NIH] Ligase Chain Reaction: A DNA amplification technique based upon the ligation of oligonucleotide probes. The probes are designed to exactly match two adjacent sequences of a specific target DNA. The chain reaction is repeated in three steps in the presence of excess probe: (1) heat denaturation of double-stranded DNA, (2) annealing of probes to target DNA, and (3) joining of the probes by thermostable DNA ligase. After the reaction is repeated for 20-30 cycles the production of ligated probe is measured. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [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-low-
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density lipoproteins and chylomicrons. [EU] Liposomal: A drug preparation that contains the active drug in very tiny fat particles. This fat-encapsulated drug is absorbed better, and its distribution to the tumor site is improved. [NIH]
Liposome: A spherical particle in an aqueous medium, formed by a lipid bilayer enclosing an aqueous compartment. [EU] Listeria: A genus of bacteria which may be found in the feces of animals and man, on vegetation, and in silage. Its species are parasitic on cold-blooded and warm-blooded animals, including man. [NIH] Listeria Infections: Infections with bacteria of the genus Listeria. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Lithium Chloride: A salt of lithium that has been used experimentally as an immunomodulator. [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 metastases: Cancer that has spread from the original (primary) tumor to the liver. [NIH]
Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Long-Term Care: Care over an extended period, usually for a chronic condition or disability, requiring periodic, intermittent, or continuous care. [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] Luciferase: Any one of several enzymes that catalyze the bioluminescent reaction in certain marine crustaceans, fish, bacteria, and insects. The enzyme is a flavoprotein; it oxidizes luciferins to an electronically excited compound that emits energy in the form of light. The color of light emitted varies with the organism. The firefly enzyme is a valuable reagent for measurement of ATP concentration. (Dorland, 27th ed) EC 1.13.12.-. [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]
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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] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocyte Depletion: Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphocytic Choriomeningitis Virus: The type species of arenavirus, part of the LCMLassa complex viruses, producing an inapparent infection in house and laboratory mice. In humans, infection with LCMV can be inapparent, or can present with an influenza-like illness, a benign aseptic meningitis, or a severe meningoencephalomyelitis. The virus can also infect monkeys, dogs, field mice, guinea pigs, and hamsters, the latter an epidemiologically important host. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lysosome: A sac-like compartment inside a cell that has enzymes that can break down cellular components that need to be destroyed. [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 dead cells, and stimulates the action of other immune system cells. [NIH] Macrophage Colony-Stimulating Factor: A mononuclear phagocyte colony-stimulating factor synthesized by mesenchymal cells. The compound stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series. M-CSF is a disulfide-bonded glycoprotein dimer with a MW of 70 kDa. It binds to a specific high affinity receptor (receptor, macrophage colony-stimulating factor). [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] 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] Mammary: Pertaining to the mamma, or breast. [EU] Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely
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expressed in behaviour. [EU] Mastitis: Inflammatory disease of the breast, or mammary gland. [NIH] Measles Virus: The type species of morbillivirus and the cause of the highly infectious human disease measles, which affects mostly children. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Meat Products: Articles of food which are derived by a process of manufacture from any portion of carcasses of any animal used for food (e.g., head cheese, sausage, scrapple). [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] 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 Fusion: The adherence of cell membranes, intracellular membranes, or artifical membrane models of either to each other or to viruses, parasites, or interstitial particles through a variety of chemical and physical processes. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] 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] Meningoencephalitis: An inflammatory process involving the brain (encephalitis) and meninges (meningitis), most often produced by pathogenic organisms which invade the central nervous system, and occasionally by toxins, autoimmune disorders, and other conditions. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Health: The state wherein the person is well adjusted. [NIH]
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Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesoderm: The middle germ layer of the embryo. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] 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] Micelles: Electrically charged colloidal particles or ions consisting of oriented molecules; aggregates of a number of molecules held loosely together by secondary bonds. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microfilament Proteins: Filaments which are composed primarily of actin and found in the cytoplasmic matrix of almost all cells. They are often associated with microtubules and may play a role in cytoskeletal function and/or mediate movement of the cell or the organelles within the cell. [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] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Milligram: A measure of weight. A milligram is approximately 450,000-times smaller than a pound and 28,000-times smaller than an ounce. [NIH] Mineralocorticoids: A group of corticosteroids primarily associated with the regulation of water and electrolyte balance. This is accomplished through the effect on ion transport in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by plasma volume, serum potassium, and angiotensin II. [NIH] Miscarriage: Spontaneous expulsion of the products of pregnancy before the middle of the
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second trimester. [NIH] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] 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] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocular: Diplopia identified with one eye only; it may be induced with a double prism, or it may occur either as a result of double imagery due to an optical defect in the eye, or as a result of simultaneous use of normal and anomalous retinal correspondence. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monotherapy: A therapy which uses only one drug. [EU] Morbillivirus: A genus of the family Paramyxoviridae (subfamily Paramyxovirinae) where all the virions have hemagglutinin but not neuraminidase activity. All members produce both cytoplasmic and intranuclear inclusion bodies. MEASLES VIRUS is the type species. [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] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] 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]
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Multigene Family: The progeny of a single open-pollinated parent or of a single cross between two individuals. [NIH] Multivalent: Pertaining to a group of 5 or more homologous or partly homologous chromosomes during the zygotene stage of prophase to first metaphasis in meiosis. [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] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [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] Nasal Mucosa: The mucous membrane lining the nasal cavity. [NIH] Natural killer cells: NK cells. A type of white blood cell that contains granules with enzymes that can kill tumor cells or microbial cells. Also called large granular lymphocytes (LGL). [NIH] 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] Neonatal: Pertaining to the first four weeks after birth. [EU] 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] 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] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to
