Sudden Infant Death Syndrome - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

SUDDEN INFANT DEATH SYNDROME 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., 1960Sudden Infant Death Syndrome: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84082-2 1. Sudden Infant Death Syndrome-Popular works. I. Title.

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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.

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

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on sudden infant death syndrome. 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 SUDDEN INFANT DEATH SYNDROME ...................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Sudden Infant Death Syndrome ................................................... 5 E-Journals: PubMed Central ....................................................................................................... 45 The National Library of Medicine: PubMed ................................................................................ 46 CHAPTER 2. NUTRITION AND SUDDEN INFANT DEATH SYNDROME............................................. 91 Overview...................................................................................................................................... 91 Finding Nutrition Studies on Sudden Infant Death Syndrome .................................................. 91 Federal Resources on Nutrition ................................................................................................... 94 Additional Web Resources ........................................................................................................... 95 CHAPTER 3. ALTERNATIVE MEDICINE AND SUDDEN INFANT DEATH SYNDROME ...................... 97 Overview...................................................................................................................................... 97 National Center for Complementary and Alternative Medicine.................................................. 97 Additional Web Resources ......................................................................................................... 103 General References ..................................................................................................................... 104 CHAPTER 4. DISSERTATIONS ON SUDDEN INFANT DEATH SYNDROME ...................................... 105 Overview.................................................................................................................................... 105 Dissertations on Sudden Infant Death Syndrome ..................................................................... 105 Keeping Current ........................................................................................................................ 106 CHAPTER 5. CLINICAL TRIALS AND SUDDEN INFANT DEATH SYNDROME ................................. 107 Overview.................................................................................................................................... 107 Recent Trials on Sudden Infant Death Syndrome ..................................................................... 107 Keeping Current on Clinical Trials ........................................................................................... 108 CHAPTER 6. PATENTS ON SUDDEN INFANT DEATH SYNDROME ................................................. 111 Overview.................................................................................................................................... 111 Patents on Sudden Infant Death Syndrome .............................................................................. 111 Patent Applications on Sudden Infant Death Syndrome........................................................... 132 Keeping Current ........................................................................................................................ 140 CHAPTER 7. BOOKS ON SUDDEN INFANT DEATH SYNDROME ..................................................... 141 Overview.................................................................................................................................... 141 Book Summaries: Federal Agencies............................................................................................ 141 Book Summaries: Online Booksellers......................................................................................... 146 The National Library of Medicine Book Index ........................................................................... 149 Chapters on Sudden Infant Death Syndrome ............................................................................ 150 Directories.................................................................................................................................. 151 CHAPTER 8. MULTIMEDIA ON SUDDEN INFANT DEATH SYNDROME .......................................... 153 Overview.................................................................................................................................... 153 Video Recordings ....................................................................................................................... 153 Bibliography: Multimedia on Sudden Infant Death Syndrome ................................................. 154 CHAPTER 9. PERIODICALS AND NEWS ON SUDDEN INFANT DEATH SYNDROME ....................... 157 Overview.................................................................................................................................... 157 News Services and Press Releases.............................................................................................. 157 Newsletters on Sudden Infant Death Syndrome........................................................................ 159 Newsletter Articles .................................................................................................................... 159 Academic Periodicals covering Sudden Infant Death Syndrome............................................... 160 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 163 Overview.................................................................................................................................... 163 NIH Guidelines.......................................................................................................................... 163 NIH Databases........................................................................................................................... 165

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Other Commercial Databases..................................................................................................... 168 The Genome Project and Sudden Infant Death Syndrome ........................................................ 168 APPENDIX B. PATIENT RESOURCES ............................................................................................... 173 Overview.................................................................................................................................... 173 Patient Guideline Sources.......................................................................................................... 173 Associations and Sudden Infant Death Syndrome .................................................................... 187 Finding Associations.................................................................................................................. 189 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 191 Overview.................................................................................................................................... 191 Preparation................................................................................................................................. 191 Finding a Local Medical Library................................................................................................ 191 Medical Libraries in the U.S. and Canada ................................................................................. 191 ONLINE GLOSSARIES................................................................................................................ 197 Online Dictionary Directories ................................................................................................... 198 SUDDEN INFANT DEATH SYNDROME DICTIONARY ................................................... 199 INDEX .............................................................................................................................................. 265

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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 sudden infant death syndrome 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 sudden infant death syndrome, 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 sudden infant death syndrome, 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 sudden infant death syndrome. 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 sudden infant death syndrome, 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 sudden infant death syndrome. The Editors

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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.

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CHAPTER 1. STUDIES ON SUDDEN INFANT DEATH SYNDROME Overview In this chapter, we will show you how to locate peer-reviewed references and studies on sudden infant death syndrome.

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

Sudden Infant Death Syndrome and The SIDS Building Blocks Program Source: Thanatos. 19(3): 24-28. Fall 1994. Contact: Available from Thanatos, Florida Funeral Directors Association, P.O. Box 6009, Tallahassee, FL 32314-6009. (904) 224-1969, (800) 226-3332, (904) 224-7965 (Fax), http://www.ffda.org (Website). 4 issues per year for $16.00; $21.00 per year for subscribers outside the U.S. Summary: This article describes the SIDS Building Blocks Program, which is designed to attend to the bereavement needs of children who have experienced the loss of a sibling or an infant close to them as a result of a sudden, unexpected death. The article also

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provides an overview of sudden infant death syndrome (SIDS), focusing on its epidemiology; a discussion of the need to provide support for individuals affected by a SIDS death; and a description of SIDS Resources, Inc., the developers of the SIDS Building Blocks Program. The primary goal of the program is to foster an exchange between grieving children and significant adults in their lives, such as parents, relatives, school counselors, health professionals, child care providers, and funeral directors. The adults are provided with information about the role they can play in helping children cope with grief. The following services are available free of charge through the program: counseling through home visits, telephone support, peer support, a quarterly newsletter, services of a lending library, educational programs for professionals and community organizations, and support and resources for professionals. The SIDS Building Blocks Task Force was established in 1993 to develop documents to serve individuals who had contact with the children in the program. The Task Force consisted of volunteers from the community and staff members from SIDS Recources, Inc. The documents developed by the Task Force are as follows: a program description, guides for adults who want to help children cope with a SIDS death, a book of suggestions for relatives and friends of SIDS families, a guide for helping children through the funeral process, two books intended for child care providers, and a bibliography. A description is provided for each of the eight documents. 4 references. •

Sudden Infant Death Syndrome: Police Can Make a Difference. FBI Law Enforcement Bulletin Source: FBI Law Enforcement Bulletin. 67(9) : 1-5. September 1998. Contact: Available from Federal Bureau of Investigation, J. Edgar Hoover Building, 935 Pennsylvania Avenue, NW, Washington, DC 20535-0001. (202) 324-3000, http://www.fbi.gov (Web Site). You can download this publication free of charge from . Summary: This journal article introduces law enforcement personnel to sudden infant death syndrome (SIDS) and sets forth some basic guidelines for officers to follow when responding to and investigating a possible SIDS case. One of the authors is a policeman who responded to an emergency call of an infant not breathing in February 1982. The victim was diagnosed as dying of SIDS. The officer recalls that he attended the infant's funeral, but on the night of the death, he did not document any of his observations of the death scene or additional information given by the family, actions that today are mandatory in states that have child death investigation laws. Following some basic information on the incidence and risk factors for SIDS, the article discusses the differential diagnosis of SIDS and child abuse. Although only qualified medical officials can diagnose SIDS, it can aid the investigation if the on-scene officers become familiar with the facts regarding SIDS and how SIDS cases compare to child abuse. Physically, most SIDS infants show no external signs of injury, whereas abused infants may exhibit bruises, bumps, cuts, welts, scars, signs of head trauma, or broken bones. Most SIDS infants will appear well-developed and well-nourished, while abused infants often show signs of malnourishment and neglect. Still, certain bodily appearances typically occur in SIDS cases due to the death process. Officers may notice discoloration of the skin, settling of the blood, frothy drainage from the nose or mouth that may be bloodtinged, and cooling rigor mortis. Parents of SIDS victims typically relate stories of placing their infants to sleep in the crib only to find them lifeless later. In child abuse cases, the parents' stories may sound suspicious or may not account for all the injuries to the child. Officers at the scene can help the investigation by carefully recording their observations, including the position of the infant when found, the presence of any

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bedding or other objects in the crib, any dangerous items in the room, any medications the child was taking, as well as room temperature and air quality. All first responders need to be good listeners. If they need more information, they can ask open-ended, nonjudgmental questions. By being sympathetic interviewers, officers will obtain the information they need while being respectful of the family's feelings. Each member of the family may react differently to the death, and in contrast to the way to officer would act. Officers need to maintain objectivity and avoid making hasty conclusions based on the family's reactions. Officers should support the family in any way they can, and keep them informed of the procedures that need to take place. They should make sure the parents get to the hospital, and that other children are taken care of at home. It is imperative that police officers and other first responders are trained to respond appropriately to possible SIDS deaths. Their observations and attention to detail could provide valuable information to researchers who are trying to find the cause of SIDS and other sudden infant and child deaths.

Federally Funded Research on Sudden Infant Death Syndrome The U.S. Government supports a variety of research studies relating to sudden infant death syndrome. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to sudden infant death syndrome. 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 sudden infant death syndrome. The following is typical of the type of information found when searching the CRISP database for sudden infant death syndrome: •

Project Title: AAV VECTOR DELIVERY TO SKELETAL MUSCLE, PLATFORM FOR THERAPEUTIC PROTEIN DELIVERY Principal Investigator & Institution: Flotte, Terence R.; Professor; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2003 Summary: Syndrome (SIDS) or with a combined cardiac and skeletal myopathy. Treatment of these disorders has consisted primarily of dietary manipulation and has been far less than optimal to this point. The recent development of recombinant adenoassociated virus (rAAV) vectors for highly efficient transduction of hepatocytes and myofibers present new tools for the study of FAO disorders. Specifically, our laboratory has produced rAAV vectors expressing FAO enzymes whose deficiency results in myopathy, such as short-chain acyl CoA dehydrogenase (SCAD) and long-chain acyl

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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CoA dehydrogenase (LCAD). Human cell lines from patients deficient in these enzymes are available, and mutant mouse models exist for both of these disorders. We propose to utilize rAAV vectors expressing FAO enzymes in an attempt to unravel the pathobiology of FAO disorders and to better define endpoints for molecular or cellbased therapies of these disorders. This will be accomplished in three specific aims: (1) To assess the extent to which genetic correction of a limited percentage of SCAD deficient or LCAD deficient cells within a cell population or organ can affect biochemical correction of fatty acid oxidation. (2) To determine whether receptor binding and entry are limiting steps for stable transduction by rAAV in a intact mammalian liver or muscle bundle. (3) To test the hypothesis that the liver pathology observed in LCAD and VLCAD deficiencies are secondary to the accumulation of toxic metabolites as opposed to primary energy failure within hepatocytes. (4) To determine whether global phenotypic correction of FAO deficiency in mice is more effective after widespread vector delivery after intrauterine or neonatal IV injection. The information gained from these studies could also be used to guide the feasibility of other organdirected therapies, potentially including stem cell transplantation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CALCIUM CHEMORECEPTORS

SIGNALING

IN

DEVELOPING

CAROTID

Principal Investigator & Institution: Sterni, Laura M.; Pediatrics; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 01-JAN-1998; Project End 31-DEC-2002 Summary: (Adapted from applicants' abstract) Dr. Laura Sterni, the PI, is an assistant professor who completed her pediatric pulmonary fellowship in 1996. In this application she outlines a program to study proposed mechanisms by which the carotid chemoreceptors increase their sensitivity in early postnatal life. The carotid chemoreceptors are oxygen sensors which are almost entirely responsible for driving the ventilatory response to hypoxia. Their sensitivity is weak at birth and requires the first few days to weeks of life to reset, increase their sensitivity to hypoxia, and assume the role of defending the infant from hypoxic stress. An understanding of the mechanisms involved in this postnatal resetting is likely to be important in understanding the pathogenesis of many disorders of neonatal respiratory control, including the Sudden Infant Death Syndrome (SIDS), the number one killer of infants over one month of age in the United States. The PI's fellowship project demonstrated that maturation of carotid chemoreceptor sensitivity to oxygen is due, at least in part, to changes within the chemosensory type I cell. These cells respond to stimuli with an increase in cytoplasmic calcium ([Ca2+]c) which then triggers neurotransmitter release. Type I cells isolated from mature animals had a significantly greater [Ca2+]c response to hypoxia and anoxia than cells isolated from newborns. These studies will investigate the role of intracellular Ca2+ stores in maturation of the [Ca2+]c response of type I cells to hypoxia. The hypotheses that will be tested are: (1) in the mature carotid chemoreceptor cell, intracellular Ca2+ stores modulate the rise in [Ca2+]c produced by voltage gated calcium entry; (2) the effect of the intracellular Ca2+ stores on the type I cell's hypoxia response changes during postnatal maturation; and (3) carotid chemoreceptor resetting is mediated partly by withdrawal of dopaminergic stimulation on Ca2+ influx and Ca2+ stores. The PI will take advantage of the strong mentoring, significant protected research time and the outstanding academic resources of the Johns Hopkins Medical Institutions to reach her goal of becoming an independent investigator in this important field. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CARDIAC CHANNEL MUTATIONS IN SIDS Principal Investigator & Institution: Ackerman, Michael J.; Assistant Professor; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002; Project Start 07-JUN-2002; Project End 31-MAY-2006 Summary: (provided by applicant): Michael J. Ackerman, M.D., Ph.D. is a board eligible pediatric cardiologist and an Assistant Professor of Medicine, Pediatrics, and Molecular Pharmacology & Experimental Therapeutics at Mayo Medical School. Dr. Ackerman is a physician-scientist directing a sudden death genomics laboratory and the Long QT Syndrome Clinic. His long-term objectives are to identify the underlying causes of sudden cardiac death in infants, children, adolescents, and young adults. In this proposal entitled Cardiac Channel Mutations in Sudden Infant Death Syndrome, the applicant sets forth to answer the fundamental question: what percentage of infants suffering a SIDS death possessed putative disease-causing mutations in the genes encoding their cardiac ion channels? Presently, SIDS continues to claim nearly 3000 apparently healthy infants each year in the United States. The fundamental causes underlying SIDS remain poorly understood. In specific aim 1, Dr. Ackerman will perform a mutational analysis of the 5 cardiac channel genes already implicated in a human arrhythmia syndrome, namely congenital long QT syndrome using temperature modulated heteroduplex analysis and denaturing high performance liquid chromatography. In specific aim 2, two non-LQTS arrhythmia syndrome ion channel genes will be investigated by mutational analysis as novel candidate SIDS genes. Finally, in specific aim 3, the possible mutations in the channel genes identified in aims 1 and 2 will be characterized functionally. These mutations will be engineered by site-directed mutagenesis into the wild type channel, expressed in transient and stable transfection cell lines, and characterized using single electrode patch clamp technologies. If the applicant's hypothesis is correct that 10% of infants with SIDS possess cardiac channel mutations, then cardiac channel genes would account for the "underlying vulnerability" for the largest identifiable subset of infants to date. Such a discovery could have significant implications on attempts to further reduce the incidence of SIDS in our country and throughout the world. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CAROTID BODY EXCITATION--NEW CONCEPT Principal Investigator & Institution: Shirahata, Machiko; Associate Scientist; Environmental Health Sciences; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 05-JUL-1999; Project End 30-JUN-2003 Summary: (Applicant's abstract): The carotid body is a major chemoreceptor organ whose excitation causes reflex responses in cardiopulmonary, renal and endocrine systems. Although the mechanisms of carotid body excitation are not yet clear, essential steps include the depolarization of chemosensitive glomus cells, the increase in glomus cell intracellular calcium and the release of neurotransmitters. Many studies point to the involvement of oxygen-sensitive potassium channels, but a causal relationship between the inhibition of these channels and the depolarization of glomus cells during hypoxia has not yet been established. Since cat glomus cells release acetylcholine even under normoxic/normocapnic conditions, we hypothesize that hypoxia augments the activity of neuronal nicotinic acetylcholine receptors and/or enhances the sensitivity of acetylcholine receptors for acetylcholine. This initiates the depolarization of glomus cells and the increase in intracellular calcium. Oxygen-sensitive potassium channels and

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voltage-gated calcium channels participate in the later phase of the changes. Preliminary data have shown that: 1) cat glomus cells expressed alpha-4 subunit containing nicotinic acetylcholine receptors, 2) acetylcholine-induced inward current and carotid body neural output were enhanced by a mild decrease in oxygen tension from normoxic levels, 3) acetylcholine increased calcium of carotid body cells, 4) oxygen-sensitive potassium current was linearly inhibited by decreasing oxygen, and 5) increased carotid body neural output in hypoxia was inhibited by L-type voltage gated calcium channels. Specific aims are to investigate: 1) the role of acetylcholine and nicotinic acetylcholine receptors for initiating the depolarization of glomus cells and the increase in calcium, 2) the contribution of oxygen sensitive potassium channels in the late phase of glomus cell depolarization during hypoxia, 3) the contribution of voltage gated calcium channels to the late phase of the calcium increase in glomus cells during hypoxia. Patch clamp, microfluorometric, and immunocytochemical techniques are to be used. This innovative proposal will advance the understanding of the excitation mechanisms of glomus cells. Once the chemotransductive mechanisms are understood, pharmacological or genetic tools can be developed to alter the carotid body function to levels desirable for treating carotid body related pathological conditions such as sudden infant death syndrome and hemodynamic changes in sleep apnea patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CELLULAR & CLINICAL PHENOTYPES OF NOVEL SCN5A MUTATIONS Principal Investigator & Institution: Makielski, Jonathan C.; Professor of Medicine and Physiology; Medicine; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-AUG-2007 Summary: (provided by applicant): SCN5A encodes the alpha subunit of the human voltage-dependent Na channel (hNaV1.5) found in heart. We have made the novel observation that up to four very common variants of NaV1.5 exist in human heart and at least some have functional implications. Mutations in this channel also cause sudden cardiac death in the congenitally acquired long QT syndrome (LQT3) and the Brugada Syndrome (BS). We have recently characterized four novel SCN5A mutations and found: 1) Two in Sudden Infant Death Syndrome (A997S, R1826H) are LQT3.2) LQT3 (M1766L) and BS (G1743) mutations have expression defects "rescued" by antiarrhythmic drugs. 3) M1766L has normal or absent current depending on the variant NaV1.5 background used to test it. We propose to investigate further the extent and mechanisms of expression defects and their "rescue" and the importance of "background". Through collaboration with Dr. Ackerman at Mayo Clinic we also have >20 additional novel SCN5A mutations to investigate for novel functional defects and arrhythrnia mechanism. We will make and express these channels in cell culture, define function by voltage clamp and immunocytochemistry, and correlate molecular function with clinical phenotype through arrhythmia mechanism. In Aim 1 we will investigate the expression and function of wild type variants, and also how mutant channel expression and function depends upon the background clone. In Aim 2 we will study novel mutants. In Aim 3 we will investigate mutants with "gain of function" and test the hypothesis that late current decay in LQT3 correlates with enhanced rate dependent QT interval adaptation, later onset, and better prognosis than mutations without late current decay. In Aim 4 we will investigate mutations with "loss of function", the mechanism for loss of function including novel trafficking defects, and test the hypothesis that this loss can be "rescued" by drugs. In Aim 5 we will co-express

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mutations with the beta1 and beta3 subunit, and assess effects of PKA stimulation, to test the hypothesis that these areas are critical to the mechanism of action. These studies on the novel findings will have implications for arrhythmia mechanism and genotypephenotype correlation in both mutation arrhythmia syndromes and more generally for the variants in "normal' hearts that may generate insight into genetic predisposition to acquired arrhythmia. At a more basic level these "natural" experiments will contribute to understanding the structure-function relationship of this important channel. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CELLULAR MECHANISMS OF MEDULLARY SEROTONERGIC NEURONS DURING DEVELOPMENT Principal Investigator & Institution: Richerson, George B.; Associate Professor; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2003; Project Start 07-JUL-2003; Project End 31-MAR-2008 Summary: The overall goal of this program is to define the cause of SIDS. With the recent discovery of abnormal LSD binding in the medulla of SIDS infants, we have focused our efforts on the medullary serotonergic system, to define what specifically happens to serotonergic neurons to cause them to malfunction. The goal of Project 5 is to define the cellular properties of serotonergic neurons, as a means of providing a neurobiological explanation for the link between serotonin and SIDS. We have previously demonstrated that serotenergic neurons closely apposed to large arteries in the rat ventral medulla increase their firing rate in response to acidosis, and we have proposed that they are chemoreceptors that stimulete breathing, arousal and other CNS changes to restore pH homeostasis: We now plan to use a rat model to determine whether the cellular properties of serotonergic neurons can explain the three risk factors in the Triple Risk Model for SIDS. We wiil use a combination of multielectrode arrays and patch clamp recordings from serotonergic neurons in culture and in brain slices. We will: 1) Study how different subsets of serotonergic neuron respond to acidosis, hypoxia, temperature and glucose. 2) Examine how muscarinic receptor activation leads to enhancement of chemoreception. 3) Define the changes in chemosensitity of serotonergic neurons as they undergo development. 4) Determine the effects of acute and chronic (during pregnancy) nicotine exposure on the function of serotonergic neurons. 5) Compare the cellular properties of serotonergic neurons from rats with those of piglets and mice, and determine whether serotonergic neurons from these species, as well as human infants, are closely associated with large arteries of the ventral medulla. These experiments will provide information critical to a full understanding of the role of serotonergic neurons in brain function, and will lead to specific testable hypotheses about how their malfunction or maldevelopment could lead to death during sleep. URimately, the results of these experiments may provide important insights that could lead to diagnostic and therapeutic tests for those infants at highest risk of SIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: COCAINE EXPOSED INFANTS--CARDIAC PROBLEMS AND OUTCOME Principal Investigator & Institution: Mehta, Sudhir K.; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 01-DEC-2000; Project End 30-NOV-2001 Summary: Infants born to mother who use cocaine during pregnancy have greater morbidity and a higher rate of sudden death. The etiology of sudden death is unclear.