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stimulation of the nervous system. [NIH] Neurologic: Having to do with nerves or the nervous system. [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] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, 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] 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] 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] Nocodazole: Nocodazole is an antineoplastic agent which exerts its effect by depolymerizing microtubules. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nucleates: Bacteria-inducing ice nucleation at warm temperatures (between zero and minus ten degrees C.). [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary
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bases in the two strains. [NIH] Nucleic Acid Probes: Nucleic acid which complements a specific mRNA or DNA molecule, or fragment thereof; used for hybridization studies in order to identify microorganisms and for genetic studies. [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] Nucleoprotein: Chromosomes consist largely of nuclei acids and proteins, joined here as complexes called nucleoproteins. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nurse Practitioners: Nurses who are specially trained to assume an expanded role in providing medical care under the supervision of a physician. [NIH] Oligonucleotide Probes: Synthetic or natural oligonucleotides used in hybridization studies in order to identify and study specific nucleic acid fragments, e.g., DNA segments near or within a specific gene locus or gene. The probe hybridizes with a specific mRNA, if present. Conventional techniques used for testing for the hybridization product include dot blot assays, Southern blot assays, and DNA:RNA hybrid-specific antibody tests. Conventional labels for the probe include the radioisotope labels 32P and 125I and the chemical label biotin. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Oncology: The study of cancer. [NIH] Oocytes: Female germ cells in stages between the prophase of the first maturation division and the completion of the second maturation division. [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] Ophthalmology: A surgical specialty concerned with the structure and function of the eye and the medical and surgical treatment of its defects and diseases. [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 eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Osmolarity: The concentration of osmotically active particles expressed in terms of osmoles of solute per litre of solution. [EU] Osmoles: The standard unit of osmotic pressure. [NIH] Osmosis: Tendency of fluids (e.g., water) to move from the less concentrated to the more
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concentrated side of a semipermeable membrane. [NIH] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] 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] Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Ovulation: The discharge of a secondary oocyte from a ruptured graafian follicle. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Ovum Implantation: Endometrial implantation of the blastocyst. [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]
Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palindrome: In genetic terms a DNA sequence which is the same (or very similar) when complementary strands are read in opposite directions. It has the property of rotational (dyad) symmetry. [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] Papilloma: A benign epithelial neoplasm which may arise from the skin, mucous membranes or glandular ducts. [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] 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]
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Parasitism: A) The mode of life of a parasite; b) The relationship between an organism (parasite) that derives benefits from, and at the expense of, another organism (host). [NIH] Particle: A tiny mass of material. [EU] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide T: N-(N-(N(2)-(N-(N-(N-(N-D-Alanyl L-seryl)-L-threonyl)-L-threonyl) L-threonyl)L-asparaginyl)-L-tyrosyl) L-threonine. Octapeptide sharing sequence homology with HIV envelope protein gp120. It is potentially useful as antiviral agent in AIDS therapy. The core pentapeptide sequence, TTNYT, consisting of amino acids 4-8 in peptide T, is the HIV envelope sequence required for attachment to the CD4 receptor. [NIH] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Pericarditis: Inflammation of the pericardium. [EU] Peripheral blood: Blood circulating throughout the body. [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] 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] Peritonitis: Inflammation of the peritoneum; a condition marked by exudations in the peritoneum of serum, fibrin, cells, and pus. It is attended by abdominal pain and tenderness,
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constipation, vomiting, and moderate fever. [EU] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Phagosomes: Membrane-bound cytoplasmic vesicles formed by invagination of phagocytized material. They fuse with lysosomes to form phagolysosomes in which the hydrolytic enzymes of the lysosome digest the phagocytized material. [NIH] Phallic: Pertaining to the phallus, or penis. [EU] 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] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phosphatidylglycerols: A nitrogen-free class of lipids present in animal and particularly plant tissues and composed of one mole of glycerol and 1 or 2 moles of phosphatidic acid. Members of this group differ from one another in the nature of the fatty acids released on hydrolysis. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipases A: Phosphatide acylhydrolases. Catalyze the hydrolysis of one of the acyl groups of phosphoglycerides or glycerophosphatidates. Phospholipase A1 hydrolyzes the acyl group attached to the 1-position (EC 3.1.1.32) and phospholipase A2 hydrolyzes the acyl group attached to the 2-position (EC 3.1.1.4). [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Physicochemical: Pertaining to physics and chemistry. [EU] 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]
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Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plant Oils: Oils derived from plants or plant products. [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] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plastids: Self-replicating cytoplasmic organelles of plant and algal cells that contain pigments and may synthesize and accumulate various substances. Plastids are used in phylogenetic studies. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH] 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
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the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [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] 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] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Pons: The part of the central nervous system lying between the medulla oblongata and the mesencephalon, ventral to the cerebellum, and consisting of a pars dorsalis and a pars ventralis. [NIH] Population Dynamics: The pattern of any process, or the interrelationship of phenomena, which affects growth or change within a population. [NIH] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiate: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Poultry Products: Food products manufactured from poultry. [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] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] 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] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Presumptive: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [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] Progeny: The offspring produced in any generation. [NIH]
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Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein 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] Proteobacteria: A class of bacteria consisting of the purple bacteria and their relatives which form a branch of the eubacterial tree. This group of predominantly gram-negative bacteria is classified based on homology of equivalent nucleotide sequences of 16S ribosomal RNA or by hybridization of ribosomal RNA or DNA with 16S and 23S ribosomal RNA. [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] Proteome: The protein complement of an organism coded for by its genome. [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
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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] Protozoal: Having to do with the simplest organisms in the animal kingdom. Protozoa are single-cell organisms, such as ameba, and are different from bacteria, which are not members of the animal kingdom. Some protozoa can be seen without a microscope. [NIH] Protozoan: 1. Any individual of the protozoa; protozoon. 2. Of or pertaining to the protozoa; protozoal. [EU] Psoralen: A substance that binds to the DNA in cells and stops them from multiplying. It is being studied in the treatment of graft-versus-host disease and is used in the treatment of psoriasis and vitiligo. [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pustular: Pertaining to or of the nature of a pustule; consisting of pustules (= a visible collection of pus within or beneath the epidermis). [EU] Pyogenic: Producing pus; pyopoietic (= liquid inflammation product made up of cells and a thin fluid called liquor puris). [EU] Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (cytosine, thymine, and
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uracil) and form the basic structure of the barbiturates. [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] Quantitative Structure-Activity Relationship: A quantitative prediction of the biological, ecotoxicological or pharmaceutical activity of a molecule. It is based upon structure and activity information gathered from a series of similar compounds. [NIH] Quaternary: 1. Fourth in order. 2. Containing four elements or groups. [EU] Quercetin: Aglucon of quercetrin, rutin, and other glycosides. It is widely distributed in the plant kingdom, especially in rinds and barks, clover blossoms, and ragweed pollen. [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] Racemic: Optically inactive but resolvable in the way of all racemic compounds. [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] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] 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] Recombinant Proteins: Proteins prepared by recombinant DNA technology. [NIH]
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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] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regional lymph node: In oncology, a lymph node that drains lymph from the region around a tumor. [NIH] Regulon: In eukaryotes, a genetic unit consisting of a noncontiguous group of genes under the control of a single regulator gene. In bacteria, regulons are global regulatory systems involved in the interplay of pleiotropic regulatory domains. These regulatory systems consist of several operons. [NIH] Rehydration: The restoration of water or of fluid content to a body or to substance which has become dehydrated. [EU] Reinfection: A second infection by the same pathogenic agent, or a second infection of an organ such as the kidney by a different pathogenic agent. [EU] 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] 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] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] 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] Resuscitation: The restoration to life or consciousness of one apparently dead; it includes such measures as artificial respiration and cardiac massage. [EU] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines
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with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Ribavirin: 1-beta-D-Ribofuranosyl-1H-1,2,4-triazole-3-carboxamide. A nucleoside antimetabolite antiviral agent that blocks nucleic acid synthesis and is used against both RNA and DNA viruses. [NIH] Ribonucleic acid: RNA. One of the two nucleic acids found in all cells. The other is deoxyribonucleic acid (DNA). Ribonucleic acid transfers genetic information from DNA to proteins produced by the cell. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Ribotyping: Restriction fragment length polymorphism analysis of rRNA genes that is used for differentiating between species or strains. [NIH] Rickettsiae: One of a group of obligate intracellular parasitic microorganisms, once regarded as intermediate in their properties between bacteria and viruses but now classified as bacteria in the order Rickettsiales, which includes 17 genera and 3 families: Rickettsiace. [NIH]
Rod: A reception for vision, located in the retina. [NIH] Rotavirus: A genus of Reoviridae, causing acute gastroenteritis in birds and mammals, including humans. Transmission is horizontal and by environmental contamination. [NIH] Ruminants: A suborder of the order Artiodactyla whose members have the distinguishing feature of a four-chambered stomach. Horns or antlers are usually present, at least in males. [NIH]
Rutin: 3-((6-O-(6-Deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranosyl)oxy)-2-(3,4dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one. Found in many plants, including buckwheat, tobacco, forsythia, hydrangea, pansies, etc. It has been used therapeutically to decrease capillary fragility. [NIH] Saline: A solution of salt and water. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] 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] Salmonellosis: Infection by salmonellae. [NIH] Sanitation: The development and establishment of environmental conditions favorable to the health of the public. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each
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consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Seafood: Marine fish and shellfish used as food or suitable for food. (Webster, 3d ed) shellfish and fish products are more specific types of seafood. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedimentation: The act of causing the deposit of sediment, especially by the use of a centrifugal machine. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Sensor: A device designed to respond to physical stimuli such as temperature, light, magnetism or movement and transmit resulting impulses for interpretation, recording, movement, or operating control. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septic: Produced by or due to decomposition by microorganisms; putrefactive. [EU] Septicaemia: A term originally used to denote a putrefactive process in the body, but now usually referring to infection with pyogenic micro-organisms; a genus of Diptera; the severe type of infection in which the blood stream is invaded by large numbers of the causal. [NIH] Septicemia: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Called also blood poisoning. [EU] Sequence Homology: The degree of similarity between sequences. Studies of amino acid and nucleotide sequences provide useful information about the genetic relatedness of certain species. [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
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synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] 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] 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] 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]
Shunt: A surgically created diversion of fluid (e.g., blood or cerebrospinal fluid) from one area of the body to another area of the body. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Sigma Factor: A protein which is a subunit of RNA polymerase. It effects initiation of specific RNA chains from DNA. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Silage: Fodder converted into succulent feed for livestock through processes of anaerobic fermentation (as in a silo). [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] Sludge: A clump of agglutinated red blood cells. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smallpox: A generalized virus infection with a vesicular rash. [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]
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Sodium Lactate: The sodium salt of racemic or inactive lactic acid. It is a hygroscopic agent used intravenously as a systemic and urinary alkalizer. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of 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] Spasmodic: Of the nature of a spasm. [EU] Spatial disorientation: Loss of orientation in space where person does not know which way is up. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectroscopic: The recognition of elements through their emission spectra. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Spermatogenesis: Process of formation and development of spermatozoa, including spermatocytogenesis and spermiogenesis. [NIH] Spermatozoa: Mature male germ cells that develop in the seminiferous tubules of the testes. Each consists of a head, a body, and a tail that provides propulsion. The head consists mainly of chromatin. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Splenomegaly: Enlargement of the spleen. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Spores: The reproductive elements of lower organisms, such as protozoa, fungi, and cryptogamic plants. [NIH] Sputum: The material expelled from the respiratory passages by coughing or clearing the throat. [NIH] Squamous: Scaly, or platelike. [EU] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells