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Preliminary observations suggest the presence of multiple cardiovascular abnormalities such as greater left ventricular mass, persistent hypertension, greater prevalence of ST segment elevations and higher vagal tone. To study the cardiovascular effects on inutero cocaine exposure the study has the following aims: to detect the cardiovasculaar abnormalities in the newborn period; to evaluate the relationship of cord blood plasma cholinesterase activity and the above abnormalities; and to study the natural history of these abnormalities during the first 2 months of life. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: COLLABORATIVE HOME INFANT MONITORING EVALUATION (CHIME) Principal Investigator & Institution: Corwin, Michael J.; Epidemiology and Biostatistics; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 30-SEP-1991; Project End 31-AUG-2002 Summary: (Adapted from applicant's description): This is an application for continued participation as the Data Coordinating and Analysis Center in an extended Collaborative Home Infant Monitoring Evaluation (CHIME) Study over the next five years. Each year, approximately 50,000 infants are placed on a home cardiorespiratory (CR) monitor. Monitors are typically prescribed for infants in one of three groups at increased risk for Sudden Infant Death Syndrome (SIDS): infants who experience an idiopathic apparent life-threatening event (apnea of infancy, AO1), SIDS siblings, and preterm infants. Despite years of experience, it is not known to what extent monitor use has reduced either infant morbidity or mortality. The CHIME study is designed to address the unresolved questions regarding who has CR events at home, the nature of these events, and their impact on neurodevelopmental outcome. We propose a 5-year extension of the CHIME study in order to complete enrollment, follow-up, and data analysis. A total of 2,115 infants will be enrolled: 375 healthy term infants, 330 SIDS siblings, 330 with AO1, and 1,080 preterm infants < 1750 g birth weight. Each infant will receive an overnight polysonogram and will be monitored at home for 4-5 months using a memory monitor developed for the CHIME study. The monitor will store all CR events occurring at home and the associated oxygen saturation and sleep position, will record periodic non-event (normative) intervals, and will continuously record R-R and breath-to-breath intervals. Apneas will be categorized as central, mixed or obstructive by the use of inductance plethysmography, a technique not previously available for home monitoring. Clinical and neurodevelopmental status will be ascertained longitudinally through 1 year of age. The CHIME study will create a comprehensive summary of the full range of CR events occurring in the home. The results will yield important insights regarding underlying mechanisms, antecedent variables predictive of events, appropriate intervention strategies, and the relationship between CR events and neurodevelopmental outcome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: COLLABORATIVE HOME INFANT MONITORING EVALUATION (CHIME) Principal Investigator & Institution: Martin, Richard J.; Professor; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 01-DEC-2000; Project End 30-NOV-2001 Summary: This protocol is a multicenter collaborative trial of Home Infant Apnea Monitors. These devices are used to monitor breathing and heart rate in infants thought

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to be at risk for SIDS as well as normal controls. This study will yield extensive descriptive information regarding the efficacy of apnea monitors, their accuracy, and the ability of these devices to detect clinically important events. The follow-up of the infants continues until approximately age 1.5 yrs. The GCRC Psychometrists assist with the developmental assessments. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: COMPARATIVE CHEMICAL ANATOMY OF THE VENTRAL MEDULLA Principal Investigator & Institution: Filiano, James J.; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001 Summary: The overall hypothesis of the Program Project is that SIDS is due to developmental abnormalities of the ventral medulla that interfere with protective cardiorespiratory responses to potentially life-threatening, but often occurring, events during sleep, such as hypoxia, hypercapnia, and apnea. In the context of the Program Project, Project IV will attempt to characterize the cyto-and chemoarchitecture of the ventral medulla of the piglet and human infant. The over-riding concept of the project is that the ventral medullary surface contains clusters of small neurons that are cytologically and neurochemically homogenous and thus form a unified class of neurons; and that his class of neurons provides a common influence on autonomic modulation, chemoreception, and cardiopulmonary coupling, although the specific role of each cluster of neurons varies in accordance with its specific somatotopic connections. First, we will test the hypothesis that, in the piglet, the small ventral neurons of the raphe pallidus, the most superficial parapyramidal neurons, and the retrotrapezoid neurons, belong to the unified class of neurons as evidenced by being cytoarchitectonically identical and expressing the same neurotransmitters and neurotransmitter receptors. Second, we will test the hypothesis that, based on cytoarchitectonic and chemoarchitectonic criteria, the human arcuate nucleus is homologous to the small ventral neurons of the piglet raphe pallidus, the piglet superficial parapyramidal nucleus, and the piglet retrotrapezoid nucleus. We will employ the traditional approach of comparative neuroanatomy by testing if neurons in both species share common cell morphology, express common receptors and share common immunohistochemical staining characteristics. Morphologic studies will employ Neurobiotin/R and standard staining methods; autoradiographic studies will test for expression for receptors for glutamate, serotonin, GABA, somatostatin, and acetylcholine (muscarinic); immunohistochemical studies will test for expression of choline acetyltransferase, tyrosine hydroxylase, glutamate decarboxylase, glutamate, substance P, cholecystokinin, and thyrotropin releasing hormone. It is goal of Project IV to develop a comparative anatomic framework that will help the physiologic studies in Projects I-III shed light on the potential significance of arcuate nucleus abnormalities reported in SIDS victims. Ultimately, this neuroanatomic framework may be useful to establish a model for SIDS in the developing piglet based on impaired behavioral and ventilatory responses to asphyxial rebreathing induced by dysfunction of the piglet arcuate homologue. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CONTROL OF BREATHING DURING PHYSIOLOGIC CONDITIONS Principal Investigator & Institution: Forster, Hubert V.; Professor; Physiology; Medical College of Wisconsin Po Box26509 Milwaukee, Wi 532264801

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Timing: Fiscal Year 2001; Project Start 01-JUN-1986; Project End 31-MAY-2005 Summary: Several theories on the neural control of breathing that were based on data from reduced preparations were not supported by our recent findings in awake and asleep goats on the effects of rostral medullary neuronal dysfunction and/or carotid body denervation (CBD). Some findings mimicked the altered breathing found in obstructive sleep apnea (OSA) and congenital central hypoventilation syndrome (CCHS). The mechanisms that mediated these effects are not established, but one likely mechanism is through intracranial chemoreceptors for years thought to exist only near the ventral medullary surface (including the retrotrapezoid nucleus RTN)). However, findings in reduced preparations of chemoreceptors at widespread brain sites have raised questions related to the location and role of chemoreceptors that affect breathing in awake and asleep states and whether brain chemoreceptor sensitivity is altered by CBD. One recently identified site of chemoreception is the medullary raphe nuclei (MRN) whose role in the control of breathing during awake and asleep states remains speculative. Accordingly, to study chemosensitivity and the role of the RTN and MRN in the control of breathing, we will implant microtubules into these nuclei of goats to: a) create a focal acidosis by dialysis of mock cerebrospinal fluid with different PCO2's, or b) induce neuronal dysfunction through injection of glutamate or serotonin receptor antagonists or agonists, or a neurotoxin. Major hypotheses are: 1) focal acidosis (equivalent to that breathing 7 percent inspired CO2, delta brain pH approximately -.05) in the RTN will increase breathing in awake, but not asleep states, while acidosis in the MRN will increase breathing in asleep, but not awake states, 2) at RTN sites where focal acidosis increases breathing, neuronal dysfunction will attenuate whole body CO2 sensitivity, but not alter rest and exercise breathing, 3) neuronal dysfunction in the MRN will attenuate CO2 sensitivity and rest and exercise breathing, 4) during the first 10 days after CBD, the effect of RTN and MRN focal acidosis will be attenuated but 15 plus days after CBD, the effect of focal acidosis will be accentuated. and 5) at most RTN and MRN sites, the acute effects of neurotoxic lesions will be hypoventilation (rest and exercise) and attenuated CO2 sensitivity; the acute effects of these lesions will be greater in CBD than in intact goats, but recovery after lesioning will be greater in intact than in CBD goats. Our unique studies are important because hypotheses generated largely from reduced preparations will be tested in awake and asleep states to enhance the understanding of medullary chemoreceptor contribution to the control of breathing and how abnormalities in this contribution may underlie diseases such as OSA, CCHS, and the Sudden Infant Death Syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CONTROL OF BREATHING IN RECOVERY FROM APNEA Principal Investigator & Institution: Thach, Bradley T.; Professor; Pediatrics; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 30-SEP-1977; Project End 31-MAY-2004 Summary: The Sudden Infant Death Syndrome (SIDS) remains a leading cause of infant deaths inspite of recent highly successful public health interventions designed to reduce SIDS risks (The U.S. "Back to Sleep" campaign, "BTS"). We propose to study several physiologic and neuro-developmental mechanisms potentially involved in the etiology of SIDS, as well as, pertinent environmental factors. The research will focus on three areas. In the first of these, we plan to study the physiology of recovery from severe hypoxia by gasping (autoresuscitation, AR). These studies will determine if the previously documented developmentally acquired defect in AR, originally described in SWR mice, is present in other inbred strains and species and, furthermore, if underlying

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mechanisms causing AR failure are similar to those in SWR mice. Additionally, the effects of increased environmental temperature on AR will be evaluated. Also, Home apnea monitor recordings of infants dying suddenly and unexpectedly while being monitored will be studied to determine if there is evidence of attempted AR and if so, potential reasons for its failure. The second part of our studies will be directed to prospectively obtaining data on the case history, death scene and postmortem examination of infant's dying with the diagnoses of SIDS, accidental suffocation and "cause of death undetermined" in the St. Louis metropolitan area. The aim is to determine how many of these deaths are preventable by public acceptance of current "BTS" guidelines and how many might be prevented by future additions or changes in the recommendations to child caretakers. In connection with this study, we will perform special death scene investigations in certain SIDS and accidental suffocation deaths combined with laboratory death scene reconstruction studies in order to determine if additional simple guidelines for parents and child equipment manufactures can be formulated in order to prevent infant deaths. Finally, we will study development of the infant's ability to avoid potentially suffocating environments during sleep, and determine the potential role of the infant's past experience on this development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DENSE ARRAY EEG FOR NEONATAL SLEEP MONITORING Principal Investigator & Institution: Tucker, Don M.; Ceo/Chief Scientist; Electrical Geodesics, Inc. 1850 Millrace Dr, Ste 3 Eugene, or 97403 Timing: Fiscal Year 2002; Project Start 01-MAY-2002; Project End 31-OCT-2002 Summary: (provided by applicant): Electroencephalography is a safe, noninvasive technique for monitoring neonatal brain function. Acute and long-term EEG monitoring of infants has clinical utility for evaluating the effects of hypoxic ischemic insults and detecting the presence of epileptic activity. The information available in neonatal EEG can be greatly enhanced by using an adequate number of electrodes to accurately map the spatial distribution of the EEG without spatial aliasing. The Geodesic Neonatal EEG Brain Monitor will be designed from experimental studies and theoretical simulations of the required sampling density for scalp potentials on the infant head. Dense Array EEG methods will be developed that incorporate the unique features of infant skull anatomy to estimate the potentials in the brain of the infant. The Geodesic Neonatal EEG Brain Monitor system will be adapted for a variety of clinical uses, initially focusing on monitoring brain function in sleep in the Neonatal Intensive Care Unit (NICU). This monitoring will examine both normal and pathological sleep states of the neonate, providing information on the maturation of arousal control in preterm and full term infants that may be important in understanding sudden infant death syndrome. PROPOSED COMMERCIAL APPLICATION: Behavioral outcome studies indicate that brain function is often at risk in the neonatal intensive care unit. An inexpensive, highresolution neonatal brain state monitor could guide medical management to support brain health and therefore improve neurological and psychological outcome in many infants. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DEVELOPMENT OF HYPOGLOSSAL MOTONEURON PROPERTIES Principal Investigator & Institution: Berger, Albert J.; Professor; Physiology and Biophysics; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-JAN-1993; Project End 30-JUN-2002

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Summary: (Adapted from the applicant's abstract): The overall research goal is to investigate postnatal development of fast synaptic transmission to hypoglossal motoneurons (HMs) and modulation of this transmission by serotonin (5-HT). HMs innervate the tongue muscle and therefor are critically important in regulation of upper airway patency. The upper airway is a site of airway obstruction; thus a comprehensive understanding of the development of systems that synaptically excite and inhibit HMs may provide new insights into certain pathologic states, including apnea of prematurity, Sudden Infant Death Syndrome and obstructive sleep apnea. Preliminary data show that during the postnatal period marked changes occur in both excitatory (primarily involving N-methyl-D-aspartate - NMDA) and inhibitory (glycinergic) synaptic responses of HMs. It is hypothesized that these changes are due to postsynaptic mechanisms involving alterations in the respective ligand-gated channels. This proposal focuses on in vitro studies of visualized rat HMs in brainstem slices, and uses whole-cell and single-channel recordings from HMs. The first three specific aims investigate developmental changes in NMDA synaptic current. The first aim is to quantify changes in evoked, spontaneous and postsynaptic NMDA currents, as well as in single NMDA channel properties. The second aim is to investigate the mechanism(s) for the reduction in NMDA synaptic current in older versus younger HMs. It is hypothesized that various factors including NMDA, Mg++ and glycine sensitivities account for these differences. The third aim investigates postnatal developmental changes in 5-HT1B receptor activated inhibition of glutamatergic synaptic transmission. The final two specific aims investigate developmental changes in glycinergic synaptic currents. Aim four quantifies the developmental changes that occur in evoked, spontaneous and postsynaptic glycinergic currents in HMs, as well as in single glycine channel properties. The fifth aim investigates postnatal changes in 5-HT1B receptor activated inhibition of glycinergic synaptic transmission. A knowledge of these developmental changes in synaptic inputs may have important functional and pathological implications for control of tongue muscle and therefore upper airway patency. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DEVELOPMENT OF SLEEP HOMEOSTASIS IN THE DEVELOPING RAT Principal Investigator & Institution: Heller, Horace Craig.; Professor and Chair; Biological Sciences; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 03-JUL-1998; Project End 31-MAY-2003 Summary: (Adapted from applicant's abstract): This proposal will investigate the development of homeostatic sleep mechanisms and emergence of distinct arousal states in the neonatal rat. Arousal states cannot be identified by EEG parameters early in postnatal development, thus, arousal states in neonates are defined behaviorally as active sleep (AS) and quiet sleep (QS). AS and QS are generally considered homologous to REM and NREM sleep in adults, however, we found that EEG slow wave activity (SWA) occurs as often during AS as it does in QS at postnatal day 12 (P12). Thus, AS may not be an immature form of adult REM sleep, rather, it may be an undifferentiated state of the nervous system out of which NREM sleep emerges first and REM sleep second. We will test this hypothesis by determining when additional physiological parameters (e.g., respiratory patterns, electro-oculogram (EOG), brain and skin temperatures, and myoclonia) coalesce and form identifiable arousal states. We have developed a system for simultaneous recording of EEG, EMG, and behavioral sleep (by videotape) in neonatal rats continuously from P12 to P30. We found that adult-like responses to sleep deprivation (SD) were not present until P24; prior to that age, SD

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elicits increases in total sleep time (TST) without affecting the intensity or amount of SWA. From P12-P24, SWA increases progressively beyond adult levels, yet is not affected by SD. Thus, critical components of adult sleep homeostatic mechanisms must be absent prior to P24. Convergent lines of evidence support a role for adenosine in regulating SWA; however, its link to homeostatic mechanisms is unknown. We found that the adenosine A~ receptor agonist, N6-Cyclopentyladenosine (CPA), mimics the effects of SD in both adult and neonatal rats. Furthermore, CPA elicits SWA at ages (P16 and P20) when 3 h of SD have no effect on SWA. Thus, A1 receptors are present and functional but apparently not activated by SD. This proposal will investigate arousal state emergence, development of sleep homeostasis, and adenosinergic regulation of sleep homeostasis in neonatal rats. These studies will contribute significantly toward clinical studies on sudden infant death syndrome (SIDS) because they investigate the mechanisms by which arousal and, hence, failure to arouse, from sleep develop. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DEVELOPMENTAL CONTROL OF THE DIAPHRAGM AND UPPER AIRWAYS Principal Investigator & Institution: Cameron, William E.; Associate Professor; Physiology and Pharmacology; Oregon Health & Science University Portland, or 972393098 Timing: Fiscal Year 2001; Project Start 01-FEB-1999; Project End 31-JAN-2004 Summary: (Adapted from the applicant's abstract): This proposal will characterize the postnatal development of the genioglossal and phrenic motoneurons, by correlating physiological changes in membrane conductance and spiking properties with changes in anatomy. The strength of respiratory muscle contraction is determined by the number of respiratory motoneurons activated and their rate of discharge. Both the order in which the neurons are activated and their discharge rates are a function of their resting conductance, that is, the number of membrane channels open at any given time. Most membrane channels are controlled by neurotransmitters and/or by the intrinsic electrical state of the cell membrane. The change in the balance of these two processes are most dramatic during postnatal development. The applicant is interested in these processes that occur in the two respiratory motoneurons that affect the performance of the diaphragm and genioglossus. Activation of these two muscles must be coordinated to move air into the lungs with the least effort; this may be particularly relevant to the pathophysiology of Sudden Infant Death Syndrome (SIDS). In the past period, the applicant established that glycine significantly contributed to the increase in resting membrane conductance that occurs at 3 weeks, and that these age-related increases in resting conductance result from an increase in the number of open potassium channels. The proposed studies will be performed on genioglossal and phrenic motoneurons in slice preparations of the rat brainstem and spinal cord. Visually identified motoneurons will be studied from four different age groups (1-2, 5-7, 13-15 and 19-22 days) with a combination of patch-clamp recording, three-dimensional neuronal reconstruction and immunocytochemical localization of certain receptors and ion channels. The application will: 1) examine the anatomy and physiology of glycine, GABA, and glutamate neurotransmitter systems at the four stages during postnatal development; 2) identify specific potassium channels that contribute to the increase in membrane conductance and spike characteristics; and 3) explore the intracellular pathways mediating the enhanced potassium conductance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EFFECTS OF PRENATAL EXPOSURE TO NICOTINE ON PRIMATE LUNG DEVELOPMENT Principal Investigator & Institution: Spindel, Eliot R.; Senior Scientist; Oregon Health & Science University Portland, or 972393098 Timing: Fiscal Year 2001 Summary: The deleterious effects of maternal smoking during pregnancy are well established. Maternal smoking is the major preventable cause of intrauterine growth retardation and prematurity. Perhaps less well appreciated, is the recent, strong evidence, that smoking during pregnancy directly and adversely affects lung development. Respiratory problems associated with in utero tobacco exposure include decreased lung function, increased respiratory diseases and increased incidence of sudden infant death syndrome (SIDS). Given the unfortunate prevalence of smoking during pregnancy and the resulting serious consequences, it is of major importance to understand the mechanisms underlying smoking-induced changes in the newborn. We have begun to investigate this by administration of nicotine to timed-pregnant rhesus monkeys. In preliminary studies we have demonstrated that exposure of pregnant rhesus monkeys to a nicotine dose consistent with that of smokers alters fetal a irway dev elopment and that related effects can be reproduced in fetal monkey lung organ culture. Immunohistochemistry shows wide expression of nicotinic receptors in developing lung and nicotine appears to alter the pattern of receptor expression. Preliminary data further suggests that some of the effects of nicotine, acting though nicotinic receptors, may be mediated by antagonism of the mitogenic effects of peptide growth factors such as GRP. From these studies will come the first description of the effects of chronic nicotine exposure on lung function, a determination of the extent to which these effects are reversible, and a beginning understanding of the mechanisms underlying these effects. FUNDING Center-supported project PUBLICATIONS Sekhon HS, Jia Y, Kuryatov A, Cole L, Raab R, Whitsett JA, Lindstrom J, Spindel ER. Interaction of nicotine with nicotinic cholinergic receptors in fetal rhesus monkey lung. Soc Neurosci Abstr 24:335, 1998. Sekhon HS, Jia Y, Kuryatov A, Cole L, Raab R, Lindstrom J, Spindel ER. Interaction between gastrin-releasing peptide (GRP) and nicotine in primate lung development. In National Heart Lung and Blood Institute workshop on Molecular Embryology of the Lung (held in Bethesda, MD, June 1, 1998) (abstract). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ELECTRICAL HETEROGENEITY AND CARDIAC ARRHYTHMIAS Principal Investigator & Institution: Antzelevitch, Charles; Masonic Medical Research Laboratory, Inc 2150 Bleeker St Utica, Ny 13501 Timing: Fiscal Year 2001; Project Start 01-MAY-1993; Project End 31-AUG-2005 Summary: Recent studies by our group and others have demonstrated that ventricular myocardium is not homogeneous as previously thought, but is comprised of at least three electrophysiologically and functionally distinct cell types: epicardium, endocardium and a unique population of cells that we termed M cells, displaying characteristics intermediate between those of ventricular myocardial and Purkinje cells. The three cell types differ with respect to early and late repolarization characteristics. These distinctions have been shown to underlie the various waveforms of the ECG and when amplified create the substrate for the development of life-threatening ventricular arrhythmias, including the polymorphic ventricular arrhythmias associated with the long QT and Brugada syndromes. We and others have recently reported that both syndromes may also be responsible for sudden death in children and infants and may

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contribute at some level to sudden infant death syndrome (SIDS). Our basis for understanding the mechanisms involved are hampered by the near total absence of data regarding the developmental aspects of electrical heterogeneity in ventricular myocardium of larger mammals. An urgent need to close this gap in our knowledge is the motivating force and the principal aim of this competing renewal. Our objectives are to define the developmental stages at which these heterogeneities normally arise in the canine heart and to probe how ion channel defects known to contribute to the long QT and Brugada syndromes may intervene to disrupt the normal electrical function of the heart and set the stage for malignant arrhythmias in the early stages of life. Our principal goals are to probe the extent to which electrical heterogeneity exists within the heart at each stage of development, to identify the underlying mechanisms as well as the conditions and interventions that amplify or diminish the intrinsic differences in regional electrical behavior and to examine to what extent transmural electrical heterogeneity is responsible for developmental changes in the ECG. To achieve these goals, we propose to use a multilevel approach designed to provide and integrate voltage clamp and action potential data from isolated myocytes, tissues and arterially perfused canine ventricular wedge preparations. Our long-range goal is to generate information that will contribute to our understanding of the causes for arrhythmic death in infants and young children. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EXPERIENCE-DEPENDENT STRUCTURAL PLASTICITY IN CNS Principal Investigator & Institution: Martinez, Joe L.; Ewing Halsell Professor of Neuroscience; Biology; University of Texas San Antonio San Antonio, Tx 78249 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-AUG-2004 Summary: A major aspiration of the Division of Life Sciences at the University of Texas at San Antonio (UTSA) is t become a national leader in neurobiology research and training of Hispanics in the next ten years, while fulfilling its regional mission to raise the level of educational achievement of people in South Texas. Th major goal of the Specialized Research Program at Minority institutions (SNRP) at UTSA is to conduct cutting edge collaborative neuroscience research with NIH health relevance, to enhance neuroscience research a he collaborating institutions, and to further the development of an vigorous academic milieu with the strengthening of an existing neuroscience seminar series. The SNRP will inspire students, and minority students in particular, to pursue research careers in neuroscience. A strong External Advisory Committee was chosen to guide the SNRP. All are members of the National Academy of Sciences and one is a Nobel Prize winner. The theme of the SNRP proposals is that experience-dependent changes in neuron morphology alter CNS function in important and exciting ways. For Derrick the addition of new neurons, as in neurogenesis, is measured in new neuron's response to long term potentiation and learning. For Gdovin the developmental changes in neurons or neuron assemblies, are measured in respiratory pace maker cells o pattern generators. For LeBaron changes in extracellular matrix proteins are measured in synaptic plasticity, as in the maintenance of long term potentiation. All of the projects have strong health relevance. Gdovin's collaborator is the James Leiter, Chief, Pulmonary and Critical Care at Dartmouth Medical School, and increased understanding of the development of respiratory oscillators and pacemakers in vertebrates has the potential to impact Sudden Infant Death Syndrome in humans. Derrick's collaborator is Bruce McEwen a Rockefeller University, and increased understanding of the mechanisms of neurogenesis in adult vertebrae brain has the potential to impact a large number of debilitating diseases in humans including any loss

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o unction due to trauma or disease, such as in Parkinson's Disease. LeBaron's collaborator is Joe L. Martinez, r. at UTSA, and increased understanding of how the brain stores information at a cellular level has the potential to suggest therapies for loss of memory function, the most dramatic being Alzheimer's Disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FAS, SIDS AND STILLBIRTHS IN CAPE TOWN, SOUTH AFRICA Principal Investigator & Institution: Jacobson, Sandra W.; Professor; Psychiatry & Behav Neuroscis; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2006 Summary: (provided by applicant):Sudden infant death syndrome (SIDS) is a leading cause of infant mortality with incidence of about 0.8/1000 live births in the U.S. and considerably higher rates in at-risk populations, including Native Americans and the Cape Coloured (mixed ancestry) community in South Africa. A recent study has implicated prenatal alcohol exposure as an important risk factor for SIDS that warrants further investigation. It has been hypothesized that medullary serotonergic network deficits may be responsible, in part, for some SIDS deaths. For the past 5 years, we have been conducting a prospective, longitudinal study on the effects of prenatal alcohol exposure in the Cape Coloured community in collaboration with researchers from the University of Cape Town School of Medicine. This research has demonstrated our ability to recruit mothers from this community; obtain valid assessments of FAS, prenatal alcohol exposure, maternal alcoholism, smoking and depression, and socioenvironmental and medical risk; and perform state-of-the-art infant neurobehavioral assessments with Cape Town infants. We have found an exceptionally high rate of alcohol abuse and dependence among pregnant women in this population and of FAS among their infants. The high incidence of both SIDS and FAS in this large metropolitan area, the readily accessible maternal heavy drinking population, and our established, productive research collaboration make Cape Town uniquely appropriate as a Comprehensive Clinical Site. The proposed cooperative agreement would expand our ongoing collaboration to include researchers in pathology and obstetrics. The aims are (1) to conduct an assessment of the incidence of SIDS and stillbirths in Cape Town, using contemporary diagnostic criteria and procedures, including neuropathological examinations of SIDS victims and controls; (2) to test the hypothesis that prenatal binge drinking increases the risk of SIDS and to evaluate that risk in relation to risks associated with prenatal maternal smoking, preterm birth, infant gender and sleeping position, seasonal variation, parental education, and maternal depression; (3) to test the hypothesis that certain moderator variables-- years of drinking, severity of maternal alcohol abuse and dependence, lower maternal weight and prenatal smoking, and the absence of an ADH2*2 allelo will increase the risk of SIDS in alcohol-exposed infants; and (4) to examine whether heavily alcohol-exposed neonates will exhibit alterations in autonomic nervous system behaviors similar to those described in SIDS victims, which are known to be regulated by the medullary serotonergic system, including arousal, cardiorespiratory reflex integration, and sleep/wake patterns. This research has the potential to improve our understanding of neurophysiological mechanisms involved in SIDS and to contribute to developing interventions for mothers and infants whose behaviors indicate that they are at risk for this adverse outcome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: FETAL NEURODEVELOPMENT--EFFECTS OF NICOTINE AND HYPOXIA Principal Investigator & Institution: Stark, Raymond I.; Professor; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2001 Summary: Prenatal exposure to nicotine through maternal smoking leads to alterations in fetal responses related to arousal and cardiorespiratory control far beyond the period of exposure. The drug pets fetuses at increased risk for growth restriction, prematurity, perinatal complications and after birth, for the Sudden Infant Death Syndrome, behavioral and learning disabilities, and attention deficit disorders; while the adolescent female offspring may be at increased risk for becoming smokers themselves. By hypoxia and direct effects of nicotine on fetal neurodevelopment have been implicated as mechanisms for this array of consequences. Our overall hypothesis is that excessive and untimely stimulation of fetal nicotinic receptors by nicotine induces wide ranging structural and functional changes in the developing nervous system leading to alterations in central regulatory mechanisms controlling autonomic and behavioral functions. While fetal regulatory mechanisms adapt to chronic nicotine exposure to maintain a relatively "normal" physiology, hypoxic stress will reveal deficiencies in physiologic competence. These structural functional alterations, established in utero produce a "vulnerable" newborn who will have a life long risk for stress related pathologies. To test these hypotheses, we will compare key markers of neurophysiologic function (coordinated fetal states, response to hypoxia and baroreceptor gain) in nicotine exposed fetuses with controls and relate their functional impairments to structural differences in brainstem and forebrain arousal and cardiorespiratory centers. Studies are carried out in a unique chronically instrumented baboon model. The homologies in neurodevelopment between the human and baboon fetus make knowledge gained from this research relevant to identifying high risk fetuses and infants. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GENE THERAPY FOR LUNG AND CARDIOVASCULAR DISEASE Principal Investigator & Institution: Muzyczka, Nicholas; Professor; Molecular Genetics & Microbiol; University of Florida Gainesville, Fl 32611 Timing: Fiscal Year 2002; Project Start 30-SEP-1997; Project End 31-AUG-2003 Summary: The long-range goal of this Program Project is to develop viral vector-based gene transfer strategies for treating genetic aqnd acquired cardiopulmonary disorders. To this end, a group of investigators with diverse, yet complementary, interdisciplinary interests and expertise and expertise has established an integrated research effort that is underscored by a common interest in practical applications of gene therapy. A major focus of the Program is the development of improved methods for gene transfer using recombinant AAV (rAAV) and lentivirus vectors. Project 3 (Muzyczka) will focus on the basic changing viral tropism through the insertion of foreign ligands into the capsid gene. Project 4 (Chang) will investigate ways of improving lentiviral vector yields and study the biodistribution of lentiviruses. Along with the vector development components, there is an emphasis on solving practical issues related to gene therapy for diseases of the heart and muscle. Project 2 (Flotte) focuses on genetic disorders of betaoxidation of fatty acids within the mitochondria. Disorders of mitochondrial fatty acid oxidation (FAO) as a group represents a relatively common class of metabolic disorders, the most common of which typically present with either Sudden Infant Death

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Sudden Infant Death Syndrome

Syndrome (SIDS) or with a combined cardiac and skeletal myopathy. The recent development of rAAV vectors for highly efficient transduction of hepatocytes and myofibers present new tools for the study of FAO disorders and project 2 will focus on short-chain acyl CoA dehydrogenase (SCAD) and long chain acyl CoA dehydrogenase (LCAD) defects, whose deficiency results in myopathy. Project 1 (Byrne) will focus on a deficiency in the lysosomal enzyme, acid alpha-glucosidase (GAA). This enzyme deficiency leads to glycogen accumulation in lysosomes of striated muscle, and in the infantile form, affected infants die of heart failure within the first year of life. Project 1 will focus on the development of alternative rAAV serotypes and targeted vectors to improve the efficiency and distribution of gene delivery for this disease. In addition, outcomes of vector distribution and biochemical effect will be tested by new MRI/MRS techniques. To assist the projects, the Program has established a Vector Core Laboratory and a Pathology Core. The Vector Core will supply vectors of uniform and reproducible quality6 to all subprojects, and investigated improved methods of generating rAAV. The Pathology Core (Core C) will carry out biodistribution and toxicology studies for all subprojects. Finally, an Administrative Core (Core A) will insure centralized fiscal management and oversight for the subprojects. The Cores will also serve as a mechanism to insure rapid exchange of information among all subprojects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETIC DETERMINANTS OF SUDDEN CARDIAC DEATH Principal Investigator & Institution: Albert, Christine M.; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 05-JUL-2003; Project End 30-JUN-2007 Summary: (provided by applicant): Sudden cardiac death (SCD) affects 400,000 individuals each year in the U.S. alone. Over half have no evidence of heart disease prior to death, and our ability to identify those at risk and therefore prevent SCD is poor. Mutations in cardiac ion channel genes including SCN5A, KVLQT1, HERG, KCNE1, KCNE2, and RyR2 have been implicated in monogenic traits with a high risk of SCD, such as the Iong-QT, Brugada, sudden infant death syndrome, and catecholaminergic polymorphic ventricular tachycardia. Alterations in ion channel function can result in life-threatening ventricular arrhythmias in diverse disease states. Therefore, sequence variants in these genes that alter function or transcription of these ion channels may confer a predisposition to ventricular arrhythmia and SCD in broader populations. This research program proposes to determine if sequence variants in the above candidate genes are associated with an increased risk of SCD in apparently healthy populations. Cases of SCD will be assembled from five NIH-funded prospective cohorts with a total of 106,314 individuals with existent blood samples. All cohorts are exceptionally wellcharacterized with respect to environmental exposures and have collected medical records on cardiovascular endpoints. We will characterize all coding sequence variation and selected non-coding sequence variation among 100 cases and controls from these cohorts. Using these novel markers, we will define the haplotype block structure (SNPs in linkage disequilibrium) for the six genes. We will then employ a nested case-control design and conditional logistic regression to test for associations between haplotypes (haplotype tag SNPs) in both coding and non-coding regions and SCD risk. We will also test directly for associations between single loci that may have functional significance and SCD risk. An estimated 600 cases of well-documented SCD will be confirmed over the first three years of the grant period, and these cases will be matched on age, sex, ethnicity, and geographic location to two control subjects from the same cohort. In addition, based upon known sex-differences in the phenotypic expression of the

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candidate genes in the primary arrhythmic disorders, we will specifically examine sexdifferences in the risk of SCD associated with sequence variation in these genes. The findings generated will have substantial implications for our understanding of the SCD syndrome and risk stratification in the general population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETIC MOUSE MODELING OF MEDULLARY SEROTONERGIC DEVELOPMENT Principal Investigator & Institution: Dymecki, Susan M.; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2003; Project Start 07-JUL-2003; Project End 31-MAR-2008 Summary: Penetrating investigations into the pathogenesis of neurological SIDS have implicated a developmental defect in the medullary serotonergic (5-HT) system, defined as an interrelated group of 5-HT and non-5-HT neurons centered around the medullary raphe. Unfortunately, littte is known about the molecules during differentiation of these neurons and how their development is affected by environmental SIDS risk factors information that is critical for determining the etiology of SIDS. To help fill this void, studies proposed in Project 6 focus on testing in mice the hypotheses that neurons of the medullary 5-HT system come from the rhombic lip; that their identities are specified, at least in part, as precursor cells in the rhombic tip, and that abnormalities in these early specification events underlie the medullary dysfunction associated with SIDS. In aim 1, we use a unique set of generic tools to establish that neurons of the medullary 5-HT system come from the rhombic lip; indeed, our preliminary fate maps indicate this is the case. We extend these analyses to characterize the dispersion of 5-HT system neurons from the rhombic lip and map their acquisition of different neurochemical identities. In most neuroepithetia, including the rhombic lip, the potential to give rise to different neuron types appears to change over time, with restrictive events occurring in the dividing progenitor cells themselves. Thus, at distinct developmental stages a given neuroepithelium is multipotent but not equipotent, presumably due in part to temporal changes in intrinsic regulators. To identify such regulators in the rhombic lip, in aim 2, we perform whole-genome expression studies of rhombic lip tissue at sequential developmental stages corresponding to its peak production times of different brainstem neurons. By comparing mRNA profiles across time points, we will identify gene sets associated with neuron subtype production. To further sift from these gene sets the best candidate regulators for future functional studies, we perform similar analyses on tissue from mice null for Pax6, a transcription factor required for producing a subset of rhombic-lip derivatives and an established regulator of CNS fate. From this, we identify mRNAs dependent on Pax6 and which may be important for a subset of 5-HT-system specification events. In aim3, we determine if prenatal exposure to nicotine (a major component of cigarette smoke and proven neuroteratogen) alters development of the 5HT system in ways that may explain the increased risk for SIDS following maternal smoking. Completion of these aims will provide a comprehensive molecular basis for delineating brainstem development and for identifying mechanisms underlying SIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: HYPERTHERMIC RESPONSE OF THE RESPIRATORY NEURAL NETWORK Principal Investigator & Institution: Tryba, Andrew K.; Organismal Biology and Anatomy; University of Chicago 5801 S Ellis Ave Chicago, Il 60637