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resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cells: Flat cells that look like fish scales under a microscope. These cells cover internal and external surfaces of the body. [NIH] Steady state: Dynamic equilibrium. [EU] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [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] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stomatitis: Inflammation of the oral mucosa, due to local or systemic factors which may involve the buccal and labial mucosa, palate, tongue, floor of the mouth, and the gingivae. [EU]
Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptococci: A genus of spherical Gram-positive bacteria occurring in chains or pairs. They are widely distributed in nature, being important pathogens but often found as normal commensals in the mouth, skin, and intestine of humans and other animals. [NIH] Streptococcus: A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stringency: Experimental conditions (e. g. temperature, salt concentration) used during the hybridization of nucleic acids. [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]
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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] 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] 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] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Superoxide Dismutase: An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Supratentorial: Located in the upper part of the brain. [NIH] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]
Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systemic disease: Disease that affects the whole body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Teichoic Acids: Bacterial polysaccharides that are rich in phosphodiester linkages. They are
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the major components of the cell walls and membranes of many bacteria. [NIH] Tenesmus: Straining, especially ineffectual and painful straining at stool or in urination. [EU] Tetracycline: An antibiotic originally produced by Streptomyces viridifaciens, but used mostly in synthetic form. It is an inhibitor of aminoacyl-tRNA binding during protein synthesis. [NIH] Tetracycline Resistance: Nonsusceptibility of a microbe (usually a bacterium) to the action of tetracycline, which binds to the 30S ribosomal subunit and prevents the normal binding of aminoacyl-tRNA. [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] 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] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thymidine: A chemical compound found in DNA. Also used as treatment for mucositis. [NIH]
Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of
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toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] 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] Trichinosis: A disease due to infection with Trichinella spiralis. It is caused by eating undercooked meat, usually pork. [NIH] Trimethoprim Resistance: Nonsusceptibility of a bacterium to the action of trimethoprim. [NIH]
Trophoblast: The outer layer of cells of the blastocyst which works its way into the endometrium during ovum implantation and grows rapidly, later combining with mesoderm. [NIH] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other
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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] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]
Typhimurium: Microbial assay which measures his-his+ reversion by chemicals which cause base substitutions or frameshift mutations in the genome of this organism. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [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] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Umbilical Cord: The flexible structure, giving passage to the umbilical arteries and vein, which connects the embryo or fetus to the placenta. [NIH] Uncoupling Agents: Chemical agents that uncouple oxidation from phosphorylation in the metabolic cycle so that ATP synthesis does not occur. Included here are those ionophores that disrupt electron transfer by short-circuiting the proton gradient across mitochondrial membranes. [NIH] Uracil: An anticancer drug that belongs to the family of drugs called alkylating agents. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] 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] Uvea: The middle coat of the eyeball, consisting of the choroid in the back of the eye and the ciliary body and iris in the front of the eye. [NIH] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccines: Suspensions of killed or attenuated microorganisms (bacteria, viruses, fungi, protozoa, or rickettsiae), antigenic proteins derived from them, or synthetic constructs, administered for the prevention, amelioration, or treatment of infectious and other diseases. [NIH]
Vaccinia: The cutaneous and occasional systemic reactions associated with vaccination using smallpox (variola) vaccine. [NIH] Vaccinia Virus: The type species of Orthopoxvirus, related to cowpox virus, but whose true origin is unknown. It has been used as a live vaccine against smallpox. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of vaccinia virus. [NIH] Vacuole: A fluid-filled cavity within the cytoplasm of a cell. [NIH]
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Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginal: Of or having to do with the vagina, the birth canal. [NIH] Vanadium: Vanadium. A metallic element with the atomic symbol V, atomic number 23, and atomic weight 50.94. It is used in the manufacture of vanadium steel. Prolonged exposure can lead to chronic intoxication caused by absorption usually via the lungs. [NIH] Variola: A generalized virus infection with a vesicular rash. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasodilators: Any nerve or agent which induces dilatation of the blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vegetative: 1. Concerned with growth and with nutrition. 2. Functioning involuntarily or unconsciously, as the vegetative nervous system. 3. Resting; denoting the portion of a cell cycle during which the cell is not involved in replication. 4. Of, pertaining to, or characteristic of plants. [EU] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebral: Of or pertaining to a vertebra. [EU] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] 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] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Vinculin: A cytoskeletal protein associated with cell-cell and cell-matrix interactions. The amino acid sequence of human vinculin has been determined. The protein consists of 1066 amino acid residues and its gene has been assigned to chromosome 10. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] 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
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kill, tumor cells. [NIH] Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached. [NIH] 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] Vulgaris: An affection of the skin, especially of the face, the back and the chest, due to chronic inflammation of the sebaceous glands and the hair follicles. [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] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] 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] Zygote: The fertilized ovum. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
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INDEX 1 1-phosphate, 75, 209 A Abdomen, 209, 218, 228, 243, 246, 255, 266, 267 Abdominal, 4, 116, 125, 209, 233, 234, 244, 254, 255 Abdominal Cramps, 4, 209 Abdominal Pain, 125, 209, 233, 234, 255 Ablate, 21, 209 Abortion, 209, 272 Abscess, 96, 97, 104, 116, 122, 125, 209 Acatalasia, 209, 219 Acceptor, 22, 209, 254 Acetaminophen, 5, 209 Acetylcholine, 209, 221, 252 Acetylgalactosamine, 209, 236 Acetylglucosamine, 89, 209, 236 Acquired Immunodeficiency Syndrome, 134, 209 Actin, 18, 24, 29, 39, 49, 60, 62, 79, 100, 108, 112, 167, 209, 234, 249 Acute renal, 209, 238 Acyl, 80, 140, 210, 256 Adaptability, 210, 219, 220 Adaptation, 13, 63, 64, 71, 84, 95, 102, 160, 210 Adenine, 172, 210, 260 Adenovirus, 183, 210 Adjustment, 210 Adjuvant, 26, 60, 171, 210, 234 Adoptive Transfer, 36, 73, 210 Adrenal Cortex, 210, 224, 239, 259 Adsorption, 87, 169, 210 Adsorptive, 210 Adverse Effect, 210, 265 Aerobic, 173, 210, 250 Aerosol, 14, 210 Affinity, 36, 53, 57, 74, 141, 160, 210, 247, 265 Agar, 76, 84, 173, 210, 225, 241, 257 Airway, 26, 211 Alanine, 6, 8, 17, 30, 82, 211 Albumin, 211, 254 Algorithms, 211, 217 Alkaline, 76, 114, 211, 212, 218 Alkaloid, 211, 222 Alkylating Agents, 211, 271