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Sudden Infant Death Syndrome

Timing: Fiscal Year 2001; Project Start 01-JUN-2001 Summary: (Applicant's abstract): Breathing is modulated as the result of changes in the internal and external environment (e.g. ionic concentration, pH, pCO2 and temperature) and the behavioral state of the animal. In response to these challenges, respiratory neural network activity is modified to affect the timing and intensity of respiratory events. While these changes are specific to respiration, the issue of how neural networks adapt a behavior during environmental changes is of interest to those studying many motor systems. In mammals, hyperthermia causes an initial increase in respiration frequency (RF) that serves to enhance heat loss through evaporative cooling, but heat loss mechanisms are not always effective. For example, hyperthermia associated with conditions such as fever and heat-stroke may lead to cardiac arrest, cessation of breathing (apnea) and death. In fact, hyperthermia is a major risk factor for sudden infant death syndrome. Despite these implications, little is known about the neural mechanisms underlying the temperature-induced changes in respiratory activity. In this proposal: 1) I will determine the effects of hyperthermia on respiratory activity generated in the isolated brain-stem respiratory neural network. The response of the pre- Botzinger Complex (pBC) respiratory network to hyperthermia will be characterized by integrating population pBC neural activity and quantifying changes in RF. 2) I will use patch-clamp recordings from pBC neurons to test whether changes in RF during hypothermia result from modulation of pacemaker neurons or the emergent properties of the respiratory neural network. 3) I will also use patch-clamp recordings from pBC neurons to examine if membrane properties and/or synaptic inputs in respiratory pacemaker neurons are modulated during hypothermia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HYPOXIA AND CONTROL OF FETAL BREATHING MOVEMENTS Principal Investigator & Institution: Koos, Brian J.; Professor; Obstetrics and Gynecology; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-AUG-1985; Project End 30-NOV-2003 Summary: Hypoxia abolishes fetal breathing (FB) through a direct effect of low P02 on the brain. We have recently shown that the parafascicular nuclear complex (Pf) in the thalamus is critically involved in hypoxic depression of FB, leading to a new paradigm regarding the neural substrate mediating hypoxic inhibition. The proposed studies in fetal sheep have four goals: 1) To determine the role of Pf in the second- phase reduction in ventilation in newborns, which undoubtedly involves the same central mechanism that mediates hypoxic inhibition of FB. Hypoxic inhibition of FB will be abolished by selectively destroying fetal Pf neurons with subsequent testing of newborn respiratory responses to hypoxia. The large size of the near-term fetal sheep brain will greatly facilitate the identification of the neural substrate mediating ventilatory "roll off" during hypoxia in the newborn. 2) To identify the Pf neural pathways involved in inhibition of FB. The lipophilic dye DiI will enable anterograde and retrograde labelling of fiber tracts which will determine the connections of these cells and thus help establish the neural network involved in hypoxic inhibition. Distinct advantages of DiI include its applicability to postmortem tissue and optimum efficiency in perinatal brains. 3) To determine the mechanism of hypoxic inhibition. Increased brain adenosine (ADO) concentrations, derived from hydrolysis of extracellular adenine nucleotides, mediate hypoxic inhibition of FB. Microdialysis with a novel inhibitor of extracellular ATPase will establish whether extracellular ATP is an essential precursor for the hypoxiainduced rise in ADO. 4) To identify the locus of ADO receptors that mediate hypoxic

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inhibition of FB. ADO receptor agonists and antagonists will be microinjected into Pf to determine whether ADO A1 or A2 receptors in or proximate to this sector inhibit FB during hypoxia. Hypoxic inhibition appears to be part of a survival mechanism whereby O2 that would otherwise be used for breathing is made available to vital organs, especially the heart and brain; thus it has relevance to hypoxia-induced perinatal brain damage. Such injury may predispose infants to Sudden Infant Death Syndrome (SIDS) by increasing the depressing effects of hypoxia on ventilation and by altering sleep state regulation of breathing postnatally. Thus, these studies on hypoxic inhibition should provide insight into mechanisms of SIDS and enhance our understanding of the clinically important transition of neural control of respiration in the perinatal period. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HYPOXIC EFFECTS ON MAMMALIAN RESPIRATORY NEURAL NETWORK Principal Investigator & Institution: Ramirez, Jan M.; Associate Professor; None; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2003; Project Start 07-DEC-1998; Project End 31-JAN-2007 Summary: (provided by applicant): The sudden infant death syndrome (SIDS) remains the leading cause of postnatal infant mortality in the USA. Increasing evidence indicates that SIDS is due to a failure of autoresuscitation, which is a protective brainstem response to asphyxia or severe hypoxia. An essential mechanism for autoresuscitation is gasping, a respiratory motor pattern which is distinct from the normal respiration occurring in normoxia. However, despite considerable relevance, the question how gasping is generated by the nervous system remains largely unknown. Transections at the pontomedullary junction transforms the motor pattern for normal respiration into gasping (Lumsden, 1923), which suggested to some researchers that different forms of breathing are generated by separate "centers" and that gasping is generated in the medulla. Using a slice preparation from the medulla of mice we demonstrated that the isolated respiratory network in the pre-Botzinger complex (PBC) generates not only one, but three forms of fictive respiratory activities with striking similarities to normal respiratory, sigh and gasping activity. Like in vivo, these three activities are generated in a stereotypic manner during the response to anoxia: An initial augmentation in the frequency of normal respiratory and sigh activities is followed by a depression and the generation of gasping. Our network characterization indicates that all three activities are generated by the reconfiguration of the same neuronal network located within the PBC. The proposed research aims at examining the cellular mechanisms that lead to the reconfiguration of the respiratory network. We specifically test the hypothesis that the transition from normal respiratory activity into gasping is associated with a change in the organization of the respiratory network: In normal respiratory activity pacemaker neurons are fully integrated in a network of inhibitory and excitatory non-pacemaker neurons. In gasping most nonpacemaker and calcium-dependent pacemaker neurons inactivate and only a small population of pacemaker neurons remains active that become essential for rhythm generation. We propose three Aims to examine this hypothesis: Aim 1 compares the synaptic modulation of pacemaker and non-pacemaker neurons, Aim 2 investigates the differential modulation of ion channel properties in pacemaker and non-pacemaker neurons and Aim 3 proposes connectivity experiments to directly test the anoxia-induced changes in the network organization. By bridging different levels of integration the proposed research will lead to a better understanding of the neuronal mechanisms that underlie normal respiratory and gasping activities. Understanding how anoxia leads to the reconfiguration of neuronal network activity is

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Sudden Infant Death Syndrome

of great general interest as every year numerous victims suffer brain damage from hypoxic insults. In the context of SIDS, our research may ultimately lead to a better understanding why certain infants fail to autoresuscitate. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HYPOXIC RESPONSES OF MEDULLARY CARDIORESPIRATORY NEURONS Principal Investigator & Institution: Neubauer, Judith A.; Associate Dean for Research; Medicine; Univ of Med/Dent Nj-R W Johnson Med Sch Robert Wood Johnson Medical Sch Piscataway, Nj 08854 Timing: Fiscal Year 2001; Project Start 01-JUL-1997; Project End 30-JUN-2003 Summary: The respiratory response to hypoxia reflects the integration of peripheral stimulation of carotid chemoreceptors and the modulation of the respiratory neuronal network by the effects of central hypoxia. The effect of central hypoxia on the net integrated respiratory output is determined by the summation of the inhibitory and excitatory effects of CNS hypoxia. Although the predominant effect of brain hypoxia is to cause a reduction in neuronal excitability, recent work suggests that there may be unique sites within the brain that are directly stimulated by hypoxia. For example, while respiratory premotor ventral respiratory group (VRG) neurons are depressed by hypoxia, sympathoexcitatory and pre-Botzinger respiratory-related neurons in the rostral ventrolateral medulla (RVLM) have been shown to increase their activity in response to local hypoxia. The cellular events that distinguish these two contrasting neuronal responses to hypoxia have not been defined. The studies outlined in this application will investigate the mechanisms underlying these responses in retrogradely labeled (fluorescent latex beads) premotor VRG (hypoxia- depressed) and RVLM (hypoxia-excited) neurons dissociated and cultured from neonatal rats using perforated patch clamp recording techniques to identify the ionic currents that distinguish the different membrane responses of these excited and depressed neurons. Identification of the ionic changes that characterize these neuronal responses to hypoxia will then allow us to explore the cellular mechanisms important for transduction of the hypoxic signal in RVLM oxygen sensing neurons. Since heme oxygenase (HO) has been shown to be an important factor in the oxygen in the oxygen sensing mechanism of excitation of the carotid body and we have found that HO is expressed in the RVLM, we will also test the hypothesis that activation of HO is important for oxygen sensitivity of RVLM neurons. Hypoxic excitation of central cardiorespiratory neurons promotes an effective autoresuscitative response (in the form of intense sympathetic discharge synchronized with respiratory gasping)which may be critical for surviving life-threatening hypoxic events. In fact, failure to gasp has been proposed as a potential cause of sudden infant death syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: INFLUENCE OF THE VENTRAL MEDULLA ON REFLEX RESPONES TO STIMULATION Principal Investigator & Institution: Leiter, James C.; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001 Summary: We propose that the sudden infant death syndrome (SIDS) results when an infant when a neuronal vulnerability is exposed to an exogenous stressor at a critical time in development. The arcuate nucleus in humans, and homologous structures in the

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piglet- the retrotrapezoid nucleus, parapyramidal neurons, caudal raphe and chemoreceptor regions along the rostral and caudal surface of the ventral medulla-are possible sites of neuronal vulnerability. The exogenous stressor may be stimulation of facial or upper airway receptors or compression of the chest. These exogenous stressors inhibit respiration and may promote cardiovascular instability, but normal protective responses arising from asphyxia (hypoxia and hypercapnia) oppose the effect of these stressors, increase breathing, stabilize blood pressure, promote arousal, which alleviates inhibitory influences on respiration and may lead to postural changes that relieve asphyxia. Disruption of the arcuate neurons or the piglet homologue diminishes or eliminates protective responses, permits the unfettered actions of stimuli inhibiting respiration and may make a fatal outcome more likely. Specific Aim 1: In the decerebrate piglet at different developmental ages, we will examine the effect of lesions in the piglet homologue of the arcuate nucleus on ventilatory and cardiovascular responses (phrenic nerve activity, heart rate and blood pressure) during stimulation of the trigeminal or superior laryngeal nerve or stimulation of a now intercostal nerve during hypercapnia or hypoxia. Specific Aim 2: In decerebrate piglets at the developmental age most susceptible to disruption of protective responses we will examine the role of muscarinic, ionotropic glutamate and thyrotropin releasing hormone receptors in brainstem regions homologous to the arcuate nucleus on ventilatory and cardiovascular responses as in Specific Aim 1. Specific Aim 3: We will examine the effect of chronic lesions in the homologue of the arcuate nucleus on ventilatory and cardiovascular responses during stimulation of the trigeminal, superior laryngeal and intercostal nerves in unanesthetized piglets during room air exposure, hypercapnia or hypoxia during wakefulness and sleep (NREM and REM). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INTERMOUNTAIN CHILD HEALTH SERVICES RESEARCH CONSORTIUM Principal Investigator & Institution: Young, Paul C.; Pediatrics; University of Utah Salt Lake City, Ut 84102 Timing: Fiscal Year 2003; Project Start 30-SEP-2001; Project End 29-SEP-2006 Summary: (provided by applicant): The goal of the Intermountain Consortium for Child Health Services Research is to launch nationally competitive research in Utah and the Intermountain West to inform the design and delivery of optimal care for children, especially those with special health care needs. The Consortium will achieve this goal by building upon the investments and accomplishments of its first two years of development. Our new objectives include completing critical components of infrastructure building, adding to the current pool of investigators through faculty development and recruitment, and conducting research projects leading to significant extramural funding. By the end of the funding period, the applicants will have a substantial and sustainable infrastructure, new key personnel, and a pool of experienced mentors, advisors, and collaborators. Their 5-year vision is that of an effective pediatric health services research program and an environment that facilitates vibrant exchange between research and practice. Our specific aims for the next three years are to: 1) Expand the Intermountain Consortium for Child Health Services Research and strengthen relationships among partners; 2) Create a Research Resource Office to coordinate and integrate health services research, clinical research, and projects designed to translate research into practice; 3) Increase the number of independent, productive health services researchers in the Intermountain West by training and supporting existing faculty and by recruiting additional faculty with training in health

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Sudden Infant Death Syndrome

services research; and 4) Complete two individual pilot research projects. Two Faculty Development Scholars will lead these studies. The first, "Measurement and Prevalence of Deformational Plagiocephaly", will validate a measure and determine the prevalence of a rapidly increasing phenomenon, flattening of the head in infancy associated with positioning to prevent sudden infant death syndrome. The second, "Use and Allocation of Home Health Care Services", will provide an analysis of pediatric home health care for children with special health care needs. These projects will provide publishable, preliminary data for grant applications for a collaborative intervention study and for a career development award. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INTRACELLULAR CHEMORECEPTORS

PH

RESPONSES

OF

CENTRAL

Principal Investigator & Institution: Putnam, Robert W.; Professor; Physiology and Biophysics; Wright State University Colonel Glenn Hwy Dayton, Oh 45435 Timing: Fiscal Year 2001; Project Start 01-JUL-1997; Project End 31-JUL-2005 Summary: Increased CO2 (hypercapnia) is a major stimulus for increased respiration and blood pressure. This pathway for cardiorespiratory control involves specialized central neurons, called chemosensitive neurons, that sense hypercapnia, but the cellular mechanisms that transduce hypercapnia into an increased neuronal firing rate are not well understood. Our work will involve the study of individual neurons from at least two chemosensitive brainstem areas (locus coeruleus and either nucleus tractus solitarius or ventrolateral medulla) and at least one nonchemosensitive area (either inferior olive or hypoglossal nucleus) using slices from neonatal rat brains. Simultaneous measurements of neuronal membrane potential (Vm) and intracellular pH (pHi) will be achieved using perforated patch recordings or whole cell recordings (WCR) combined with pH- sensitive fluorescent dyes and fluorescence imaging microscopy. Our first aim is to identify the signal pathways that transduce hypercapnia into an increased firing rate. It will consist of 4 separate aims: i) study the roles of molecular CO2, external pH (pHO) and pHi as the proximate signal of chemoreception by exposing neurons to solutions that vary in each of these parameters; ii) examine the phenomenon of "washout", whereby the Vm response to hypercapnia is lost during WCR measurements, to see if additional signal molecules (e.g. Cai, polyamines or carbonic anhydrase) are also involved in chemoreception; iii) study the "hypoxia paradox" (hypoxia-induced acidification does not appear to increase firing rate in chemosensitive neurons) to see if it is due to the lack of additional signal molecules; and iv) study the changes in the Vm and pHi response to hypercapnia in chemosensitive neurons from rats with reduced chemosensitivity (induced by chronic exposure to hypercapnia). Our second aim is to study the effects of the signals, identified in Aim 1, on various K+ channels and determine the role of each of these channels in modifying the shape of the action potential and neuronal firing rate. Three K+ channels will be studied: i) inward rectifying K+ channels, important in determining the slope of the interspike depolarization and thereby the firing rate of the neuron; ii) Ca2+-activated K+ channels, important in determining the shape of the action potential and the magnitude of the after hyperpolarization; and iii) TWIK-related acid sensitive K+ channels (TASK), important in determining the resting Vm. This work should indicate the precise nature of the proximate signal of chemosensitivity, elucidate the way in which hypercapnic stimuli affect various K+ channels and give insight into how these effects are integrated to result in the final neuronal response. Further, by comparing the findings in neurons from 2 chemosensitive areas, our findings should help clarify why there are numerous

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chemosensitive regions in the brainstem. These studies will contribute to our understanding of respiratory diseases thought to be due in part to central chemoreceptor dysfunction, such as sudden infant death syndrome (SIDS) and central alveolar hypoventilation syndromes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISM OF CARDIORESPIRATORY RHYTHM IN NEONATES Principal Investigator & Institution: Mendelowitz, David S.; Professor; Pharmacology; George Washington University 2121 I St Nw Washington, Dc 20052 Timing: Fiscal Year 2002; Project Start 01-APR-1998; Project End 31-MAR-2007 Summary: (Provided By Applicant) The neural control of the cardiovascular and respiratory systems is highly interrelated. During each respiratory cycle, the heart beats more rapidly in inspiration and slows during post-inspiration, which is referred to as respiratory sinus arrhythmia. This cardio-respiratory interaction occurs within the central nervous system and is mediated largely, if not entirely, via the parasympathetic innervation of the heart. Respiratory sinus arrhythmia is diminished in many disease states and it has been speculated that an abnormality of cardio-respiratory control may be involved in sudden infant death syndrome (SIDS). This proposal is a logical extension of the results obtained during the previous funding period and will build a unifying framework that identifies the neurons and mechanisms responsible for respiratory modulation of cardiac parasympathetic vagal activity. We will use a novel in-vitro preparation that maintains rhythmic respiratory activity with an innovative transsynaptic virus that evokes expression of green fluorescent protein (GFP) that identifies neurons that project to cardiac vagal neurons in-vitro without altering their electrophysiological properties. Specifically, we will test whether cardiac vagal neurons are inhibited during inspiration by an increased frequency of inhibitory GABAergic inputs, and that the increased GABA frequency is mediated by activation of presynaptic nicotinic receptors. We will also test the hypothesis that cardiac vagal neurons are directly excited during post-inspiration via electrical synapses which can be abolished by gap junction blockers. Furthermore, we will identify and characterize the rhythmic respiratory activity of the neurons that synapse upon, and make gap junction contacts with, cardiac vagal neurons. This work will not only address hypotheses fundamental to understanding the basis and mechanisms of cardiorespiratory rhythms in the neonatal rat that originate in the medulla, but will also suggest which receptors and processes could be altered in diseases of the cardiorespiratory system such as SIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: EXCITATION

MEDULLARY

MECHANISMS

OF

HYPOXIC

RESPIRATORY

Principal Investigator & Institution: Solomon, Irene C.; Assistant Professor; Physiology and Biophysics; State University New York Stony Brook Stony Brook, Ny 11794 Timing: Fiscal Year 2001; Project Start 01-SEP-2000; Project End 31-JUL-2004 Summary: (Applicant's abstract): Severe brain hypoxia results in respiratory and sympathetic excitation. Respiratory excitation takes the form of gasping which is characterized by an abrupt onset, short duration, high amplitude burst of activity, associated exclusively with inspiratory discharge. Survival during hypoxia exposures appears to be critically dependent upon this integrated cardiorespiratory reflex which has been referred to as "autoresuscitation", and is associated with rapid reoxygenation of arterial blood and restoration of blood pressure. Failure to gasp has been proposed as a