Allergen, 26, 211, 227 Allografts, 211, 239 Alpha Particles, 211, 261 Alternative medicine, 186, 211 Amino Acid Sequence, 10, 17, 212, 213, 235, 272 Ammonia, 212, 236 Amnion, 212, 221 Ampicillin, 71, 72, 92, 212 Amplification, 9, 62, 66, 86, 131, 178, 212, 245 Amyloid, 46, 212 Anaemia, 98, 212 Anaerobic, 62, 72, 173, 212, 231, 263, 265 Anaesthesia, 212, 242 Anal, 156, 212, 230, 232 Analgesic, 209, 212 Analog, 55, 212 Anaphylatoxins, 212, 223 Anaplasia, 212 Androgens, 210, 212, 225 Anemia, 116, 212, 218 Anesthesia, 129, 211, 212 Aneurysm, 212, 214, 240 Animal model, 9, 16, 25, 32, 42, 51, 53, 54, 55, 212 Anions, 211, 213, 244, 268 Annealing, 213, 245, 257 Anorexia, 213, 234 Anthrax, 9, 17, 38, 51, 213 Anthropogenic, 28, 213 Antiallergic, 213, 225 Antibacterial, 44, 48, 63, 88, 125, 138, 141, 146, 173, 213, 266 Antibiotic, 9, 16, 40, 51, 66, 79, 88, 96, 109, 176, 212, 213, 215, 218, 231, 233, 255, 266, 269 Antibodies, 38, 63, 83, 87, 89, 166, 167, 170, 171, 177, 213, 214, 237, 238, 239, 240, 241, 247, 250, 257 Antibody-Dependent Cell Cytotoxicity, 213, 244 Anticoagulant, 213, 259 Antigen-Antibody Complex, 213, 223 Antigen-presenting cell, 213, 226 Anti-inflammatory, 209, 214, 225, 235, 258 Anti-Inflammatory Agents, 214, 225 Antimetabolite, 214, 263
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Listeria monocytogenes
Antineoplastic, 211, 214, 225, 252 Antipyretic, 209, 214 Antiserum, 171, 214, 215 Antiviral, 12, 45, 214, 243, 255, 263 Anus, 212, 214, 215, 218, 223 Aorta, 214, 272 Aortic Aneurysm, 173, 214 Apolipoproteins, 214, 234, 245 Apoptosis, 19, 152, 214 Applicability, 174, 214 Aqueous, 62, 73, 155, 214, 226, 229, 240, 246 Archaea, 214, 249 Arenavirus, 214, 247 Arginine, 212, 214, 252 Arterial, 214, 240, 259 Arteries, 214, 215, 217, 224, 240, 249, 271 Arterioles, 215, 217, 218 Artery, 212, 214, 215, 217, 224, 260, 272 Ascites, 165, 215 Aseptic, 215, 247, 253, 267 Assay, 18, 57, 62, 69, 73, 80, 83, 89, 92, 111, 132, 147, 148, 156, 170, 171, 215, 240, 271 Astrovirus, 183, 215 Ataxia, 215, 239 Atresia, 95, 215 Attenuated, 6, 15, 23, 24, 27, 33, 41, 46, 53, 60, 73, 85, 122, 167, 215, 271 Attenuation, 40, 45, 65, 215 Atypical, 93, 215, 242 Autoimmune disease, 215 Autoimmunity, 26, 215 Autologous, 32, 215 Avidity, 10, 215 Azithromycin, 92, 98, 116, 215 B Bacillus, 16, 17, 29, 38, 44, 47, 50, 56, 76, 80, 89, 149, 165, 170, 175, 213, 215 Bacteraemia, 98, 215 Bacteremia, 29, 215, 263 Bacterial Infections, 4, 18, 59, 177, 215, 220 Bacterial Physiology, 210, 215 Bacterial Proteins, 11, 40, 43, 216 Bactericidal, 147, 216, 231 Bacteriocins, 160, 169, 174, 216 Bacteriophage, 73, 74, 174, 216, 243, 257, 263, 270, 272 Bacteriophage lambda, 216, 243 Bacterium, 7, 11, 13, 19, 20, 22, 27, 32, 33, 39, 45, 60, 74, 88, 104, 152, 160, 164, 168, 169, 173, 174, 176, 177, 179, 216, 222, 224, 238, 269, 270
Basement Membrane, 216, 231, 245 Basophils, 216, 237, 245 Beer, 166, 216 Benign, 216, 218, 237, 247, 251, 254, 261 Benzene, 216, 219 Benzoic Acid, 140, 151, 216 Beta-pleated, 212, 216 Bile, 64, 95, 216, 234, 239, 246, 267 Bile Acids, 216, 267 Bile Acids and Salts, 216 Binding Sites, 29, 86, 87, 216 Bioavailability, 43, 216 Biochemical, 13, 15, 16, 19, 28, 31, 34, 37, 59, 168, 170, 172, 214, 217, 233, 245 Biodegradation, 177, 217 Biological therapy, 217, 237 Biological Warfare, 6, 217 Biosynthesis, 8, 47, 130, 169, 177, 217, 265 Biotechnology, 61, 90, 103, 186, 193, 217 Bioterrorism, 12, 44, 217 Bladder, 217, 242, 271 Blastocyst, 217, 223, 254, 257, 270 Blood Coagulation, 217, 218, 269 Blood Platelets, 217, 269 Blood pressure, 217, 219, 240, 250, 265 Blood vessel, 217, 219, 220, 229, 230, 238, 247, 249, 265, 266, 267, 269, 272 Blood-Brain Barrier, 177, 217 Blot, 83, 134, 147, 217, 240, 253 Blotting, Western, 217, 240 Body Fluids, 217, 218, 265 Bone Marrow, 38, 58, 153, 216, 217, 235, 237, 240, 247 Bowel, 183, 209, 212, 218, 242, 243, 245, 255, 267 Bowel Movement, 183, 218, 267 Brachytherapy, 218, 243, 244, 261, 273 Bradykinin, 218, 252 Brain Neoplasms, 218, 239 Brain Stem, 124, 218 Broad-spectrum, 16, 212, 218 Buccal, 218, 246, 267 Bypass, 24, 218 C Cadmium, 66, 83, 218 Cadmium Poisoning, 218 Calcium, 29, 39, 120, 139, 218, 221, 223, 234 Cancer vaccine, 7, 32, 218 Capillary, 132, 218, 263, 272 Capping, 29, 218 Carbohydrate, 155, 218, 225, 236, 258
277
Carbon Dioxide, 160, 219, 221, 232, 257, 262 Carboxy, 175, 219 Carcinogenic, 211, 216, 219, 242, 253, 259, 267 Carcinogens, 219, 221 Carcinoma, 41, 45, 219 Cardiac, 219, 229, 230, 251, 262, 267 Cardiovascular, 18, 19, 219 Cardiovascular disease, 18, 219 Cardiovirus, 219, 229 Carnitine, 64, 71, 74, 89, 95, 140, 141, 219 Case report, 96, 104, 115, 117, 122, 126, 219 Catalase, 64, 79, 209, 219 Catechols, 133, 219 Cations, 219, 244 Causal, 90, 134, 219, 230, 243, 264 Cell Adhesion, 219, 243 Cell Cycle, 219, 272 Cell Death, 35, 68, 214, 219, 251 Cell Differentiation, 19, 42, 219 Cell Division, 54, 100, 167, 215, 219, 220, 237, 250, 257, 259, 264 Cell membrane, 44, 166, 220, 244, 248, 256 Cell motility, 19, 39, 49, 220 Cell Movement, 39, 220 Cell proliferation, 27, 159, 220 Cell Size, 220, 233 Cell Survival, 58, 220, 237 Central Nervous System, 24, 209, 211, 216, 218, 220, 236, 237, 239, 248, 258 Central Nervous System Infections, 220, 237, 239 Centrifugation, 13, 220 Cerebral, 81, 82, 122, 215, 217, 218, 220, 230, 239 Cerebral hemispheres, 218, 220 Cerebrospinal, 70, 220, 239, 265 Cerebrospinal fluid, 70, 220, 239, 265 Cerebrovascular, 219, 220 Cerebrum, 220 Cervical, 40, 220 Cervix, 209, 220 Chemokines, 27, 220 Chemotactic Factors, 220, 223 Chemotaxis, 39, 221 Chemotherapy, 9, 40, 60, 91, 92, 98, 103, 109, 116, 123, 221 Chimeras, 30, 221 Chlorine, 87, 155, 221 Cholera, 9, 183, 221, 265, 272
Cholesterol, 37, 216, 221, 224, 234, 245, 248, 267 Choline, 175, 221 Chorioamnionitis, 106, 221 Chorion, 221 Chromatin, 214, 221, 230, 266 Chromium, 43, 221 Chromosomal, 38, 101, 178, 179, 212, 221, 257, 263 Chromosome, 8, 51, 221, 224, 245, 264, 272 Chronic, 14, 18, 57, 96, 98, 113, 118, 221, 223, 231, 242, 246, 260, 268, 272, 273 Ciprofloxacin, 116, 221 CIS, 22, 221, 262 Citric Acid, 47, 221 Citric Acid Cycle, 47, 221 Clathrin, 222, 229 Cleave, 218, 222 Clinical Medicine, 222, 258 Clinical trial, 6, 8, 9, 32, 33, 40, 42, 193, 222, 261 Clone, 87, 222 Cloning, 39, 66, 74, 80, 92, 98, 217, 222, 245 Clostridium, 4, 16, 161, 174, 175, 182, 183, 198, 222, 234 Clostridium botulinum, 16, 182, 198, 222 Clostridium perfringens, 161, 175, 182, 183, 222 Coated Vesicles, 222, 229 Codon, 20, 222, 235 Cofactor, 222, 259, 269 Colchicine, 156, 222 Coliphages, 216, 222 Colitis, 4, 222, 242 Collagen, 58, 211, 216, 222, 223, 232, 234, 239, 257, 259 Collagen disease, 223, 239 Colloidal, 211, 223, 228, 249 Colon, 33, 41, 60, 222, 223, 228, 242, 245 Colorectal, 60, 223 Complement, 57, 60, 212, 213, 223, 235, 243, 247 Complementary and alternative medicine, 145, 158, 223 Complementary medicine, 145, 223 Complementation, 88, 223 Computational Biology, 193, 223 Conception, 21, 209, 223, 232, 267 Conjugated, 36, 57, 149, 171, 216, 224 Conjugation, 79, 224 Conjunctiva, 224, 242 Conjunctivitis, 173, 224
278
Listeria monocytogenes
Connective Tissue, 218, 222, 223, 224, 234, 246, 249, 259, 268 Consciousness, 212, 224, 226, 227, 260, 262 Constipation, 224, 256 Contamination, 4, 53, 72, 86, 117, 124, 148, 164, 165, 166, 174, 176, 177, 179, 182, 224, 263 Contraindications, ii, 224 Coordination, 17, 52, 139, 224 Coronary, 219, 224, 249 Coronary heart disease, 219, 224 Coronary Thrombosis, 224, 249 Cortex, 215, 224, 254 Corticosteroid, 36, 224, 258 Cortisone, 225, 258 Co-trimoxazole, 103, 225 Cowpox, 225, 271 Cowpox Virus, 225, 271 Craniocerebral Trauma, 225, 237, 239 Crossing-over, 225, 262 Cryptosporidiosis, 215, 225 Cues, 19, 225 Culture Media, 211, 225 Cultured cells, 28, 225 Curative, 225, 269 Cutaneous, 173, 213, 225, 244, 246, 271 Cyclic, 74, 225, 237, 252 Cysteine, 19, 31, 146, 173, 220, 225, 268 Cystine, 225 Cytokine, 6, 10, 15, 18, 21, 26, 35, 41, 50, 52, 107, 148, 225, 243 Cytomegalovirus, 4, 36, 225 Cytoplasm, 7, 24, 29, 30, 33, 39, 45, 49, 57, 60, 167, 214, 216, 220, 226, 230, 263, 271 Cytoplasmic Vesicles, 226, 256 Cytosine, 172, 226, 260 Cytoskeleton, 24, 104, 226, 243, 249 Cytotoxic, 8, 15, 21, 45, 46, 62, 63, 77, 118, 156, 167, 226, 241, 261 Cytotoxicity, 102, 226 D Dairy Products, 141, 170, 173, 179, 182, 226 Decidua, 226, 257 Degenerative, 226, 238 Dehydration, 29, 174, 182, 221, 226 Deletion, 42, 53, 85, 100, 214, 226 Delivery of Health Care, 226, 235 Dementia, 209, 226 Denaturation, 226, 245, 257 Dendrites, 226, 252