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potential cause of sudden infant death syndrome. The principle hypothesis of this proposal is that the putative respiratory pacemaker is located in the pre-Botzinger complex (the proposed locus of respiratory rhythm generation; pre-BotC), is hypoxia chemosensitive, and when released from strong GABAergic inhibition, exhibits chemosensitivity to systemic hypoxia over the range associated with chemoreception of the carotid bodies. Additionally, we propose that both disinhibition of GABA" ?receptors and direct hypoxic excitation of neurons (i.e., hypoxic chemosensitivity) located in the pre-BotC play complimentary roles in the genesis of hypoxia related gasping. The goal of the experiments proposed in this application is to examine the roles of direct hypoxic excitation of pre-BotC neurons, GABAergic disinhibition of pre-BotC neurons, and ionotropic excitatory amino acid (EAA) receptor activation of pre-BotC neurons as potential mechanisms for the respiratory excitation seen during gasping in response to severe brain hypoxia. Microinjection of neurotransmitter agonists and antagonists in conjunction with whole nerve and medullary single unit extracellular recordings will be used. Experiments will be conducted in both decerebrate and chloralose-anesthetized, vagotomized, deafferented, paralyzed, and ventilated cats. The specific aims are: (1) test whether pre-inspiratory (I-driver) neurons located in the preBotC are activated by focal hypoxia, and whether focal hypoxia phase shifts and synchronizes other respiratory-modulated subtypes or respiratory neurons located in the pre-BotC to a gasp-synchronous discharge, (2) test whether pre-inspiratory (I-driver) neurons located in the pre-BotC are activated during severe systemic hypoxia phase shifts and synchronizes other inspiratory-modulated subtypes of respiratory neurons located in the pre-BotC to a gasp-synchronous discharge, (3) test whether GABA" mediated disinhibition neurons located in the pre-BotC plays a facilitatory role in the production of respiratory excitation seen during hypoxia, and (4) test whether ionotropic EAA receptor activation of neurons located in the pre-BotC plays a modulatory role in the respiratory excitation seen during hypoxia-induced gasping. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MEDULLARY THERMOREG

SEROTONERGIC

INVOLVEMENT

IN

SLEEP,

Principal Investigator & Institution: Darnall, Robert A.; Professor; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2003; Project Start 07-JUL-2003; Project End 31-MAR-2008 Summary: The important findings that a substantial subset of SIDS infants have decreases in serotonin receptor binding the ventral medulla form the basis for the hypothesis that abnormalities in the 'medullary 5-HT system' play an important rote in SIDS. Neurons in this region participate in widespread autonomic functions including cardiorespiratory control, thermoregutation, and based on recent new information from our laboratory, sleep. The overall aim of this proposal is to investigate the roles of phenotypically specific neurons in the medullary 5-HT system on sleep homeostasis, responses to a thermal stress, and on cardiorespiratory variability. Our strategy will be to use novel neurochemicals to locally inhibit or destroy serotonergic neurons and/or neurons expressing the 5-HT(1A), NK1, or m1 muscarinic receptor in chronically instrumented piglets. 8-OH DPAT will be used to selectively activate 5-HT(1A) autoreceptors on 5-HT neurons, and 5,7-DHT or the neurotoxin saporin conjugated to an antibody to the serotonin transporter protein (SERT-SAP) will be used to selectively destroy serotonergic neurons. Analogous methods will be usedto inhibit or destroy neurons expressing the NK1 or m1 muscarinic receptor with SP-SAP or a powerful toxin obtained from the venom of the green mamba highly selective for m1 muscarinic

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receptors (m1-toxin1). We will evaluate the effects of these specific 'lesions' on sleep architecture in piglets using EEG wavelet analysis and behavioral observations during short (6 hr) plethysmograph recordings, and long (12-24 hr) recordings in their natural habitat (with the sow and siblings) using telemetry. We will also evaluate responses to thermal stresses focusing on shivering and non-shivering thermogenesis, skin blood flow, and hyperpnea. Finally, we will use the sensitive techniques of fractal analysis to evaluate the complexity of cardiorespiratory variability, the decrease in which is associated with decreased ability of a control system to respond to a perturbation. Indeed, infants who subsequently die of SIDS have decreases in heart rate variability. Lesions will be made in the midline and lateral columns and all areas simultaneously to test the hypothesis that neurons are organized in a functionally specific manner. We hypothesize that the medullary 5-HT system is a major site for the integration of cardiorespiratory, thermoregulatory, and sleep and arousal mechanisms, and that abnormalities in this region could produce local or widespread effects that might contribute to sudden death. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MOLECULAR STRUCTURE OF THE 900 KD BOTULINUM NEUROTOXIN COMPLEX Principal Investigator & Institution: Stevens, Raymond C.; University of Calif-Lawrenc Berkeley Lab Lawrence Berkeley National Laboratory Berkeley, Ca 94720 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2002 Summary: Botulinum neurotoxin complex serotype A is a 900 kiloDalton (kDa) protein produced as one of eight serotypes (A-G) by the anaerobic bacterium Clostridium botulinum. Among the most potent biological toxins known to man, botulinum neurotoxin causes inhibition of synaptic vesicle release at the neuromuscular junction resulting in flaccid paralysis and ultimately death. Botulinum neurotoxin type A (BoNT/A) is a potent disease agent in both food-borne botulism and Sudden Infant Death Syndrome (SIDS), an established biological weapon, and a novel therapeutic in the treatment of involuntary muscle disorders. Previously, we have determined the 3-D structure of the 150 kDNA neurotoxin component of the 900 kDa complex by x-ray crystallography. We have also completed antibody mapping experiments to determine how the 150 kDa neurotoxin is bound into the 900 kDa toxin complex. We have conducted a series of biophysical stability experiments in order to understand how the two assemblies (150 kDa toxin and 750 kDa non-toxic component) combine and stabilize the 900 kDa complex. Lastly, based on the work above, and preliminary electron microscopy work, we are designing an alternative vaccine strategy for botulism. Current vaccine programs for botulism are not very effective. The preliminary objective of this proposal is to obtain a three- dimensional structure of the 900 kDa botulinum neurotoxin complex, and understand how the neurotoxin component fits into the complex. To accomplish this goal, we will use a 2-D crystals of the 900 kDa complex to conduct 3-D image reconstruction experiments. We have already obtained 2-D crystals of the 900 kDa complex to conduct 3-D image reconstruction experiments. We have already obtained 2-D crystals of the 900 kDa complex that diffract weakly to 14 Angstroms resolution in negative strain, and a density projection map has been produced at 30 Angstroms resolution. Based on the crystal quality and the frequency with which defects were observed in the crystals used in our earlier investigation, it appears as though much higher quality crystals can be obtained. Specifically, our transfer technique is presently crude due to our new venture into this area of research, and several suggestions have been made by other program project members on how to

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Sudden Infant Death Syndrome

improve our transfer techniques. We are also investigating alternative buffer conditions to help stabilize the protein further. Once optimization of the 2-D crystals has been completed, we will complete the negative stain work at the maximum resolution possible using data collection in a tilt series followed by 3-D image reconstruction. This work will be followed by attempting higher resolution studies with cryo-techniques. We will crystallize the 900 kDa complex in the presence of scFv antibody molecules that have a high affinity for exposed regions of the neurotoxin when bound to the 900 kDn complex. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MONITORING A SIDS MODEL IN NEONATAL SWINE Principal Investigator & Institution: Sica, Anthony L.; Physiology and Pharmacology; Suny Downstate Medical Center 450 Clarkson Ave New York, Ny 11203 Timing: Fiscal Year 2001; Project Start 30-SEP-1991; Project End 30-JUN-2003 Summary: The long-term objective of the proposed research is to evaluate the role of cardiac mechanisms in the etiology of sudden death in the Sudden Infant Death Syndrome (SIDS). Thus this project is directly related to a problem in infant survival and health. The specific aims of the proposed research are designed to test the hypothesis that a developmental anomaly in cardiac innervation could reduce ventricular electrical stability and favor the onset of sudden cardiac death. The research design and surgical methods have been worked out in the previous grant period; newborn swine with surgically induced imbalance in cardiac autonomic innervation will be continuously monitored (24 hrs.) throughout eight postnatal weeks. Those surviving and similarly surgically prepared littermates will be tested (at ages 2,4,6,8 wks) for cardiovascular responses to: (i) hypoxia, (ii) hypercapnia, (iii) stimulation of cardiopulmonary receptors, and (iv) alterations in baroreceptor afferent inputs. Results obtained from study of these possible precipitating factors should reveal the increased susceptibility of the neonate at risk for sudden death. Sleep is the predominant behavioral state of the neonate and ontogeny of EEG sleep in neonates can be monitored by serial EEG recordings. We plan to examine ECG recordings as a function of state determined by VCR tapes of behavior, diaphragmatic EMG and EEG, and correlate these variables against both age and type of denervation. Nonlinear analysis of heart rate variability in infants has revealed an increase in complexity with maturation and our own results included similar findings in piglets. This grant proposal would pursue these findings and the effects of selected cardiac denervation on this complexity, correlating results with sudden death in denervated piglets. Such studies should confirm our working hypothesis regarding the importance of cardiac innervation in the etiology of sudden death in infants. We are, therefore, postulating an abnormality at the effector level, i.e., at the cardiac level, specifically: maturation of the normal innervation of the heart and its reflex control. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: BRAINSTEM

MU

OPIOID

RECEPTOR

REGULATION

IN

NEONATAL

Principal Investigator & Institution: Olsen, George D.; Professor; Physiology and Pharmacology; Oregon Health & Science University Portland, or 972393098 Timing: Fiscal Year 2003; Project Start 15-DEC-1993; Project End 31-MAR-2007 Summary: (provided by applicant): The long-term goal of the proposed research is to understand mechanisms by which chronic in utero morphine and methadone exposure

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affect regulation and function of mu opioid receptors (MOR) in respiratory control areas of newborn brainstem. Respiratory depression is induced by endogenous opioid peptides and exogenous opioids that activate MOR. A critical brainstem site for these effects is the nucleus tractus solitarius (NTS), which integrates sensory signals and drives respiratory muscles. Profound disturbance of neonatal breathing is a welldocumented consequence of maternal opioid abuse. These neonates exhibit withdrawal hyperventilation and an increased incidence of sudden infant death syndrome (SIDS). The proposed studies are essential for understanding normal respiratory development, drug-induced changes, and effective treatment of pregnant heroin addicts and methadone maintained patients. The exact role of NTS MOR in neonatal congenital narcotic dependence and these respiratory disturbances is unknown. For anatomical, physiological, and pharmacological reasons, the guinea pig is a superb model for study of maternal opioid abuse. Guinea pig kappa opioid receptor has been cloned, but only partial sequences of MOR and delta opioid receptors have been available. However, our laboratory has recently determined the complete guinea pig MOR cDNA sequence. Availability of this sequence will enable us to define for the first time guinea pig MOR pharmacology, and systematically compare it to human and mouse MOR. Research is guided by four hypotheses: 1) guinea pig MOR is functionally similar to human MOR with respect to mu agonist efficacy, binding kinetics, and activation of G-protein, but different from murine MOR; 2) methadone induces respiratory depression and is equipotent to, but of longer duration than morphine in the neonatal guinea pig; 3) chronic in utero morphine and methadone exposure results in increased functional MOR on the cell surface, but decreases the coupling efficiency of MOR with G-proteins in the NTS; 4) chronic in utero morphine and methadone exposure up-regulates MOR mRNA in the NTS. Hypotheses are explored through four specific aims: 1) to compare mu agonist selectivity and potency, and development of cellular tolerance for guinea pig, human and murine MOR each expressed in stably transfected CHO cells; 2) to prove that the respiratory effects of methadone are similar to morphine in the neonatal guinea pig; 3) to study the effects of morphine and methadone on guinea pig MOR in NTS of brainstem sections from guinea pig neonates exposed in utero; and 4) to quantitate MOR mRNA in NTS from guinea pig neonates exposed to morphine and methadone in utero. These studies will provide developmental information on guinea pig NTS MOR following chronic in utero opioid exposure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEUROCHEMICAL CHEMOSENSORY NEURONS

ORGANIZATION

OF

CENTRAL

Principal Investigator & Institution: Pete, Gina M.; Howard University 2400 6Th St Nw Washington, Dc 20059 Timing: Fiscal Year 2001 Summary: This proposal consists of research focused on: 1) the central neurochemical organization of sensory neurons that triggers integrated respiratory responses to changes in CO2/H+, 2) the receptor systems of these neurons, activation of which may modulate their response to CO2/H+ signal, and 3) their connectivity with respiratory output neurons such as hypoglossal motor cells. Recently, it has been shown that expression of immediate-early genes are sensitive, inducible, and broadly applicable markers for neurons activated by extracellular stimuli. In the proposed studies, we will use expression of c-fos gene encoded protein (cFos) to identify neurons activated by hypercapnia, in order to investigate neurotransmitter content and receptor systems of these cells. The connectivity of chemosensory neurons with the respiratory-related

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Sudden Infant Death Syndrome

motoneuron pools will be determined by combining retrograde tracer technique with cFos immunohistochemistry. The data derived from these studies will provide basic information related to the central chemosensory network, neurochemical organization, and chemical nature of communications between chemosensitive ells and brainstem output neurons. These results will have indirect bearing on the understanding of neurochemical mechanisms underlying centrally mediated respiratory and cardiovascular dysfunctions, as might occur in idiopathic alveolar hypoventilation, sleep apnea and sudden infant death syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEURONAL RHYTHMOGENESIS

DETERMINANTS

OF

RESPIRATORY

Principal Investigator & Institution: Butera, Robert J.; Electrical and Computer Engr; Georgia Institute of Technology 225 North Ave Nw Atlanta, Ga 30332 Timing: Fiscal Year 2001; Project Start 01-MAY-2001; Project End 30-APR-2004 Summary: (Applicant's abstract): The neuronal circuitry underlying respiratory rhythm genesis is a complex system with complex neuronal dynamics involving various neuronal populations within the mammalian brainstem. This rhythm persists in reduced in vitro preparations, including the en bloc brainstem-spinal cord and the transverse slice. While these reduced preparations have greatly advanced the study of respiratory rhythm genesis at the cellular level, the neuronal dynamics of even these reduced preparations are not completely understood. The objective of this particular application is to fully understand mechanisms for respiratory rhythm genesis in both in vitro and in vivo preparations; our particular approach is the use of computational models and quantitative data analysis techniques. We hypothesize that the aspiratory phase of the respiratory rhythm is generated by neurons in the pre-Botzinger complex (pBc) that display adaptive ion channel properties, and that this population interacts via excitatory and inhibitory connections with other respiratory regions to produce the complete respiratory rhythm in vivo. We further hypothesize that the nature of the excitatory synaptic connectivity within the pBc not only coordinates the aspiratory phase but also makes the respiratory rhythm more robust in the presence of cell-to-cell variability and external disturbances. Our specific aims are 1) determine how intrinsic ion channel properties and extrinsic synaptic input regulate burst frequency and duration and action potential firing rates of aspiratory pBc neurons; 2) determine how cellular heterogeneity and synaptic properties affect the synchronization and stability of the respiratory rhythm; and 3) determine the role of pacemaker-based and network-based modes of respiratory rhythm generation by extending our model to consider the en bloc brainstem spinal cord preparation. This research will increase our understanding of basic cellular and synaptic mechanisms underlying respiratory rhythm generation and may ultimately lead to new pharmacological techniques for clinical intervention and prophylaxis for such disorders as sudden infant death syndrome, sleep apnea and apnea of prematurity, central alveolar syndrome, and other forms of respiratory control failure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NICOTINE INDUCED NEUROPLASTICITY IN THE CAROTID BODY Principal Investigator & Institution: Gauda, Estelle B.; Associate Professor; Pediatrics; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-JAN-2005

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Summary: (Scanned from the applicant's description): Nicotine, a major component of tobacco smoke, is a neuroteratogen that binds to nicotinic cholinergic receptors on catecholamine-containing neurons and induces neuroplasticity. Catecholaminergic systems are vulnerable to the effects of prenatal exposure to nicotine since these systems develop early in ontogeny and have trophic influences on the development of multiple neuronal networks. Perturbations in neurotransmission in dopaminergic and noradrenergic neurons in the central nervous system induced by nicotine exposure are associated with postnatal morbidities which include, impaired cognitive function, attention deficit disorders and abnormalities in locomotion. Prenatal nicotine exposure also affects maturation of adrenal chromaffin cells resulting in altered stress responses. We present data that prenatal nicotine exposure increases catecholaminergic traits in peripheral arterial chemoreceptors that are involved in cardiorespiratory control. An increase in inhibitory catecholaminergic traits in peripheral arterial chemoreceptors may in part account for the striking epidemologic association between prenatal exposure to tobacco smoke and sudden infant death syndrome (SIDS). Infants born to smoking mothers have depressed hypoxic arousal responses, reduced respiratory drive, and blunted ventilatory responses to hypoxia. Similarly, animals exposed prenatally to nicotine have abnormalities in hypoxic ventilation, delayed autoresuscitation and increased mortality with exposure to hypoxia. Comparable to nigrostriatal neurons and adrenal chromaffin cells, peripheral arterial chemoreceptors are rich in catecholamines and express nicotinic receptors. Plasticity of neurons in the central nervous system induced by nicotine exposure involves regulation of catecholaminergic traits mediated by cAMP/calcium and the neurotrophins, basic fibroblast growth factor (bFGF) and brain-derived nerve growth factor (BDNF). Our preliminary data show that prenatal nicotine increases tyrosine hydroxylase (TH) mRNA expression, the rate-limiting enzyme for catecholamine synthesis, in peripheral arterial chemoreceptors. However, the mechanism for this effect is unknown. Yet, it is known that the expression of catecholaminergic traits in peripheral arterial chemoreceptors during development is neurotrophin dependent. In the current proposal, we hypothesize that nicotine exposure during development up-regulates catecholaminergic systems in peripheral arterial chemoreceptors via cAMP/calcium mechanisms and the induction of neurotrophins. Thus, using an in vitro rat model of peripheral arterial chemoreceptors, the goals of this proposal are to 1) determine the plasticity of peripheral arterial chemoreceptors induced by late fetal and early postnatal nicotine exposure and 2), elucidate the cellular and molecular mechanisms involved in this plasticity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NORTHERN CONSORTIUM

PLAINS

PRENATAL

AND

INFANT

HEALTH

Principal Investigator & Institution: Elliott, Amy J.; Pediatrics; University of South Dakota 414 E Clark St Vermillion, Sd 57069 Timing: Fiscal Year 2003; Project Start 26-SEP-2003; Project End 31-JUL-2006 Summary: (provided by applicant): The 'Northern Plains Prenatal and Infant Health Consortium' is comprised of three institutions that each have existing links to communities across South and North Dakota and an Advisory Board with representatives from numerous community agencies and disciplines. The primary purpose behind the formation of this consortium is to provide a structure in which collaborative research projects can be conducted to clarify the role prenatal alcohol exposure plays in fetal death, stillbirth, and sudden infant death syndrome. Deciphering the impact of prenatal alcohol exposure on fetal/infant mortality and