Dendritic, 21, 26, 32, 58, 63, 72, 77, 112, 125, 160, 226, 248 Dendritic cell, 21, 26, 32, 58, 112, 125, 160, 226 Dengue Virus, 46, 47, 226 Density, 14, 220, 226, 233, 245, 253 Deoxyribonucleic, 171, 226, 263 Deoxyribonucleotides, 226 Depressive Disorder, 226, 246 Desensitization, 227, 241 Deuterium, 227, 240 Diacetyl, 160, 227 Diagnostic procedure, 163, 170, 186, 227 Diarrhea, 4, 29, 182, 183, 225, 227, 231, 233 Diarrhoea, 227, 234 Diathesis, 58, 227 Digestion, 178, 216, 218, 222, 227, 243, 246, 267 Digestive tract, 227, 265, 267 Digoxigenin, 83, 227 Dilation, 218, 227, 239 Diploid, 223, 227, 257 Direct, iii, 30, 34, 41, 62, 68, 71, 73, 88, 123, 170, 183, 222, 227, 246, 262 Disaccharides, 56, 227 Discrete, 24, 29, 227 Discrimination, 64, 67, 70, 71, 101, 227 Disinfectant, 95, 227, 231 Dissection, 19, 25, 227 Dissociation, 210, 227 Distal, 60, 227 Dizziness, 182, 227 Drive, ii, vi, 4, 18, 27, 39, 51, 137, 138, 228 Drug Interactions, 228 Drug Resistance, 4, 228 Drug Tolerance, 228, 269 Duodenum, 216, 228, 267 Dura mater, 228, 248, 254 Dyes, 212, 216, 228, 233 Dysentery, 9, 228 E Effector, 10, 14, 21, 36, 39, 42, 49, 53, 209, 213, 223, 228, 244 Effector cell, 21, 42, 213, 228, 244 Efficacy, 7, 8, 10, 12, 16, 17, 32, 39, 40, 46, 139, 141, 228 Elastic, 228, 268 Elastin, 222, 228, 232 Electrolyte, 225, 228, 249, 258, 265 Electrons, 228, 244, 254, 261 Electrophoresis, 20, 63, 66, 67, 81, 86, 89, 97, 98, 110, 114, 121, 126, 178, 228, 241
279
Emaciation, 209, 228 Embryo, 209, 212, 217, 219, 229, 242, 249, 257, 271 Emulsion, 229, 233 Encapsulated, 7, 77, 139, 167, 229, 246 Encephalitis, 46, 47, 70, 96, 118, 124, 166, 219, 229, 248 Encephalitis, Viral, 229 Encephalomyelitis, 229 Encephalomyocarditis Virus, 19, 229 Endemic, 221, 229, 266 Endocarditis, 94, 105, 109, 126, 173, 229 Endocardium, 229 Endocrine System, 229, 251 Endogenous, 39, 42, 59, 72, 110, 119, 150, 229 Endometrium, 226, 229, 270 Endophthalmitis, 110, 119, 229 Endosomes, 31, 48, 229 Endothelial cell, 58, 113, 149, 152, 217, 229, 269 Endothelium, 230, 252 Endothelium-derived, 230, 252 Endotoxins, 223, 230 Enterocytes, 55, 128, 230 Environmental Health, 130, 192, 194, 230 Enzymatic, 17, 47, 80, 211, 218, 223, 230, 238, 248, 257, 262 Enzyme-Linked Immunosorbent Assay, 86, 128, 230 Eosinophils, 230, 237, 245 Epidemic, 12, 65, 70, 74, 87, 105, 108, 128, 230, 266 Epidemiologic Studies, 230, 235 Epidemiological, 67, 70, 80, 117, 121, 132, 168, 230 Epidermis, 230, 260 Epidermoid carcinoma, 230, 267 Epinephrine, 230, 252, 271 Epithelial, 26, 40, 55, 58, 79, 87, 91, 120, 127, 131, 152, 154, 183, 226, 230, 231, 236, 245, 254 Epithelial Cells, 58, 87, 91, 127, 131, 152, 154, 183, 231, 245 Epithelium, 216, 230, 231, 254 Epitope, 28, 31, 45, 62, 73, 77, 89, 231 Erythrocytes, 212, 218, 231, 262 Erythromycin, 215, 231 Esophagitis, 4, 231 Esophagus, 215, 227, 231, 256, 267 Ethanol, 18, 36, 57, 85, 231, 232 Eukaryotic Cells, 39, 94, 231, 253, 271
Excitation, 231, 233, 252 Excitatory, 231, 236 Exogenous, 8, 40, 59, 71, 133, 210, 229, 231 Exotoxin, 222, 231 External-beam radiation, 231, 244, 261, 273 Extracellular Matrix, 39, 224, 231, 232, 243 Extracellular Matrix Proteins, 39, 231 Extracellular Space, 61, 231, 232 Eye Infections, 210, 232 F Family Planning, 193, 232 Fat, 19, 134, 216, 217, 224, 225, 232, 245, 246, 266, 268 Fatigue, 182, 232 Febrile, 80, 128, 226, 232 Feces, 123, 125, 224, 232, 246, 267 Fermentation, 20, 95, 149, 166, 216, 232, 263, 265 Fetal Blood, 221, 232 Fetal Death, 167, 232 Fetus, 21, 22, 209, 221, 232, 257, 258, 271 Fibroblasts, 58, 232 Fibronectin, 86, 98, 232 Filtration, 13, 232 Fish Products, 232, 264 Fixation, 20, 232 Flagellin, 15, 128, 233 Flow Cytometry, 18, 132, 233 Fluorescence, 34, 69, 76, 84, 179, 233 Fluorescent Dyes, 233 Fold, 15, 43, 60, 233 Food and Beverages, 175, 233 Food Chain, 165, 233 Food Contamination, 3, 4, 182, 198, 233 Food Handling, 5, 233 Food Services, 168, 233 Foodborne Illness, 3, 4, 42, 176, 182, 198, 233 Fosfomycin, 16, 116, 233 Fovea, 233 Frameshift, 233, 234, 271 Frameshift Mutation, 234, 271 Fungi, 61, 224, 229, 232, 234, 249, 266, 271, 273 G Gallbladder, 209, 234 Gamma irradiation, 102, 150, 234 Gangrenous, 234, 265 Gas, 212, 219, 221, 222, 234, 240, 252, 268 Gas Gangrene, 222, 234 Gastric, 219, 234, 239
280
Listeria monocytogenes
Gastrin, 234, 239 Gastroenteritis, 4, 49, 80, 108, 128, 176, 198, 215, 234, 263 Gastrointestinal, 3, 4, 108, 145, 183, 218, 221, 230, 231, 233, 234, 268, 272 Gastrointestinal tract, 231, 234 Gelatin, 225, 234, 236, 269 Gelsolin, 29, 108, 234 Gemfibrozil, 40, 234 Gene Expression, 20, 26, 38, 51, 55, 68, 70, 73, 86, 121, 123, 159, 235 Gene Expression Profiling, 26, 235 Gene Therapy, 57, 95, 210, 235 Genetic Code, 235, 252 Genetic Engineering, 217, 222, 235 Genetic Markers, 164, 235 Genetic testing, 235, 258 Genetics, 23, 27, 41, 45, 51, 101, 112, 174, 224, 235 Genital, 221, 235 Genotype, 129, 211, 235, 256 Geographic Locations, 109, 235 Germ Cells, 235, 253, 254, 266 Gestation, 235, 257 Gland, 21, 58, 210, 225, 235, 246, 248, 254, 257, 264, 267, 269 Glucocorticoid, 235, 239, 258 Glucose, 74, 75, 84, 104, 110, 145, 221, 235, 236, 238, 264 Glucuronic Acid, 236, 238 Glutamate, 22, 47, 236 Glutamic Acid, 9, 236, 252, 259 Glutamine, 47, 236 Glycerol, 236, 256 Glycerophospholipids, 236, 256 Glycine, 66, 74, 76, 82, 86, 89, 140, 172, 211, 216, 236, 252, 265 Glycoprotein, 116, 232, 236, 245, 247, 269, 270 Glycosaminoglycans, 55, 232, 236, 259 Glycoside, 227, 236, 263 Goats, 226, 236 Goblet Cells, 230, 236 Gonadal, 236, 267 Gout, 222, 236 Governing Board, 236, 258 Gp120, 236, 255 Grade, 173, 236 Graft, 127, 211, 237, 241, 260 Graft Rejection, 237, 241 Graft-versus-host disease, 237, 260
Gram-negative, 16, 29, 52, 55, 176, 231, 237, 259, 263, 272 Gram-Negative Bacteria, 55, 237, 259 Gram-Positive Bacteria, 55, 56, 166, 170, 222, 237 Granule, 237, 263 Granulocyte, 114, 237 Growth factors, 21, 237 Guanine, 31, 172, 237, 260 Guanylate Cyclase, 237, 252 Guinea Pigs, 237, 247 H Habitat, 237, 252 Haematological, 111, 237 Haematology, 237 Hair follicles, 237, 273 Half-Life, 19, 237 Haptens, 210, 237 Headache, 4, 237, 239, 242 Heart attack, 219, 238 Hemoglobin, 212, 231, 238, 245 Hemoglobinopathies, 235, 238 Hemolysins, 50, 238 Hemolytic, 4, 34, 51, 68, 75, 111, 116, 173, 238 Hemostasis, 238, 243 Heparin, 55, 238 Hepatic, 141, 211, 238 Hepatitis, 98, 118, 182, 238, 242 Hepatocyte, 81, 238 Hepatomegaly, 238, 242 Heredity, 234, 235, 238 Herpes, 4, 38, 171, 238 Herpes Zoster, 238 Heterodimers, 238, 243 Heterogeneity, 111, 210, 238 Heterotrophic, 234, 238 Histamine, 212, 238, 239 Histidine, 15, 174, 239 Histocompatibility, 46, 239 Homeostasis, 10, 239 Homologous, 38, 50, 51, 75, 76, 122, 142, 225, 235, 239, 251, 264 Hormonal, 225, 239 Hormone, 21, 224, 225, 230, 234, 239, 259, 269 Horseradish Peroxidase, 230, 239 Host-cell, 60, 239 Humoral, 6, 29, 51, 58, 75, 167, 178, 237, 239, 241 Humour, 239 Hybrid, 222, 239, 253
281
Hybridomas, 170, 239 Hydration, 17, 239 Hydrocephalus, 107, 113, 239, 244 Hydrocortisone, 141, 239 Hydrogen, 172, 175, 209, 219, 226, 227, 231, 239, 240, 250, 252, 254, 259, 268 Hydrogen Bonding, 240, 252 Hydrogen Peroxide, 219, 240, 268 Hydrolysis, 168, 227, 240, 256, 258, 259 Hydrophobic, 37, 44, 68, 77, 236, 240, 244, 245 Hydroxylysine, 222, 240 Hydroxyproline, 211, 222, 240 Hyperaemia, 224, 240 Hypersensitivity, 73, 140, 153, 211, 227, 240 Hypertension, 219, 240, 244 Hypothalamic, 36, 240 Hypothalamus, 218, 240, 257 I Iliac Aneurysm, 126, 240 Immune function, 58, 147, 155, 240, 241 Immune Sera, 240 Immune system, 7, 11, 14, 15, 18, 21, 26, 28, 29, 40, 51, 52, 57, 58, 121, 167, 178, 214, 215, 217, 228, 240, 241, 247, 256, 273 Immunization, 6, 15, 26, 27, 37, 42, 44, 45, 73, 77, 160, 210, 240, 241 Immunoassay, 146, 154, 230, 240 Immunoblotting, 86, 128, 240 Immunocompetence, 43, 241 Immunocompromised, 5, 7, 29, 30, 31, 42, 82, 123, 125, 167, 168, 170, 173, 179, 241 Immunodeficiency, 37, 51, 77, 209, 241 Immunodiffusion, 211, 241 Immunoelectrophoresis, 211, 241 Immunogenic, 8, 16, 46, 241 Immunoglobulin, 26, 213, 241, 250 Immunologic, 52, 57, 210, 221, 238, 240, 241, 261 Immunologic Factors, 238, 241 Immunomodulator, 241, 246 Immunosuppression, 18, 141, 241, 247, 253 Immunosuppressive, 57, 235, 241 Immunosuppressive Agents, 241 Immunosuppressive therapy, 241 Immunotherapy, 9, 32, 41, 171, 178, 210, 217, 227, 241 Implant radiation, 241, 243, 244, 261, 273 Implantation, 223, 241, 254 In situ, 38, 43, 72, 241
In vitro, 11, 16, 18, 19, 25, 34, 36, 42, 53, 56, 57, 86, 113, 114, 117, 139, 235, 241, 242, 257, 269 Incision, 242, 244 Incontinence, 239, 242 Incubation, 170, 242 Induction, 6, 13, 14, 18, 22, 40, 43, 45, 53, 55, 72, 77, 78, 86, 112, 212, 242 Infarction, 224, 239, 242, 249 Infectious Mononucleosis, 173, 242 Infertility, 20, 242 Inflammatory bowel disease, 100, 117, 242 Influenza, 6, 12, 15, 24, 46, 47, 242, 247 Ingestion, 4, 58, 72, 73, 176, 213, 218, 242, 257 Inhalation, 6, 43, 210, 242, 257 Initiation, 25, 55, 242, 265 Initiator, 242, 243 Inoculum, 51, 242 Inorganic, 43, 242, 250 Insight, 43, 49, 52, 56, 60, 242 Integrase, 19, 243 Integrins, 58, 243 Interferon, 21, 31, 33, 52, 65, 70, 71, 79, 83, 102, 108, 118, 150, 243 Interferon-alpha, 243 Interleukin-1, 25, 72, 138, 243 Interleukin-12, 138, 243 Interleukin-2, 243 Intermittent, 243, 246, 255 Internal radiation, 243, 244, 261, 273 Interstitial, 218, 232, 243, 244, 248, 273 Intervention Studies, 12, 243 Intestinal, 4, 48, 54, 55, 91, 100, 116, 117, 177, 183, 222, 225, 230, 243 Intestinal Mucosa, 48, 100, 117, 230, 243 Intestine, 24, 183, 216, 218, 231, 243, 245, 267 Intoxication, 243, 272, 273 Intracellular Membranes, 226, 243, 248 Intracranial Hemorrhages, 239, 244 Intracranial Hypertension, 237, 239, 244 Intraocular, 229, 244 Intraperitoneal, 18, 124, 244 Intraspecific, 169, 244 Intravenous, 18, 67, 129, 244 Intrinsic, 52, 210, 216, 244 Invasive, 54, 56, 66, 97, 118, 128, 152, 244 Ionophores, 105, 244, 271 Ions, 44, 227, 228, 234, 240, 244, 249 Irradiation, 5, 244, 273 Irritants, 228, 244