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Sudden Infant Death Syndrome

development will require the input of individuals from a variety of disciplines, in addition to input regarding community needs and concerns. The Northern Plains Consortium is committed to participating in the multidisciplinary steering committee that will result from this RFA and will work in a cooperative manner with the other Comprehensive Clinical Sites, the Developmental Biology and Pathology Center, the Data Coordinating and Analysis Center, and the NIH to design protocols that can be implemented across numerous clinical sites. It is hoped that this collaborative effort will result in answers that will decrease fetal and infant mortality rates, thereby improving child health in the communities we serve. The primary goal for Phase I of this project will be to formalize the collaborative relationships, with both the Steering Committee and the Northern Plains Advisory Board, which will serve as the basis for conducting multi-site research projects. These relationships will be formed through meetings which will occur 4 times in the first year for the Steering Committee and twice with the Advisory Board. We will meet with our advisory board twice each year, coincident with the bi-annual meetings of the Aberdeen Area Perinatal Infant Mortality Review Committee (PIMR). These meetings will lead to the creation of the collaborative structure and processes through which research projects suitable for multi-site implementation will be designed. Furthermore, the Advisory Board, which contains many community leaders, will help develop ways to strengthen the functional community partnerships that will be necessary to successfully carry out this research agenda. A final goal will be to refine the design of a potential pilot study that draws upon our expertise in the areas of exposure assessment and measurement of physiologic function during the fetal and early newborn period. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PERINATAL ASSESSMENT OF AT RISK POPULATIONS Principal Investigator & Institution: Fifer, William P.; Professor; New York State Psychiatric Institute 1051 Riverside Dr New York, Ny 10032 Timing: Fiscal Year 2001; Project Start 30-SEP-1994; Project End 30-APR-2004 Summary: (adapted from investigator's abstract) The long-term objectives of this proposal are to elucidate physiologic mechanisms that underlie the Sudden Infant Death Syndrome, and to develop age-appropriate, non-invasive tests that will identify infants who are at the greatest risk for SIDS. These tests focus on assessments of peripheral and central mechanisms involved in the integrated control of cardiac, blood pressure, and respiratory function. Subjects are the fetuses and infants of mothers from a low-socioeconomic status population in New York City and from a rural Native American population on the Pine Ridge Reservation in South Dakota, which is at unusually high risk for SIDS. The proposed studies begin with measurements made during late gestation. Assessments then continue through infancy to document the physiologic changes that coincide with the period of maximal risk for SIDS. These postnatal studies incorporate measurements made during sleep under basal conditions as well as during head-up and head-down tilting. The principal dependent variables are heart rate and several indices of heart rate variability, respiratory rate and variability, body temperature, and electrocortical activity and beat-to-beat blood pressure. Five experiments will address the following aims; Patterns of developmental change in cardiorespiratory activity measured from the late fetal period through infancy will distinguish groups of infants at increased risk for SIDS How postnatal development of heart rate, blood pressure and respiratory responses to the challenge of head-up and head-down tilting will be altered in groups of infants at increased risk for SIDS Physiologic responses to tilt are dependent upon sleep state and this dependency may

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change with age Blood pressure decreases to head-up tilt are larger in the prone sleeping position Head-up tilting will induce cortical activation which will be diminished during the period of greatest vulnerability to SIDS Respiratory and heart rate responses to tilt will be diminished in the morning hours and Responses to tilt will vary with time after feeding. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PHYSIOLOGICAL DEVELOPMENT IN SIDS Principal Investigator & Institution: Harper, Ronald M.; Professor; Neurobiology; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-DEC-1986; Project End 30-JUN-2003 Summary: The objective is to identify brain structures which mediate controlling influences on breathing and blood pressure during waking and quiet sleep, and thus to assist determination of the mechanisms of failure in the Sudden Infant Death syndrome (SIDS). Blood oxygen level dependent (BOLD) functional magnetic resonance imaging will be used to visualize neural activity in 1) twenty-two patients with Congenital Central Hypoventilation Syndrome (CCHS), a disorder characterized by absence of central chemoreception, loss of breathing drive during sleep, impaired breathing responses to hyperthermia, and occasional waking hypotonia; 2) twnety-two PraderWalli patients, who show diminished peripheral, but intact central chemoreception; and 3) twenty-two age- and gender-matched controls. Images will be acquired during baseline, and during hyperoxic, hypercapnic, hypoxic, inspiratory loading, hyperthermic, paced breathing and passive motion challenges, and during cold pressor application, while respiratory measures, heart rate and variability, non-invasive blood pressure, and an index of sympathetic outflow (sweating" are collected. Brain images from baseline conditions will be compare to images collected during experimental challenges in waking for all three groups, and in quiet sleep for CCHS and control subjects. The extent of activation and time course of changes in activated brain regions during challenges will be compared between groups. The timing of signal changes in different brain sites will be correlated with physiological changes accompanying the challengers. The studies have the potential to reveal the rain sites underlying breathing and blood pressure control, and the potential mechanisms of failure in SIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: POSTNATAL RESETTING OF CAROTID CHEMORECEPTOR SENSITIVITY Principal Investigator & Institution: Carroll, John L.; Associate Professor; Arkansas Children's Hospital Res Inst Research Institute Little Rock, Ar 72202 Timing: Fiscal Year 2001; Project Start 01-AUG-1995; Project End 31-AUG-2004 Summary: The main sensors of arterial oxygen (02) tension are the carotid bodies (CB). Although they are critically important during infancy, they are not fully developed at birth, and take time to mature. The site of O2 sensing is believed to be the type I cell, which depolarizes in response to hypoxia, leading to Ca2+ influx through calcium channels, a rise in intracellular calcium and release of neurotransmitters which are thought to stimulate carotid sinus nerve endings. We previously reported that the type I cell calcium response to hypoxia matures after birth, and our recent studies suggest that several aspects of this cascade change after birth, as follows: (a) depolarization of type I cells by hypoxia is minimal in cells from newborns and increases with age; (b)the O2-

36

Sudden Infant Death Syndrome

sensitivity of a background K+ conductance is small in cells from newborns and increases with age; and (c) calcium currents of immature, but not mature, type cells are inhibited 50% by hypoxia. The proposed work will test the hypothesis that developmental changes in the O2-sensitivity of a background "leak" K+ conductance account, in part, for postnatal maturation of carotid chemoreceptor O2 sensitivity. In addition, we will determine whether (1) background K+ conductance is carried by one major background K+ channel type, the O2 sensitivity of which increases with age; or (2) background K+ conductance in type I cells is carried by at least 2 channel types, one O2sensitive and one non-O2-sensitive, and development involves a change in the ratio of the O2-sensitive to non-O2-sensitive channels. We will also seek to understand whether developmental shifts occur in 0a-sensitive calcium channels during maturation. The results will answer important questions about the mechanisms underlying postnatal development of carotid chemoreceptor function. The ultimate goal of the proposed studies is to understand how the carotid chemoreceptors mature and how development is modulated, so that a number of potentially life threatening disorders such as asthma, bronchopulmonary dysplasia, apnea and sudden infant death syndrome (SIDS) can be better treated or prevented. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PREDICTING LIFE-THREATENING EVENTS IN CHIME INFANT DATA Principal Investigator & Institution: Schuckers, Stephanie A.; Electrical and Computer Engr; Clarkson University Division of Research Potsdam, Ny 136995630 Timing: Fiscal Year 2002; Project Start 27-JUL-2002; Project End 30-JUN-2004 Summary: (provided by applicant): Sudden infant death syndrome (SIDS) is the sudden death of an infant under one year old without any apparent warning signs. It is the leading cause of death of infants between the age of one month and one year in the developed countries. Previous studies have indicated that SIDS victims may suffer from cardiorespiratory failure, which reflects immaturity of autonomic nervous system (ANS) control. Heart variability (HRV) has been shown to be a noninvasive and inexpensive way to assess the ANS. Increased heart rate and decreased heart rate variability have been observed in SIDS victims. While it is unclear whether there is a relationship between SIDS and infants who have apparent life-threatening events (ALTE) like apnea and bradycardia, there is a desire to gain a better understanding of the nature of ALTE, their frequency and severity, and the ability of home monitors to detect events and provide an alarm. The Collaborative Home Infant Monitoring Evaluation (CHIME) study group, formed by NIH, sought to study these issues through the collection of a massive clinical database, which includes physiological, signals from 529 infants recorded in polysomnographic (PSG) studies. The infants were then studied several months using a home monitor which recorded life-threatening events. A classification is available regarding which infants had verified, apparent life-threatening events. Given the wealth of information linking SIDS and heart rate variability (HRV), we desire to investigate whether heart rate variability is effective predictor for life-threatening events. This research will investigate whether HRV can differentiate infants at risk for future apparent life-threatening events (FALTE). First statistical methods will be used to determine if there is significant difference in HRV between normal and FALTE infant groups. Next, the major goal is to design a method to classify infants using HRV, exploring various prediction models including logistic regression, decision tree, and neural networks. The relationship between HRV parameters and all the affected factors will also be studied to provide a clearer understanding of the parameters, and to help

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determine how to use HRV as a classifier. Successful prediction of infants with future apparent life-threatening events could have clinical significance and provide physicians with an opportunity for treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PROFILING THE NEEDS OF DYING CHILDREN Principal Investigator & Institution: Feudtner, John C.; Pediatrics; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-AUG-2000; Project End 31-JUL-2002 Summary: Addressing the needs of dying children- a benchmark of societal compassion and a gauge of health care quality-rises as a challenge for the 21st century. As deaths due to injury, prematurity, and sudden infant death syndrome are prevented, the remaining deaths may be increasingly associated with chronic conditions. I hypothesize that deaths attributable to complex chronic conditions (CCCs) constitute an increasing proportion of all pediatric deaths, both at a population level and more specifically among patients cared for by children's hospitals, and that the prolongation of life has led to a rising prevalence of these conditions. Furthermore, I postulate that quality of care and support for these dying children and their families deteriorates over the last two years of life, with declining continuity of care and untimely referral to hospice and other social support services. This five-year research plan will profile the needs of dying children specifically aiming to: 1. Determine whether the prevalence of terminal congenital CCCs is rising in the national population. 2. Measure the change in prevalence of children with terminal CCCs in tertiary children's hospitals, thereby assessing the magnitude of need for hospital-based pediatric palliative care services. 3. Test whether the 'intensity' of medical care increases in the 30-day interval prior to the day on which death compared to the preceding 23 month interval, so as to improve clinicians prognostic inferences regarding likelihood of death. 4. Examine two markers of quality of care of children with CCCs by: Testing whether the continuity of care deteriorates in the last two years of life for children with CCCs; and 5. Examining the timing of referral to hospice. This research seeks to improve the care and health policy for dying children in three ways. First, evidence of a 'epidemiological transition' in pediatric mortality-from mostly accidental and sudden death to deaths that occur somewhat inevitably with a longer yet unpredictable dying process-would motivate the redesign of pediatric health care services and physician training at both the regional and national level. Second, this research will produce several techniques to monitor health utilization data for indicators of the quality of care provided to terminally ill children. Finally, the results of these studies will ultimately inform the development and trial of a longitudinal needs assessment program for children with complex chronic conditions. These studies of the epidemiology of pediatric death and the needs of dying children will help enhance the individual care provided to these children and their families as well as broader policy. They will also foster the development of the applicant's research skills so as to become an independent researcher addressing the needs of children with complex chronic conditions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: PROTECTIVE VENTILATORY RESPONSES TO HYPOXIA Principal Investigator & Institution: St. John, Walter; Professor; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2002

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Sudden Infant Death Syndrome

Summary: The protective response to hypoxia is organized in two layers. With initial exposure, eupneic ventilation increase. In severe hypoxia, eupnea is replaced by gasping, which promotes "autoresuscitation." The eupneic ventilatory response to hypoxia changes with development. In the newborn, ventilation rises and then falls. With age, the hypoxia- induced augmentation becomes more sustained. We hypothesize that hypoxia- induced ventilatory depression results from activation of a mesencephalicpontine "central oxygen detector." Piglets will be studied. We will identify the region containing the "central oxygen detector." Hypoxia-induced depressions of ventilation will be attenuated if neurons of this central oxygen are destroyed. Neuronal activities of this detector will be characterized. These activities are hypothesized to increased during depressions of phrenic activity in hypoxia or during localized hypoxia by applications of sodium cyanide. We will then examine the role of neurons in the ventral medulla in hypoxia-induced ventilatory depressions and in the neurogenesis of gasping. These ventral medullary neuronal activities may provide a generalized tonic input for ventilatory activity. Yet gasping will not be altered since the mechanisms underlying the neurogenesis of eupnea and gasping differ fundamentally. In unanesthetized piglets, ventilatory activity will be recorded during wakefulness and sleep. We hypothesize that apneic episodes will be recorded following ablation of neurons in the medullary gasping center and those in the ventral medulla. Our results will have profound implications as to the mechanisms of apnea and the sudden infant death syndrome. Mechanisms of central apnea may be elucidated by our studies of the "direct" influence of hypoxia on the brainstem ventilatory control system, of the role of ventral medullary mechanisms in this hypoxia-induced depression and the role of medullary gasping mechanisms in the control of eupnea. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF CAROTID BODY AFFERENT DEVELOPMENT Principal Investigator & Institution: Katz, David M.; Professor; Neurosciences; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 01-JUL-1989; Project End 30-JUN-2004 Summary: The proposed research seeks to define the role of neuronal growth factors in development of chemoafferent neurons and peripheral chemoreflexes in rats and mice. Chemoafferent neurons in the petrosal are the afferent link between the carotid body and central autonomic pathways and thereby play a pivotal role in regulating chemoreceptor control of cardiorespiratory function. Until recently, relatively little was known about mechanisms that underlie development of the chemoafferent pathway, despite evidence that derangements of chemoreflex maturation may contribute to developmental disorders of cardiorespiratory control, including Sudden Infant Death Syndrome and hypoventilation and apneic syndromes in neonates and infants. This continuation proposal is based on our recent discovery that Brain-Derived Neurotrophic Factor (BDNF), a member of the neurotrophin family of neuronal growth factors, is expressed in the fetal carotid body and is required for survival of chemoafferent neurons and development of peripheral chemoreflexes. The proposed studies are designed to further define the role of BDNF in development of chemoreflex function and to elucidate the role of Glial Cell Line-Derived Neurotrophic Factor (GDNF), a newly discovered growth factor in the developing chemoafferent pathway. To approach these issues, the proposed research seeks to define growth factor influences on chemoafferent development and chemoreflex maturation, using rat fetuses and neonates, as well as genetically engineered mice lacking functional growth factor alleles. Specifically, we plan to define 1) Growth factor regulation of chemoafferent survival and

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differentiation, in vivo and in vitro, 2) Growth factor regulation of chemoreflex development, using plethysmographic recording in intact animals, 3) Regulation of chemoafferent survival by oxygen availability in vivo, and 4) The role of endogenous BDNF in chemoafferent neurons. By defining growth factor regulation of chemoafferent pathway development, the proposed research aims to shed light on cellular and molecular mechanisms relevant to understanding and improved management of hypoventilation and apnea syndromes in neonates and infants. Already, molecular genetic studies have identified bdnf and gdnf as candidate genes for at least one developmental disorder of breathing, Congenital Central Hypoventilation Syndrome. In addition, by elucidating how oxygen availability regulates chemoafferent survival after birth, these studies are designed to provide insight into potential links between supplemental oxygen therapy and delayed maturation of peripheral chemoreflexes in preterm infants. Moreover, it is hoped that defining development of this system will, in turn, create a model of growth factor function and regulation that is applicable to the nervous system as a whole. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: RESPIRATORY PATTERN GENERATION STUDIED IN VITRO Principal Investigator & Institution: Feldman, Jack L.; Chairman; Neurobiology; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2001; Project Start 01-JUL-1988; Project End 30-JUN-2004 Summary: The brain is vigilant in control of breathing, regulating blood O2 and CO3 over an order of magnitude range in metabolic demand, wide ranges of posture and body movements, compromises in muscle or cardiopulmonary function, from birth till death without lapses beyond a few minutes. This grant continues our effort to determine the sites and mechanisms underlying the nervous system generation and modulation of breathing rhythm. Determination of these properties is critical for understanding pathologies where ventilatory failure results from dysfunction of nervous system, including such diseases as apnea of prematurity, congenital central hypoventilation, central alveolar hypoventilation, sleep apnea and, perhaps, sudden infant death syndrome. Significant progress in identifying critical sites and cellular mechanisms involved in the generation of the respiratory rhythm followed the development of novel in vitro preparations. These preparations generate a respiratory-related rhythm, and their exploitation led to two hypotheses that are the focus of this application: SITE HYPOTHESIS: The preBotzinger Complex (preBotC) contains the kernel for respiratory rhythm generation. The preBotC is the limited portion of the ventrolateral respiratory column necessary and sufficient for in vitro neonatal rodent medullary slice preparations to generate respiratory-related motor nerve output. We discovered that the anatomical extent of the preBotC in rodent is demarked by neurons expressing Neurokinin 1 receptors. Two goals of this project are to use this information to: i) test the SITE HYPOTHESIS, and; ii) identify the preBotC in neonatal and adult human brain. RHYTHMOGENESIS HYPOTHESIS: Endogenous bursting, i.e., pacemaker(-like), neurons in the preBotC are the cellular kernel for respiratory rhythm. There are three questions that must be answered to understand the generation of the respiratory rhythm: i) Which neurons are necessary and/or sufficient for the rhythm?; ii) By what mechanism do these neurons generate the rhythm?; How is the rhythm modulated? Of the various neurons which are candidates for this role, we propose a population of neurons called Type-1. Two additional goals are to: ) test whether Type- 1 neurons are required for generation of respiratory rhythm, and; ii) determine the synaptic

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Sudden Infant Death Syndrome

interactions amongst preBotC neurons that define the respiratory rhythm generating network. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SIDS DATA COORDINATING AND ANALYSIS CENTER Principal Investigator & Institution: Dukes, Kimberly A.; Dm-Stat, Inc. 407 Rear Mystic Ave, Unit 11A Medford, Ma 02155 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-JUL-2006 Summary: (provided by applicant): In multi-center studies or collaborative projects, a centralized Data Coordinating and Analysis Center (DCAC) with strong leadership, organization and analytic skills is critical to the success of the project. DMSTAT, Inc. proposes to serve as the DCAC for the multi-disciplinary research network on prenatal alcohol exposure and sudden infant death syndrome (SIDS) that will be established through responses to RFA HD- 03-004. DM-STAT has a proven track record of success as the designated DCAC on NICHD and NIAAA sponsored multi-center trials and collaborations. Our goal is to make life easier for participating staff so that they can focus on their areas of expertise. To achieve that goal, DM-STAT will create and maintain a study-wide infrastructure to support the activities of and facilitate information sharing between members of the Network, including the NICHD, NIAAA, and governing boards. This infrastructure will revolve around a Network website containing administrative and data management components. The website will provide instant access to all project documentation and materials, data management reports, statistical analysis summaries, and will provide a forum (the Meeting Center) for sharing ideas and issues. The first phase (of two phases) calls for formalizing a collaborative structure between, Comprehensive Clinical Sites (CCS), Developmental Biology and Pathology Center(s) (DBPC) and the DCAC to investigate the relationship between prenatal alcohol exposure and the risk for sudden infant death syndrome (SIDS) and adverse pregnancy outcomes (e.g., stillbirth and fetal alcohol syndrome (FAS)). In addition, the Network will investigate social and behavioral factors that may be related to a woman's decision to drink alcohol during pregnancy and lactation. Phase I will require development of testable hypotheses, pilot testing of the core and sitespecific protocols and producing an executive summary with recommendations based upon the results of these pilot studies in order to assess feasibility and justification for Phase II. DM-STAT will provide leadership and guidance to the network with respect to study design, protocol development, data management and statistical analysis. With a cohesive Network in place, DM-STAT will then be responsible for coordinating safe and consistent implementation of the core protocol, monitoring key indicators of quality, and performing analysis of pilot data. DM-STAT is committed to quality; it is the focal point of everything we do. We are proactive as opposed to reactive, innovative in streamlining and organizing processes and procedures, able to educate and communicate with study staff at all levels, and we are passionate and committed to getting the job done right the first time. We believe that DM-STAT is best positioned to serve the needs of this Network in an efficient and effective manner. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: SPATIOTEMPORAL DEVELOPMENT

EEG

QUALIFICATION

IN

INFANT

Principal Investigator & Institution: Grieve, Philip G.; Pediatrics; Columbia University Health Sciences New York, Ny 10032

Studies

41

Timing: Fiscal Year 2001; Project Start 10-JUL-2000; Project End 30-JUN-2002 Summary: A program of research and career development has been developed for the PI to devise new methods for quantitative assessment of spatiotemporal patterns of brain activity in the scalp electroencephalogram (EEG) of developing infants. Previously, scalp surface voltage or current measurement was limited by inadequacies in sampling sites which resulted in spatial aliasing and electrical patterns that were quantitatively in error and spatially distorted. Recent advances in bioengineering make possible collection and processing of EEG data from hundreds of sites and accurate measurement of spatial electrical waveforms; however, the enormous quantities of information that are created make impractical standard techniques for EEG analysis and interprutation. New quantitative analytical techniques are proposed which draw on the PI's experience as an electrical engineer in the processing of stochastic space-time signals in radar/sonar arrays and in the recognition of patterns in images. These methods will be especially tailored to account the unique and evolving anatomy of the infant brain and cranial vault. Techniques will be validated in clinical studies of response to arousal stimuli of normal infants and those at increased risk for Sudden Infant Death Syndrome. With establishment of normative developmental trends, infants in the neonatal intensive care unit who have suffered hypoxic/ischemic event will be studied to detect deviations from norms that may be predictive of abnormal neurodevelopment. In addition to a more precise understanding of the correlates of brain electrical function, assessment of its localization will be initiated in anticipation of future research from chronic recordings of intracerebral electrical activity in fetal baboon. A formal training program has been designed for the P.I specifically tailored to his academic needs which complement his prior postdoctoral experience. This will include the following: mentoring by experts in neuro-development, electroencephalography and clinical research for hands-on experience; course work in neurobiology and research ethics; participation in a fellows training program in EEG and a seminar series in perinatal physiology; and collaboration with bioengineers, psychobiologists, and clinical neonatologists. The goal of this coordinated program of research/training is to complete the preparation of the PI for a career as an independent researcher, with skills multidisciplinary collaborative investigation and further his capacity to define new directions for quantitative biomedical research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: STACHYBOTRYS INDUCED HEMORRHAGE IN THE DEVELOPING LUNG Principal Investigator & Institution: Dearborn, Dorr G.; Associate Professor of Biochemistry; Pediatrics; Case Western Reserve University 10900 Euclid Ave Cleveland, Oh 44106 Timing: Fiscal Year 2001; Project Start 05-FEB-1999; Project End 31-JAN-2004 Summary: Over the past 4 years in Cleveland, Ohio there have been 34 cases of pulmonary hemorrhage and hemosiderosis in young infants. To date, ten infants have died. A CDC case-controlled study found an association with water damaged homes and the toxigenic fungus called Stachybotrys atra which requires water-saturated cellulose to grow. The spores of this fungus do not germinate in the lung, but do not contain very potent mycotoxins which appear to be particularly toxic to the rapidly developing lungs of young infants. Secondary stresses, e.g. environmental tobacco smoke, appear to be important triggers for overt hemorrhage. Concern that there may be a large number of undetected infants with the disorder ted to examination of all infant coroner cases, which revealed six sudden infant death syndrome cases with major

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Sudden Infant Death Syndrome

amounts of pulmonary hemosiderin-laden macrophages, indicating extensive hemosiderosis existing prior to death. All of these infants lived in the same contiguous area as the majority of the hemosiderosis patients. This disorder may extend beyond Cleveland, since toxigenic fungi are widespread. We are aware of 122 infants with idiopathic pulmonary hemorrhage in this country in the past 4 years. The purpose of this proposal is to establish an original rat pup model for Stachybotrymycotoxicosis which can be used to understand the developmental pathophysiology by which fungal spores induces hemorrhage, address practical problems in clinical care, and foster public health prevention. This model uses tracheal instillation of toxic Stachybotrys spores in neonatal to weanling rats to initiate the pathologic process. Specific aim 1 will evaluate dose response to Stachybotrys spore inhalation, critical age of vulnerability, histopathology, inflammatory mediator response, and change in lung function during injury and recovery. Specific aim 2 will explore the vulnerability of pulmonary capillaries to leakage in the Stachybotrys exposed pups in vivo and in vitro, specific stress triggers of hemorrhage, and efficacy of anti- inflammatory therapy. Specific aim 3 will develop and test biochemical markers for Stachybotrys exposure including toxins and antibody production. The experiments in this proposal will provide fundamental new information on Stachybotrys exposure applicable to detection and treatment of this new disorder. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: THE UPPER AIRWAY AND THE SUDDEN INFANT DEATH SYNDROME Principal Investigator & Institution: Bartlett, Donald; Professor and Chair; Physiology; Dartmouth College 11 Rope Ferry Rd. #6210 Hanover, Nh 03755 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Despite recent progress in its prevention, the Sudden Infant Death Syndrome (SIDS) remains the most frequent cause of infant mortality between the ages of one month and one year in the United States. A striking epidemiological finding is that more victims than expected are found in the prone position, often with the face in the bedclothes. Campaigns to encourage putting infants to sleep on their backs have led to a gratifying reduction in the incidence of SIDS in several countries, yet the influence of posture remains mysterious. This project will use decerebrate neonatal piglets to explore the possibility that the risk of prone sleeping is determined by reflex responses involving the upper airway, and that these responses may be aggravated by CO2 in the upper airway (from re-breathing), by abnormalities of the ventral medulla (for which there is evidence in some SIDS victims), or from elevated body temperature (for which there is epidemiologic evidence and an intriguing report of a study in puppies). We will examine the influence of each of these conditions on three upper airway reflex responses: the "diving" response, the laryngeal chemo reflex and the load-compensating reflex response to upper airway obstruction. Our general hypothesis is that some combination of conditions and stimuli will exaggerate the reflex interruption of breathing, possibly contributing to the pathogenesis of SIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TRIGEMINAL AUTONOMIC INTERACTIONS Principal Investigator & Institution: Mcculloch, Paul F.; Physiology; Midwestern University 555 31St St Downers Grove, Il 60515 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 29-SEP-2004

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Summary: (provided by applicant): The long-term goal of this application to establish the mechanisms and circuitry by which signals from the upper respiratory tract integrate within the brainstem to produce reflex autonomic responses. Stimulation of the upper respiratory tract can produce an intense functional reorganization of the cardiovascular and respiratory systems. This reflex includes central apnea, parasympathetic bradycardia and sympathetically mediated vasoconstriction. Initiation of this response results from stimulation of trigeminal receptors that innervate the face and nasal passages. This autonomic response is primarily a defensive reflex, and is only elicited when a potentially life threatening external stimulus is presented. Because an animal is in imminent danger during such an event, homeostatic control, such as the maintenance or arterial blood pressure, should no longer be primary objective of the animal?s autonomic nervous system. In this situation a defensive reflex should temporarily become more powerful than a homeostatic reflex. It is hypothesized that stimulation of the trigeminal inhibits the baroreflex at the level of the nucleus tractus solitarius (NTS). The objectives of this proposal are to determine 1) the response of brainstem trigeminal neurons during nasal stimulation; 2) the relationship between the trigeminal system and secondary brainstem neurons located in the NTS and rostral ventrolateral medulla (RVLM); and 3) if trigeminal stimulation inhibits second-order barosensitive NTS neurons. It is expected that extracellular recordings will determine that neurons located within the superficial laminae of the trigeminal medullary dorsal horn (MDH) respond to nasal stimulation with an increase in firing rate that positively correlates with the cardiorespiratory changes elicited by the nasal stimulation. It is also expected that electrical stimulation of the NTS and RVLM will antidromically stimulate these same MDH neurons. This would determine that these nuclei are part of the brainstem circuitry of this response. Finally, it is expected that extracellular recordings will determine that trigeminal stimulation inhibits barosensitive neurons within the NTS, thus inhibiting the brainstem baroreflex pathway. This would indicate that a defensive reflex (upper respiratory tract stimulation) can inhibit a homeostatic reflex (arterial baroreflex). This proposal has clinical implications because it investigates the relationship between a defensive reflex and a homeostatic reflex, and explores the mechanisms of integrative cardiorespiratory control within the brainstem. Also, stimulation of the upper respiratory tract may be a casual factor in Sudden Infant Death Syndrome (SIDS). Some infants at risk for SIDS present autonomic dysfunction and abnormalities of respiratory and/or cardiovascular control mechanisms, especially after stimulation of the upper respiratory tract. Having a better understanding of brainstem cardiorespiratory integration might provide a neurological basis for the etiology of SIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VENTRAL MEDULLA AND THE SUDDEN INFANT DEATH SYNDROME Principal Investigator & Institution: Kinney, Hannah C.; Associate Professor; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001; Project Start 01-APR-1998; Project End 31-MAR-2003 Summary: Our overall hypothesis is that the sudden infant death syndrome (SIDS), or a subset of SIDS, is due to developmental abnormalities of the ventral medulla that interfere with normal protective cardiorespiratory responses to potentially lifethreatening, but often occurring, events during sleep, such as hypoxia, hypercapnia, and apnea. We recently reported in SIDS victims neurotransmitter receptor binding deficiencies in the arcuate nucleus, which contains ventral medullary surface neurons

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Sudden Infant Death Syndrome

that are considered homologous to neurons located in similar areas in cats that are necessary for the protective responses to hypercapnia and asphyxia. We propose a triple-risk model of SIDS in which an infant will die of SIDS only if he/she possesses: 1) an underlying vulnerability, e.g., an abnormality in the ventral medulla; 2) a critical period in the development of homeostatic control, i.e., early infancy; and 3) an exogenous stressor, e.g., positional asphyxia. This model will be examined in Projects IIII, both in decerebrate piglets and in chronically instrumented piglets during wakefulness and natural sleep. In Project I, we will define the role of the arcuate homologue in cardiorespiratory control in the piglet across early development, and determine the effect of structural and neurochemical lesions of the arcuate homologue on response to hypercapnia and asphyxia. In Project II, we will delineate in piglets the mechanisms of protective ventilatory response to hypoxia, especially the depressive phase of the biphasic response and autoresuscitation by gasping. In Project III, we will determine the effects of trigeminal, superior laryngeal, and intercostal nerve stimulation in piglets with arcuate homologue lesions during room air exposure, hypercapnia, and hypoxia. In Project IV, we will define the comparative cyto-and chemoarcitectonic anatomy of the human arcuate nucleus and the piglet homologue. In Project V, the objective is to apply information from Projects I-IV in the definition of abnormalities in SIDS brainstems, in addition to those in the arcuate nucleus. The A. Administrative Core will provide the necessary administrative framework. The B. Anatomy Core will provide cellular and neurochemical services for animal and human brainstem studies. The C. Animal Physiology Core will provide an animal research laboratory in which Projects I-IV will be performed by the individual investigators. This program should advance our understanding of the role of ventral medullary abnormalities in the pathogenesis of SIDS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VENTRAL CHEMORECEPTION

MEDULLA,

BREATHING,

AND

CENTRAL

Principal Investigator & Institution: Nattie, Eugene E.; Professor of Physiology; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2001 Summary: We proposed that SIDS results from abnormalities in the ventral medulla that interfere with normal protective cardiorespiratory reflexes. In this project we shall disrupt experimentally in piglets, at two developmental times, the homologue of the human arcuate nucleus found to be abnormal in SIDS victims. This homologue is proposed to contain the retrotrapezoid nucleus (RTN) and parapyramidal regions, the medullary raphe region, and the central chemoreceptor regions of the caudal ventrolateral medulla. In adult animals, disruption of the RTN/parapyramidal and raphe regions is known to diminish respiratory output and the sensitivity of the respiratory response to increased carbon dioxide. The magnitude of the effects is greater in anesthesia. Denervation of peripheral chemoreceptors magnifies the deleterious effects of this disruption in adult animals; when performed in newborn animals with intact brainstem function, it results in hypoventilation, more frequent apneas, and death. We shall, in the decerebrate piglet with and without intact carotid bodies, alter arcuate homologue function by microinjection of 1) an excitatory amino acid neurotoxin to produce lesions, and 2) muscarinic and ionotropic glutamate agonists/antagonists, and thyrotropin releasing-hormone. Phrenic nerve output and blood pressure in the baseline state and their responses to hypercapnia and asphyxia will be measured. In the unanesthetized chronic piglet preparations with and without intact carotid bodies, we

Studies

45

will examine the effect of arcuate homologue lesions on breathing and blood pressure during natural wakefulness and sleep and on the responses to hypercapnia and asphyxia. Our goal is to examine the relative roles of arcuate homologue neurons and carotid body inputs on breathing and blood pressure in the absence of anesthesia and in natural sleep and wakefulness. In respect to the Triple Risk Model for SIDS pathogenesis, we are 1) experimentally creating a vulnerability by means of our lesions or injections, at 2) two separate developmental ages, and 3) examining, as exogenous stresses, responses to hypercapnia and asphyxia in wakefulness and sleep with and without afferent input from the carotid body. 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 “sudden infant death syndrome” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for sudden infant death syndrome in the PubMed Central database: •

Babies sleeping with parents: case-control study of factors influencing the risk of the sudden infant death syndrome. by Blair PS, Fleming PJ, Smith IJ, Platt MW, Young J, Nadin P, Berry PJ, Golding J.; 1999 Dec 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28288

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Facial structure in the sudden infant death syndrome: case-control study. by Rees K, Wright A, Keeling JW, Douglas NJ.; 1998 Jul 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28609

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Functional and Developmental Studies of the Peripheral Arterial Chemoreceptors in Rat: Effects of Nicotine and Possible Relation to Sudden Infant Death Syndrome. by Holgert H, Hokfelt T, Hertzberg T, Lagercrantz H.; 1995 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41382

•

Used infant mattresses and sudden infant death syndrome in Scotland: case-control study. by Tappin D, Brooke H, Ecob R, Gibson A.; 2002 Nov 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=131017

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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Sudden Infant Death Syndrome

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 sudden infant death syndrome, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “sudden infant death syndrome” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for sudden infant death syndrome (hyperlinks lead to article summaries): •

A case of murder and the BMJ. Was it truly murder or sudden infant death syndrome? Author(s): Lowry RB. Source: Bmj (Clinical Research Ed.). 2002 May 4; 324(7345): 1096-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11993496&dopt=Abstract

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A comparison of respiratory symptoms and inflammation in sudden infant death syndrome and in accidental or inflicted infant death. Author(s): Krous HF, Nadeau JM, Silva PD, Blackbourne BD. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 2003 March; 24(1): 1-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604990&dopt=Abstract

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A nested case-control study of oxytocin and sudden infant death syndrome. Author(s): Kraus JF, Bulterys M, Greenland S. Source: American Journal of Obstetrics and Gynecology. 1990 February; 162(2): 604-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2309851&dopt=Abstract

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A possible relation between oxytocin for induction of labor and sudden infant death syndrome. Author(s): Einspieler C, Kenner T. Source: The New England Journal of Medicine. 1985 December 26; 313(26): 1660. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4069181&dopt=Abstract

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

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•

A serotonin malfunction hypothesis by finding clear mutual relationships between several risk factors and symptoms associated with sudden infant death syndrome. Author(s): Okado N, Narita M, Narita N. Source: Medical Hypotheses. 2002 March; 58(3): 232-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12018976&dopt=Abstract

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A statistical analysis of the seasonality in sudden infant death syndrome. Author(s): Helweg-Larsen K, Bay H, Mac F. Source: International Journal of Epidemiology. 1985 December; 14(4): 566-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4086143&dopt=Abstract

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A study on how to increase the sudden infant death syndrome (SIDS) autopsy rate. Author(s): Matoba R. Source: Forensic Science International. 2002 September 14; 130 Suppl: S104-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12350311&dopt=Abstract

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A triple-risk model for the sudden infant death syndrome (SIDS) and the apparent life-threatening episode (ALTE): the stressed magnesium deficient weanling rat. Author(s): Caddell JL. Source: Magnes Res. 2001 September; 14(3): 227-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11599557&dopt=Abstract

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Addendum: Distinguishing Sudden Infant Death Syndrome From Child Abuse Fatalities. Author(s): American Academy of Pediatrics. Committee on Child Abuse and Neglect. Source: Pediatrics. 2001 September; 108(3): 812. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11547803&dopt=Abstract

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Altered cardiac repolarization in some victims of sudden infant death syndrome. Author(s): Sadeh D, Shannon DC, Abboud S, Saul JP, Akselrod S, Cohen RJ. Source: The New England Journal of Medicine. 1987 December 10; 317(24): 1501-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3683486&dopt=Abstract

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Amitriptyline overdose versus sudden infant death syndrome in a two-month-old white female. Author(s): Perrot LJ. Source: J Forensic Sci. 1988 January; 33(1): 272-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3351466&dopt=Abstract

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•

Analysis of breathing patterns in a prospective population of term infants does not predict susceptibility to sudden infant death syndrome. Author(s): Waggener TB, Southall DP, Scott LA. Source: Pediatric Research. 1990 February; 27(2): 113-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2314938&dopt=Abstract

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Analysis of the heart rate and breathing patterns of infants destined to suffer sudden infant death syndrome: probability density function analysis. Author(s): Stevens V, Wilson AJ, Southall DP, Barber DC, Franks CI. Source: Pediatric Research. 1985 December; 19(12): 1327-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4080453&dopt=Abstract

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Analysis of the mitochondrial genome in sudden infant death syndrome. Author(s): Divne AM, Rasten-Almqvist P, Rajs J, Gyllensten U, Allen M. Source: Acta Paediatrica (Oslo, Norway : 1992). 2003; 92(3): 386-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12725556&dopt=Abstract

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Apnea, sudden infant death syndrome, and home monitoring. Author(s): Committee on Fetus and Newborn. American Academy of Pediatrics. Source: Pediatrics. 2003 April; 111(4 Pt 1): 914-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671135&dopt=Abstract

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Are risk factors for sudden infant death syndrome different at night? Author(s): Williams SM, Mitchell EA, Taylor BJ. Source: Archives of Disease in Childhood. 2002 October; 87(4): 274-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12243991&dopt=Abstract

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Are substitutions in the first hypervariable region of the mitochondrial DNA displacement-loop in sudden infant death syndrome due to maternal inheritance? Author(s): Arnestad M, Opdal SH, Musse MA, Vege A, Rognum TO. Source: Acta Paediatrica (Oslo, Norway : 1992). 2002; 91(10): 1060-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12434891&dopt=Abstract

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Association between sudden infant death syndrome and prone sleep position, bed sharing, and sleeping outside an infant crib in Alaska. Author(s): Gessner BD, Ives GC, Perham-Hester KA. Source: Pediatrics. 2001 October; 108(4): 923-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11581445&dopt=Abstract