282
Listeria monocytogenes
Isoprenoid, 130, 244 K Kb, 11, 192, 244 Kidney Transplantation, 126, 244 Killer Cells, 36, 244 Kinetic, 17, 244 L Labile, 223, 244 Lactoperoxidase, 72, 78, 138, 245 Laminin, 58, 216, 232, 245 Large Intestine, 227, 243, 245, 262, 265 Latency, 5, 245 Laxative, 211, 245 Lectins, 141, 245 Lesion, 42, 245, 246, 265, 271 Lethal, 3, 63, 82, 85, 128, 169, 174, 177, 216, 245 Lethargy, 239, 245 Leucine, 75, 245 Leukemia, 151, 235, 245 Leukocytes, 58, 216, 218, 220, 221, 230, 243, 245, 271 Life cycle, 13, 234, 245 Ligands, 15, 75, 243, 245 Ligase, 19, 69, 71, 245 Ligase Chain Reaction, 69, 71, 245 Ligation, 245 Linkage, 218, 235, 245 Lipid, 37, 53, 214, 221, 234, 236, 244, 245, 246 Lipopolysaccharide, 78, 113, 216, 237, 245 Lipoprotein, 237, 245 Liposomal, 57, 246 Liposome, 71, 77, 139, 246 Listeria Infections, 168, 198, 246 Lithium, 62, 173, 246 Lithium Chloride, 173, 246 Liver, 58, 60, 115, 209, 211, 216, 219, 225, 229, 232, 234, 236, 238, 246, 258 Liver metastases, 60, 246 Liver Transplantation, 115, 246 Localization, 26, 29, 32, 48, 79, 246 Localized, 19, 33, 173, 209, 229, 232, 242, 245, 246, 254, 257, 271 Locomotion, 18, 246, 257 Long-Term Care, 9, 246 Lucida, 245, 246 Luciferase, 15, 73, 246 Lupus, 246, 268 Lymph, 220, 229, 230, 239, 242, 246, 247, 262 Lymph node, 220, 246, 247, 262
Lymphadenopathy, 242, 246 Lymphatic, 230, 242, 246, 247, 249, 266, 269 Lymphatic system, 246, 247, 266, 269 Lymphocyte, 8, 15, 33, 41, 45, 47, 53, 57, 62, 77, 209, 213, 241, 244, 247, 248 Lymphocyte Count, 209, 247 Lymphocyte Depletion, 241, 247 Lymphocytic, 12, 45, 247 Lymphocytic Choriomeningitis Virus, 12, 45, 247 Lymphoid, 16, 26, 36, 48, 213, 241, 247 Lysosome, 30, 247, 256 Lytic, 64, 74, 247, 265, 272 M Macrophage, 17, 21, 33, 39, 43, 51, 71, 78, 92, 98, 114, 130, 152, 213, 243, 247 Macrophage Colony-Stimulating Factor, 114, 247 Major Histocompatibility Complex, 46, 82, 247 Malignancy, 32, 37, 105, 247, 254 Malignant, 33, 209, 214, 218, 247, 251, 261 Mammary, 21, 58, 247, 248 Manic, 246, 247 Manifest, 58, 247 Mastitis, 86, 166, 248, 265 Measles Virus, 15, 248 Meat, 5, 77, 85, 89, 100, 106, 109, 110, 120, 150, 156, 160, 165, 176, 183, 198, 248, 270 Meat Products, 106, 109, 120, 248 Mediate, 25, 26, 34, 37, 74, 75, 87, 89, 167, 244, 248, 249 Mediator, 75, 113, 243, 248 MEDLINE, 193, 248 Melanin, 248, 256, 271 Melanocytes, 248 Melanoma, 46, 248 Membrane Fusion, 30, 248 Membrane Lipids, 248, 256 Memory, 10, 11, 27, 36, 41, 48, 50, 56, 58, 59, 73, 149, 213, 226, 248 Meninges, 220, 225, 228, 248 Meningoencephalitis, 49, 72, 167, 173, 177, 248 Mental, iv, 5, 192, 194, 226, 227, 232, 248, 260, 264 Mental Health, iv, 5, 192, 194, 248, 260 Mercury, 233, 249 Mesenchymal, 247, 249 Mesoderm, 249, 270 Metabolite, 47, 249
283
Metastasis, 60, 249 Metastatic, 60, 218, 249, 264 Methionine, 59, 249, 268 MI, 166, 207, 249 Micelles, 123, 249 Microbe, 23, 48, 176, 249, 269 Microfilament Proteins, 87, 249 Microorganism, 6, 176, 222, 249, 255, 273 Micro-organism, 120 Micro-organism, 170 Micro-organism, 174 Micro-organism, 249 Micro-organism, 264 Microtubules, 249, 252 Migration, 40, 49, 58, 60, 249 Milligram, 14, 249 Mineralocorticoids, 210, 225, 249 Miscarriage, 166, 249 Mitochondria, 250, 253 Mitosis, 214, 245, 250 Mobility, 111, 250 Modification, 120, 174, 211, 235, 250, 261 Molecule, 14, 38, 39, 47, 49, 59, 213, 216, 223, 227, 228, 230, 231, 236, 238, 240, 244, 250, 252, 253, 254, 257, 259, 261, 270, 272 Monitor, 8, 34, 250, 252 Monoclonal, 56, 81, 83, 89, 160, 170, 239, 240, 244, 250, 261, 273 Monoclonal antibodies, 56, 81, 170, 240, 250 Monocular, 39, 250 Monocyte, 57, 108, 113, 117, 213, 247, 250 Mononuclear, 21, 39, 141, 242, 247, 250, 271 Monotherapy, 102, 250 Morbillivirus, 248, 250 Morphological, 42, 81, 229, 248, 250 Morphology, 42, 65, 72, 93, 103, 110, 151, 214, 237, 250 Motility, 19, 24, 29, 39, 49, 60, 64, 93, 100, 108, 164, 167, 234, 250 Mucins, 230, 236, 250 Mucosa, 15, 49, 246, 250, 267 Mucositis, 250, 269 Mucus, 228, 250 Multigene Family, 76, 251 Multivalent, 215, 251 Mutagenesis, 30, 76, 81, 251 Mutagens, 234, 251 Myalgia, 242, 251 Myeloid Cells, 53, 251
Myeloma, 56, 170, 251 Myocarditis, 219, 229, 251 Myocardium, 249, 251 N Nasal Mucosa, 242, 251 Natural killer cells, 36, 58, 98, 243, 251 Nausea, 234, 251 NCI, 1, 191, 221, 251 Necrosis, 214, 229, 242, 249, 251 Neonatal, 16, 49, 106, 123, 149, 251 Neoplasm, 251, 254 Neoplastic, 212, 239, 251 Nerve, 212, 215, 226, 248, 251, 254, 267, 270, 272 Nervous System, 220, 248, 251, 252, 255, 272 Networks, 39, 251 Neural, 81, 139, 212, 239, 251 Neuroendocrine, 21, 251 Neurologic, 239, 252 Neuronal, 19, 252 Neurons, 226, 231, 252 Neurotransmitter, 209, 211, 218, 236, 239, 252, 268 Neutrons, 211, 244, 252, 261 Neutrophil, 37, 39, 43, 85, 252 Niche, 22, 49, 252 Nitric Oxide, 34, 83, 114, 140, 149, 252 Nitrogen, 20, 34, 47, 130, 211, 212, 231, 232, 236, 252, 256, 270 Nocodazole, 156, 252 Nuclear, 224, 228, 231, 251, 252 Nucleates, 19, 252 Nuclei, 211, 224, 228, 235, 250, 252, 253, 259 Nucleic acid, 57, 62, 164, 166, 168, 169, 171, 177, 179, 226, 235, 251, 252, 253, 260, 263, 267 Nucleic Acid Hybridization, 168, 169, 252 Nucleic Acid Probes, 171, 253 Nucleolus, 253, 263 Nucleoprotein, 45, 253 Nucleus, 57, 214, 215, 216, 221, 225, 226, 227, 230, 231, 250, 252, 253, 259, 267 Nurse Practitioners, 4, 253 O Oligonucleotide Probes, 179, 245, 253 Oncogenic, 243, 253 Oncology, 253, 262 Oocytes, 39, 253 Opacity, 226, 253 Open Reading Frames, 50, 253
284
Listeria monocytogenes
Operon, 76, 82, 253, 262 Ophthalmology, 119, 232, 253 Opportunistic Infections, 209, 253 Organ Culture, 253, 269 Organelles, 34, 220, 222, 226, 248, 249, 253, 257 Osmolarity, 81, 140, 253 Osmoles, 253 Osmosis, 253, 254 Osmotic, 64, 82, 85, 211, 253, 254 Osteomyelitis, 104, 254 Ovalbumin, 56, 254 Ovaries, 32, 254 Ovary, 21, 254, 257 Ovulation, 21, 254 Ovum, 226, 235, 245, 254, 259, 270, 273 Ovum Implantation, 254, 270 Oxidation, 19, 209, 221, 225, 254, 271 P Pachymeningitis, 248, 254 Palate, 254, 267 Palindrome, 131, 254 Palliative, 254, 269 Pancreas, 209, 254 Pancreatic, 219, 254 Papilloma, 9, 40, 131, 254 Papillomavirus, 45, 254 Parasite, 31, 48, 233, 254, 255 Parasitic, 225, 228, 246, 254, 263 Parasitism, 167, 255 Particle, 246, 255, 270 Patch, 18, 255 Pathogenesis, 8, 12, 18, 25, 29, 30, 44, 49, 51, 54, 55, 66, 80, 85, 123, 129, 130, 138, 154, 255 Pathologic, 26, 214, 224, 240, 255, 260, 262 Pathologic Processes, 214, 255 Patient Education, 198, 202, 204, 207, 255 Pelvis, 209, 254, 255, 271 Penicillin, 82, 212, 255 Peptide, 7, 11, 15, 26, 27, 43, 46, 58, 59, 82, 88, 160, 173, 174, 175, 211, 255, 258, 259 Peptide T, 174, 255 Perforation, 30, 34, 255 Pericarditis, 106, 255 Peripheral blood, 132, 243, 255 Peripheral Nervous System, 252, 255, 268 Peritoneal, 18, 71, 98, 118, 133, 139, 215, 244, 255 Peritoneal Cavity, 215, 244, 255 Peritoneal Dialysis, 118, 133, 255 Peritoneum, 255
Peritonitis, 118, 133, 255 Pesticides, 217, 256 Phagocyte, 141, 247, 256 Phagocytosis, 14, 30, 31, 33, 63, 103, 256 Phagosomes, 30, 33, 48, 102, 256 Phallic, 232, 256 Pharmacologic, 212, 237, 256, 269 Pharynx, 242, 256 Phenotype, 21, 50, 61, 81, 223, 256 Phenylalanine, 256, 271 Phosphatidylglycerols, 80, 140, 256 Phospholipases, 30, 37, 88, 94, 256 Phospholipases A, 94, 256 Phospholipids, 123, 232, 245, 248, 256 Phosphorus, 218, 256 Phosphorylated, 22, 256 Phosphorylation, 22, 30, 73, 256, 271 Physicochemical, 43, 256 Physiologic, 217, 237, 256, 261, 262 Physiology, 30, 34, 39, 145, 245, 256 Pigment, 248, 257 Pilot study, 8, 257 Pituitary Gland, 224, 257 Placenta, 21, 24, 232, 257, 259, 271 Plant Oils, 140, 151, 257 Plants, 72, 80, 211, 217, 219, 221, 233, 235, 236, 250, 257, 263, 266, 270, 272 Plaque, 79, 82, 257 Plasma, 19, 22, 39, 211, 213, 220, 226, 232, 234, 238, 249, 251, 257 Plasma cells, 213, 251, 257 Plasmid, 16, 37, 66, 104, 109, 169, 257, 272 Plastids, 253, 257 Platelet Aggregation, 212, 252, 257 Platelets, 19, 33, 58, 153, 252, 257, 269 Pneumonia, 6, 125, 173, 224, 257 Poisoning, 3, 4, 157, 173, 176, 182, 183, 198, 218, 222, 233, 234, 243, 249, 251, 257, 263, 264 Pollen, 257, 261 Polymerase, 19, 61, 63, 69, 70, 85, 90, 100, 131, 147, 148, 156, 257, 262, 265 Polymerase Chain Reaction, 61, 63, 69, 70, 85, 90, 100, 131, 147, 148, 156, 257 Polymorphic, 11, 66, 70, 90, 131, 134, 258 Polymorphism, 63, 65, 70, 258, 263 Polypeptide, 7, 15, 19, 21, 66, 79, 211, 212, 222, 258, 259, 273 Polysaccharide, 213, 258, 259 Pons, 218, 258 Population Dynamics, 49, 258 Post-translational, 173, 174, 258
285
Potassium, 120, 249, 258 Potentiate, 60, 258 Poultry Products, 66, 77, 121, 165, 258 Practice Guidelines, 194, 258 Preclinical, 38, 41, 258 Precursor, 30, 31, 46, 173, 174, 221, 228, 230, 256, 258, 270, 271 Prednisolone, 258 Prednisone, 106, 258 Prenatal, 95, 229, 258 Presumptive, 164, 258 Probe, 9, 29, 32, 62, 63, 66, 68, 69, 73, 76, 83, 132, 154, 166, 168, 171, 245, 253, 258 Progeny, 167, 224, 251, 258 Progesterone, 259, 267 Progression, 12, 33, 213, 259 Progressive, 38, 219, 226, 228, 251, 259 Proline, 9, 22, 71, 222, 240, 259 Promoter, 10, 68, 259 Prone, 179, 259 Prophase, 251, 253, 259 Prophylaxis, 12, 259, 271 Protease, 19, 31, 86, 176, 259 Protein C, 19, 45, 113, 115, 211, 212, 214, 216, 222, 245, 259, 272 Protein Conformation, 212, 259 Protein Kinases, 112, 259 Protein S, 22, 30, 44, 54, 59, 120, 217, 231, 235, 259, 263, 269 Proteobacteria, 20, 259 Proteoglycan, 55, 259 Proteolytic, 31, 222, 223, 259 Proteome, 69, 100, 259 Protons, 211, 240, 259, 261 Protozoa, 9, 224, 228, 249, 259, 260, 266, 271 Protozoal, 4, 225, 260 Protozoan, 28, 48, 220, 225, 260 Psoralen, 33, 260 Psoriasis, 260 Psychiatry, 96, 122, 232, 260 Psychoactive, 260, 273 Public Health, 5, 15, 42, 104, 165, 177, 194, 260 Public Policy, 193, 260 Publishing, 61, 182, 260 Pulmonary, 17, 26, 43, 217, 221, 260, 268, 272 Pulmonary Edema, 221, 260 Pulse, 30, 250, 260 Purines, 260, 265 Purulent, 229, 260
Pustular, 173, 260 Pyogenic, 231, 254, 260, 264 Pyrimidines, 260, 265 Q Quality of Life, 53, 261 Quantitative Structure-Activity Relationship, 139, 261 Quaternary, 64, 79, 96, 259, 261 Quercetin, 29, 261 R Race, 249, 261, 266 Racemic, 261, 266 Radiation, 9, 20, 231, 233, 234, 241, 243, 244, 261, 273 Radiation therapy, 231, 234, 243, 244, 261, 273 Radioactive, 237, 240, 241, 243, 244, 250, 252, 253, 261, 273 Radioisotope, 253, 261 Radiolabeled, 217, 244, 261, 273 Radiotherapy, 218, 244, 261, 273 Randomized, 228, 261 Reactive Oxygen Species, 34, 261 Reagent, 64, 168, 221, 246, 261 Recombinant Proteins, 15, 261 Recombination, 38, 224, 235, 262 Rectum, 214, 218, 223, 227, 234, 242, 245, 262 Recurrence, 60, 262 Red blood cells, 173, 231, 238, 262, 264, 265 Refer, 1, 218, 223, 227, 232, 234, 238, 246, 252, 262, 270 Refraction, 262, 266 Regeneration, 19, 262 Regimen, 228, 262 Regional lymph node, 17, 262 Regulon, 13, 55, 67, 262 Rehydration, 183, 262 Reinfection, 37, 262 Relapse, 32, 127, 262 Remission, 262 Repressor, 253, 262 Resorption, 239, 262 Respiration, 125, 219, 250, 262 Resuscitation, 70, 262 Retinal, 250, 262 Retroviral vector, 235, 263 Retrovirus, 51, 263 Reversion, 263, 271 Rhinitis, 263, 265 Ribavirin, 118, 263
286
Listeria monocytogenes
Ribonucleic acid, 171, 263 Ribosome, 13, 263, 270 Ribotyping, 64, 67, 109, 132, 178, 263 Rickettsiae, 263, 271 Rod, 215, 216, 231, 263 Rotavirus, 183, 263 Ruminants, 70, 84, 236, 263 Rutin, 261, 263 S Saline, 15, 110, 160, 263 Salivary, 225, 263 Salivary glands, 225, 263 Salmonellosis, 176, 263 Sanitation, 9, 263 Saponins, 263, 267 Schizoid, 264, 273 Schizophrenia, 264, 273 Schizotypal Personality Disorder, 264, 273 Screening, 17, 23, 25, 40, 43, 222, 264 Seafood, 80, 173, 198, 264 Sebaceous, 244, 264, 273 Secondary tumor, 249, 264 Secretion, 11, 33, 39, 44, 45, 50, 54, 74, 85, 225, 239, 249, 250, 264 Secretory, 40, 264 Sedimentation, 220, 264 Segregation, 262, 264 Sensor, 19, 264 Sepsis, 8, 106, 119, 264 Septic, 118, 215, 264 Septicaemia, 106, 166, 264, 265 Septicemia, 102, 134, 167, 173, 177, 264 Sequence Homology, 255, 264 Sequencing, 17, 79, 80, 98, 258, 264 Serine, 9, 22, 52, 86, 173, 264 Serologic, 240, 265 Serotypes, 53, 63, 71, 89, 91, 92, 122, 170, 176, 179, 215, 226, 265 Serum, 65, 149, 171, 210, 211, 212, 214, 223, 234, 240, 247, 249, 255, 265, 270 Sessile, 40, 265 Shedding, 24, 85, 265 Shock, 55, 73, 87, 118, 239, 265, 270 Shunt, 133, 265 Side effect, 210, 217, 265, 269 Sigma Factor, 55, 76, 151, 265 Signs and Symptoms, 262, 265 Silage, 246, 265 Skeleton, 209, 265 Sludge, 99, 111, 124, 265 Small intestine, 183, 228, 239, 243, 265, 272 Smallpox, 9, 12, 265, 271
Smooth muscle, 212, 239, 265, 268 Sneezing, 265 Social Environment, 261, 265 Sodium, 64, 86, 120, 125, 129, 160, 236, 249, 265, 266 Sodium Lactate, 125, 266 Soft tissue, 217, 234, 265, 266 Solvent, 216, 231, 236, 254, 266 Somatic, 239, 250, 255, 266 Spasmodic, 209, 266 Spatial disorientation, 227, 266 Specialist, 199, 227, 266 Specificity, 27, 34, 36, 43, 52, 59, 81, 98, 160, 171, 210, 266 Spectroscopic, 17, 266 Spectrum, 44, 266 Sperm, 212, 221, 257, 266 Spermatogenesis, 20, 266 Spermatozoa, 266 Spinal cord, 218, 220, 221, 228, 229, 248, 251, 254, 255, 266 Spleen, 18, 170, 225, 247, 266 Splenomegaly, 242, 266 Sporadic, 66, 97, 179, 266 Spores, 17, 242, 266 Sputum, 171, 266 Squamous, 9, 230, 266, 267 Squamous cell carcinoma, 9, 230, 266, 267 Squamous cells, 266, 267 Steady state, 17, 267 Steel, 267, 272 Sterility, 242, 267 Steroid, 21, 216, 225, 264, 267 Stimulant, 165, 239, 267 Stimulus, 228, 231, 245, 267 Stomach, 4, 182, 209, 227, 231, 234, 239, 251, 255, 256, 263, 265, 266, 267 Stomatitis, 11, 267 Stool, 5, 115, 125, 223, 242, 245, 267, 269 Strand, 172, 257, 267 Streptococci, 113, 166, 267 Streptococcus, 20, 44, 65, 97, 101, 104, 169, 267 Stress, 13, 55, 58, 64, 67, 75, 84, 85, 86, 89, 95, 119, 131, 145, 154, 177, 182, 234, 251, 267 Stringency, 164, 267 Stroke, 192, 219, 267 Subacute, 242, 268 Subclinical, 42, 242, 268 Subspecies, 174, 266, 268, 271 Substance P, 138, 231, 249, 264, 268
287
Substrate, 19, 32, 39, 44, 172, 176, 230, 268 Suction, 232, 268 Sulfur, 173, 231, 249, 268 Superoxide, 34, 64, 268 Superoxide Dismutase, 64, 268 Supplementation, 149, 268 Suppression, 87, 110, 225, 268 Supratentorial, 122, 268 Surfactant, 87, 160, 268 Survival Rate, 9, 32, 60, 268 Symptomatic, 170, 268 Synergistic, 140, 151, 161, 268 Systemic disease, 53, 264, 268 Systemic lupus erythematosus, 106, 223, 268 T Tachycardia, 215, 268 Tachypnea, 215, 268 Teichoic Acids, 237, 268 Tenesmus, 228, 269 Tetracycline, 109, 269 Tetracycline Resistance, 109, 269 Therapeutics, 165, 269 Thermal, 89, 110, 160, 227, 252, 257, 269 Threonine, 10, 22, 52, 173, 255, 265, 269 Thrombin, 257, 259, 269 Thrombocytes, 257, 269 Thrombocytopenia, 116, 269 Thrombomodulin, 259, 269 Thrombosis, 243, 259, 267, 269 Thymidine, 172, 269 Thymus, 240, 247, 269 Thyroid, 10, 269, 271 Tissue Culture, 23, 24, 30, 55, 74, 79, 269 Tolerance, 7, 26, 33, 41, 62, 65, 66, 67, 76, 77, 85, 104, 105, 114, 128, 133, 210, 269 Tooth Preparation, 210, 269 Topical, 231, 240, 269 Toxic, iv, 30, 34, 211, 216, 224, 226, 229, 231, 238, 269, 270 Toxicity, 16, 43, 165, 228, 249, 269 Toxicology, 41, 194, 269 Toxin, 5, 38, 182, 183, 269, 270 Trace element, 221, 270 Trachea, 256, 269, 270 Transcriptase, 263, 270 Transduction, 25, 31, 52, 75, 88, 108, 112, 270 Transfection, 217, 235, 270 Transfer Factor, 240, 270 Translation, 211, 231, 270 Translational, 270
Translocation, 63, 83, 92, 231, 270 Transmitter, 209, 248, 270 Transplantation, 7, 57, 115, 240, 247, 270 Trauma, 55, 231, 251, 270 Trichinosis, 182, 270 Trimethoprim Resistance, 72, 270 Trophoblast, 21, 130, 217, 270 Tropism, 12, 24, 270 Tryptophan, 222, 270 Tuberculosis, 7, 13, 14, 18, 46, 47, 48, 59, 246, 270 Tumor Necrosis Factor, 40, 114, 118, 119, 127, 150, 270 Tunica, 250, 271 Typhimurium, 9, 25, 36, 41, 48, 53, 56, 61, 85, 93, 104, 146, 165, 176, 271 Typhoid fever, 9, 271 Tyrosine, 112, 154, 245, 271 U Ubiquitin, 19, 271 Ulcer, 99, 271 Umbilical Cord, 221, 271 Uncoupling Agents, 244, 271 Uracil, 172, 261, 271 Urethra, 271 Urinary, 83, 221, 239, 242, 266, 271 Urine, 171, 217, 242, 271 Uterus, 21, 209, 220, 226, 229, 254, 259, 271, 272 Uvea, 229, 271 V Vaccination, 7, 8, 10, 12, 33, 45, 48, 51, 60, 171, 271 Vaccines, 6, 7, 8, 9, 12, 15, 16, 27, 33, 37, 41, 45, 53, 58, 59, 60, 167, 178, 183, 271, 272 Vaccinia, 6, 9, 11, 16, 56, 271 Vaccinia Virus, 6, 11, 271 Vacuole, 17, 22, 30, 32, 37, 87, 88, 167, 271 Vagina, 220, 272 Vaginal, 51, 272 Vanadium, 43, 272 Variola, 271, 272 Vascular, 126, 230, 242, 252, 257, 272 Vasodilators, 252, 272 Vector, 6, 7, 8, 14, 15, 17, 24, 37, 40, 73, 92, 160, 270, 271, 272 Vegetative, 17, 272 Vein, 212, 244, 252, 271, 272 Venous, 259, 272 Ventricle, 240, 260, 272 Ventricular, 239, 272 Venules, 217, 218, 272
288
Listeria monocytogenes
Vertebral, 104, 272 Vesicular, 11, 31, 238, 265, 272 Veterinary Medicine, 104, 138, 193, 272 Vibrio, 4, 9, 37, 53, 183, 221, 272 Villi, 239, 272 Vinculin, 29, 272 Viral, 4, 8, 24, 36, 38, 168, 174, 183, 229, 242, 253, 263, 270, 272 Virulent, 7, 14, 30, 42, 50, 74, 90, 108, 122, 124, 134, 140, 272 Vitiligo, 260, 273 Vitro, 11, 36, 40, 58, 81, 238, 273 Vivo, 11, 14, 16, 18, 19, 22, 27, 32, 36, 38, 40, 48, 50, 52, 53, 56, 57, 58, 72, 76, 79, 97, 114, 235, 238, 241, 242, 247, 273 Vulgaris, 151, 273
W White blood cell, 209, 213, 237, 242, 245, 247, 250, 251, 252, 257, 273 Windpipe, 256, 269, 273 Withdrawal, 58, 273 Womb, 271, 273 Wound Healing, 18, 243, 273 X Xenograft, 213, 273 X-ray, 14, 16, 233, 234, 244, 252, 261, 273 X-ray therapy, 244, 273 Y Yeasts, 176, 234, 256, 273 Z Zygote, 224, 273 Zymogen, 259, 273