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Autopsies and sudden infant death syndrome. Author(s): Bass M. Source: Am J Dis Child. 1990 February; 144(2): 137-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2301309&dopt=Abstract

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Awareness of sudden infant death syndrome risk factors among mothers of Pacific infants in New Zealand. Author(s): Paterson J, Tukuitonga C, Butler S, Williams M. Source: N Z Med J. 2002 February 8; 115(1147): 33-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11942511&dopt=Abstract

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Babies sleeping with parents and sudden infant death syndrome. Down with smoking and babies sleeping in separate rooms. Author(s): Mermer CA. Source: Bmj (Clinical Research Ed.). 2000 October 21; 321(7267): 1019; Author Reply 1020. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11203210&dopt=Abstract

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Babies sleeping with parents and sudden infant death syndrome. Invoking sudden infant death syndrome in cosleeping may be misleading. Author(s): Carter N, Rutty GN. Source: Bmj (Clinical Research Ed.). 2000 October 21; 321(7267): 1019; Author Reply 1020. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11039984&dopt=Abstract

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Babies sleeping with parents and sudden infant death syndrome. Smoking may be residual confounder in bed sharing. Author(s): Ezeonyeji A, Jewitt S, Poyser L, Stadward T. Source: Bmj (Clinical Research Ed.). 2000 October 21; 321(7267): 1019-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11203209&dopt=Abstract

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Babies sleeping with parents: case-control study of factors influencing the risk of the sudden infant death syndrome. CESDI SUDI research group. Author(s): Blair PS, Fleming PJ, Smith IJ, Platt MW, Young J, Nadin P, Berry PJ, Golding J. Source: Bmj (Clinical Research Ed.). 1999 December 4; 319(7223): 1457-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10582925&dopt=Abstract

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Bed sharing and smoking in the sudden infant death syndrome. Author(s): Farooqi IS, Lip GY, Beevers DG. Source: Bmj (Clinical Research Ed.). 1994 January 15; 308(6922): 204-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8312792&dopt=Abstract

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Bed sharing and sudden infant death syndrome. Author(s): Bourne AJ, Beal SM, Byard RW. Source: Bmj (Clinical Research Ed.). 1994 February 19; 308(6927): 537-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8136691&dopt=Abstract

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Bed sharing and the sudden infant death syndrome. Author(s): Klonoff-Cohen H, Edelstein SL. Source: Bmj (Clinical Research Ed.). 1995 November 11; 311(7015): 1269-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7496236&dopt=Abstract

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Biovolatilization of antimony and sudden infant death syndrome (SIDS). Author(s): Jenkins RO, Craig PJ, Goessler W, Irgolic KJ. Source: Human & Experimental Toxicology. 1998 April; 17(4): 231-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9617636&dopt=Abstract

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Birth weight- and gestational age-specific sudden infant death syndrome mortality: United States, 1991 versus 1995. Author(s): Malloy MH, Freeman DH Jr. Source: Pediatrics. 2000 June; 105(6): 1227-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10835061&dopt=Abstract

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Blood ferritin concentrations in newborn infants and the sudden infant death syndrome. Author(s): Raha-Chowdhury R, Moore CA, Bradley D, Henley R, Worwood M. Source: Journal of Clinical Pathology. 1996 February; 49(2): 168-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8655686&dopt=Abstract

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Bottle feeding and the sudden infant death syndrome. Author(s): Mitchell EA, Stewart AW, Ford RP. Source: Bmj (Clinical Research Ed.). 1995 July 8; 311(6997): 122-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7613372&dopt=Abstract

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Bottle feeding and the sudden infant death syndrome. Study was not large enough to show effect. Author(s): Tappin DM. Source: Bmj (Clinical Research Ed.). 1995 April 22; 310(6986): 1070; Author Reply 1071. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7728081&dopt=Abstract

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Bottle feeding and the sudden infant death syndrome. Type of formula was not specified. Author(s): Walker-Smith JA. Source: Bmj (Clinical Research Ed.). 1995 April 22; 310(6986): 1070; Author Reply 1071. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7728082&dopt=Abstract

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Brain stem lesions in the sudden infant death syndrome: variability in the hypoplasia of the arcuate nucleus. Author(s): Matturri L, Biondo B, Suarez-Mier MP, Rossi L. Source: Acta Neuropathologica. 2002 July; 104(1): 12-20. Epub 2002 March 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12070659&dopt=Abstract

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Brain stem nuclei in sudden infant death syndrome (SIDS): volumes, neuronal numbers and positions. Author(s): Lamont P, Murray N, Halliday G, Hilton J, Pamphlett R. Source: Neuropathology and Applied Neurobiology. 1995 June; 21(3): 262-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7477735&dopt=Abstract

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Brainstem 3H-nicotine receptor binding in the sudden infant death syndrome. Author(s): Nachmanoff DB, Panigrahy A, Filiano JJ, Mandell F, Sleeper LA, ValdesDapena M, Krous HF, White WF, Kinney HC. Source: Journal of Neuropathology and Experimental Neurology. 1998 November; 57(11): 1018-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9825938&dopt=Abstract

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Brainstem immaturity in sudden infant death syndrome: a quantitative rapid Golgi study of dendritic spines in 95 infants. Author(s): Quattrochi JJ, McBride PT, Yates AJ. Source: Brain Research. 1985 January 28; 325(1-2): 39-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3978432&dopt=Abstract

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Brainstem research in sudden infant death syndrome. Author(s): Kinney HC, Filiano JJ. Source: Pediatrician. 1988; 15(4): 240-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3068663&dopt=Abstract

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Breast feeding and the sudden infant death syndrome in Scandinavia, 1992-95. Author(s): Alm B, Wennergren G, Norvenius SG, Skjaerven R, Lagercrantz H, HelwegLarsen K, Irgens LM. Source: Archives of Disease in Childhood. 2002 June; 86(6): 400-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12023166&dopt=Abstract

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Bronchus-associated lymphoid tissue (BALT) in the lungs of children who had died from sudden infant death syndrome and other causes. Author(s): Tschernig T, Kleemann WJ, Pabst R. Source: Thorax. 1995 June; 50(6): 658-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7638809&dopt=Abstract

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Cardiac sodium channel gene mutations and sudden infant death syndrome: confirmation of proof of concept? Author(s): Towbin JA, Ackerman MJ. Source: Circulation. 2001 September 4; 104(10): 1092-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11535560&dopt=Abstract

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Cerebral cortical function in infants at risk for sudden infant death syndrome. Author(s): Clancy RR, Spitzer AR. Source: Annals of Neurology. 1985 July; 18(1): 41-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4041162&dopt=Abstract

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Cerebrospinal fluid and plasma beta-endorphin concentrations in prolonged infant apnea (near-miss sudden infant death syndrome). Author(s): Sankaran K, Hindmarsh KW, Wallace SM, McKay RJ, O'Donnell M. Source: Dev Pharmacol Ther. 1986; 9(4): 224-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2944729&dopt=Abstract

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Changes in the epidemiological pattern of sudden infant death syndrome in southeast Norway, 1984-1998: implications for future prevention and research. Author(s): Arnestad M, Andersen M, Vege A, Rognum TO. Source: Archives of Disease in Childhood. 2001 August; 85(2): 108-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11466184&dopt=Abstract

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Changes in the epidemiology of sudden infant death syndrome in Sweden 1973-1996. Author(s): Alm B, Norvenius SG, Wennergren G, Skjaerven R, Oyen N, Milerad J, Wennborg M, Kjaerbeck J, Helweg-Larsen K, Irgens LM; Nordic Epidemiological SIDS Study. Source: Archives of Disease in Childhood. 2001 January; 84(1): 24-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11124779&dopt=Abstract

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Chlamydia and sudden infant death syndrome. A study of 166 SIDS and 30 control cases. Author(s): Lundemose JB, Lundemose AG, Gregersen M, Helweg-Larsen K, Simonsen J. Source: International Journal of Legal Medicine. 1990 December; 104(1): 3-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11453089&dopt=Abstract

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Circumstances leading to a change to prone sleeping in sudden infant death syndrome victims. Author(s): Cote A, Gerez T, Brouillette RT, Laplante S. Source: Pediatrics. 2000 December; 106(6): E86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11099629&dopt=Abstract

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Clinical implications of sudden infant death syndrome epidemiology. Author(s): Peterson DR. Source: Pediatrician. 1988; 15(4): 198-203. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3266011&dopt=Abstract

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Commentary: the prevention of sudden infant death syndrome: is there a role for home monitoring? Author(s): Southall DP. Source: Journal of Medical Engineering & Technology. 1985 November-December; 9(6): 259-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4087279&dopt=Abstract

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Comparative analysis of differences by gender in sudden infant death syndrome in Hungary and Japan. Author(s): Toro K, Sawaguchi T, Sawaguchi A, Rozsa S, Sotonyi P. Source: Forensic Science International. 2001 April 15; 118(1): 15-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11343850&dopt=Abstract

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Comparative epidemiology of sudden infant death syndrome and sudden intrauterine unexplained death. Author(s): Froen JF, Arnestad M, Vege A, Irgens LM, Rognum TO, Saugstad OD, StrayPedersen B. Source: Archives of Disease in Childhood. Fetal and Neonatal Edition. 2002 September; 87(2): F118-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12193518&dopt=Abstract

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Comparative evaluation of diagnostic guidelines for sudden infant death syndrome (SIDS) in Japan. Author(s): Sawaguchi T, Sawaguchi A, Matoba R. Source: Forensic Science International. 2002 September 14; 130 Suppl: S65-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12350304&dopt=Abstract

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Comparison of infants dying from the sudden infant death syndrome with matched live controls. Author(s): Bartholomew S, MacArthur BA. Source: Social Science & Medicine (1982). 1988; 27(4): 393-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3175722&dopt=Abstract

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Confounding in the study of pacifier use in sudden infant death syndrome. Author(s): Schlaud M, Poets CF. Source: European Journal of Pediatrics. 2000 July; 159(7): 542-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10923233&dopt=Abstract

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Considering suffocatory abuse and Munchausen by proxy in the evaluation of children experiencing apparent life-threatening events and sudden infant death syndrome. Author(s): Truman TL, Ayoub CC. Source: Child Maltreatment. 2002 May; 7(2): 138-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12020070&dopt=Abstract

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Cost-effectiveness and implications of newborn screening for prolongation of QT interval for the prevention of sudden infant death syndrome. Author(s): Zupancic JA, Triedman JK, Alexander M, Walsh EP, Richardson DK, Berul CI. Source: The Journal of Pediatrics. 2000 April; 136(4): 481-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10753246&dopt=Abstract

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Could Pneumocystis carinii have a role in sudden infant death syndrome? Author(s): Orellana C. Source: Lancet. 2001 July 7; 358(9275): 43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11454387&dopt=Abstract

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Coxsackie B3 myocarditis in 4 cases of suspected sudden infant death syndrome: diagnosis by immunohistochemical and molecular-pathologic investigations. Author(s): Dettmeyer R, Baasner A, Schlamann M, Haag C, Madea B. Source: Pathology, Research and Practice. 2002; 198(10): 689-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12498225&dopt=Abstract

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Cree infant care practices and sudden infant death syndrome. Author(s): Wilson CE. Source: Canadian Journal of Public Health. Revue Canadienne De Sante Publique. 2000 March-April; 91(2): 133-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10832180&dopt=Abstract

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Curliated Escherichia coli, soluble curlin and the sudden infant death syndrome (SIDS). Author(s): Goldwater PN, Bettelheim KA. Source: Journal of Medical Microbiology. 2002 November; 51(11): 1009-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12448686&dopt=Abstract

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Debate on cot death. In 1994, 29% of suspicious deaths were officially recorded as due to sudden infant death syndrome. Author(s): Reder P, Duncan S. Source: Bmj (Clinical Research Ed.). 2000 January 29; 320(7230): 311. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10722290&dopt=Abstract

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Decreased autonomic responses to obstructive sleep events in future victims of sudden infant death syndrome. Author(s): Franco P, Szliwowski H, Dramaix M, Kahn A. Source: Pediatric Research. 1999 July; 46(1): 33-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10400131&dopt=Abstract

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Decreased kainate receptor binding in the arcuate nucleus of the sudden infant death syndrome. Author(s): Panigrahy A, Filiano JJ, Sleeper LA, Mandell F, Valdes-Dapena M, Krous HF, Rava LA, White WF, Kinney HC. Source: Journal of Neuropathology and Experimental Neurology. 1997 November; 56(11): 1253-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9370236&dopt=Abstract

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Decreased serotonergic receptor binding in rhombic lip-derived regions of the medulla oblongata in the sudden infant death syndrome. Author(s): Panigrahy A, Filiano J, Sleeper LA, Mandell F, Valdes-Dapena M, Krous HF, Rava LA, Foley E, White WF, Kinney HC. Source: Journal of Neuropathology and Experimental Neurology. 2000 May; 59(5): 37784. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10888367&dopt=Abstract

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Defects of metabolism of fatty acids in the sudden infant death syndrome. Author(s): Howat AJ, Bennett MJ, Variend S, Shaw L, Engel PC. Source: British Medical Journal (Clinical Research Ed.). 1985 June 15; 290(6484): 1771-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3924247&dopt=Abstract

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Deficient heat shock protein expression: a potential mechanism for the sudden infant death syndrome. Author(s): Gozal D. Source: Medical Hypotheses. 1996 January; 46(1): 52-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8746129&dopt=Abstract

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Defining the sudden infant death syndrome. Author(s): Beckwith JB. Source: Archives of Pediatrics & Adolescent Medicine. 2003 March; 157(3): 286-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622679&dopt=Abstract

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Definition of the sudden infant death syndrome. Author(s): Rambaud C, Guilleminault C, Campbell PE. Source: Bmj (Clinical Research Ed.). 1994 May 28; 308(6941): 1439. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7993420&dopt=Abstract

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Dendritic development of motor neurons in the cervical anterior horn and hypoglossal nucleus of normal infants and victims of sudden infant death syndrome. Author(s): Takashima S, Mito T, Becker LE. Source: Neuropediatrics. 1990 February; 21(1): 24-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2314554&dopt=Abstract

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Deprivation and sudden infant death syndrome. Author(s): Mitchell EA, Stewart AW, Crampton P, Salmond C. Source: Social Science & Medicine (1982). 2000 July; 51(1): 147-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10817477&dopt=Abstract

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Detection of pyrogenic toxins of Staphylococcus aureus in sudden infant death syndrome. Author(s): Zorgani A, Essery SD, Madani OA, Bentley AJ, James VS, MacKenzie DA, Keeling JW, Rambaud C, Hilton J, Blackwell CC, Weir DM, Busuttil A. Source: Fems Immunology and Medical Microbiology. 1999 August 1; 25(1-2): 103-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10443497&dopt=Abstract

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Developmental abnormalities of medullary “respiratory centers” in sudden infant death syndrome. Author(s): Takashima S, Becker LE. Source: Experimental Neurology. 1985 December; 90(3): 580-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4065274&dopt=Abstract

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Developmental and environmental factors that enhance binding of Bordetella pertussis to human epithelial cells in relation to sudden infant death syndrome (SIDS). Author(s): Saadi AT, Blackwell CC, Essery SD, Raza MW, el Ahmer OR, MacKenzie DA, James VS, Weir DM, Ogilvie MM, Elton RA, Busuttil A, Keeling JW. Source: Fems Immunology and Medical Microbiology. 1996 November; 16(1): 51-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8954353&dopt=Abstract

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Developmental brain-stem pathology in sudden infant death syndrome. Author(s): Takashima S, Mito T, Yamanouchi H. Source: Acta Paediatr Jpn. 1994 June; 36(3): 317-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7522391&dopt=Abstract

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Developmental characteristics of apnea in infants who succumb to sudden infant death syndrome. Author(s): Kato I, Groswasser J, Franco P, Scaillet S, Kelmanson I, Togari H, Kahn A. Source: American Journal of Respiratory and Critical Care Medicine. 2001 October 15; 164(8 Pt 1): 1464-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11704597&dopt=Abstract

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Developmental neurotransmitter pathology in the brainstem of sudden infant death syndrome: a review and sleep position. Author(s): Ozawa Y, Takashima S. Source: Forensic Science International. 2002 September 14; 130 Suppl: S53-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12350301&dopt=Abstract

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Do differences in the prevalence of risk factors explain the higher mortality from sudden infant death syndrome in New Zealand compared with the UK? Author(s): Mitchell EA, Esmail A, Jones DR, Clements M. Source: N Z Med J. 1996 September 27; 109(1030): 352-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8890859&dopt=Abstract

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DPT-OPV immunization and sudden infant death syndrome. Author(s): John TJ. Source: Indian Pediatrics. 1997 November; 34(11): 1045-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9567540&dopt=Abstract

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Dummy sucking and sudden infant death syndrome (SIDS) Author(s): Cozzi F, Cardi E, Cozzi DA. Source: European Journal of Pediatrics. 1998 November; 157(11): 952. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9835447&dopt=Abstract

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Dynamics of respiratory patterning in normal infants and infants who subsequently died of the sudden infant death syndrome. Author(s): Schechtman VL, Lee MY, Wilson AJ, Harper RM. Source: Pediatric Research. 1996 October; 40(4): 571-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8888285&dopt=Abstract

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Early and late MR findings in near-miss sudden infant death syndrome. Author(s): Demaerel P, Lagae L, Schraepen T, Baert AL. Source: Journal of Computer Assisted Tomography. 1998 January-February; 22(1): 133-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9448777&dopt=Abstract

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Effect of a sudden infant death syndrome risk reduction education program on risk factor compliance and information sources in primarily black urban communities. Author(s): Rasinski KA, Kuby A, Bzdusek SA, Silvestri JM, Weese-Mayer DE. Source: Pediatrics. 2003 April; 111(4 Pt 1): E347-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671150&dopt=Abstract

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Effect of time post mortem on the concentration of endotoxin in rat organs: implications for sudden infant death syndrome (SIDS). Author(s): Sayers NM, Crawley BA, Humphries K, Drucker DB, Oppenheim BA, Hunt LP, Morris JA, Telford DR. Source: Fems Immunology and Medical Microbiology. 1999 August 1; 25(1-2): 125-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10443500&dopt=Abstract

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Effects of hypomagnesemia on reactivity of bovine and ovine platelets: possible relevance to infantile apnea and sudden infant death syndrome. Author(s): Miller JK, Schneider MD, Ramsey N, White PK, Bell MC. Source: Journal of the American College of Nutrition. 1990 February; 9(1): 58-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2307807&dopt=Abstract

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Elevated serum concentrations of beta-tryptase, but not alpha-tryptase, in Sudden Infant Death Syndrome (SIDS). An investigation of anaphylactic mechanisms. Author(s): Buckley MG, Variend S, Walls AF. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 2001 November; 31(11): 1696-704. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11696045&dopt=Abstract

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Endotoxin in blood and tissue in the sudden infant death syndrome. Author(s): Crawley BA, Morris JA, Drucker DB, Barson AJ, Morris J, Knox WF, Oppenheim BA. Source: Fems Immunology and Medical Microbiology. 1999 August 1; 25(1-2): 131-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10443501&dopt=Abstract

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Enhanced reactivity of Alz-50 antibody in brains of sudden infant death syndrome victims versus brains with lethal hypoxic/ischemic injury. Diagnostic significance after application of the ImmunoMax technique on routine paraffin material. Author(s): Oehmichen M, Theuerkauf I, Bajanowski T, Merz H, Meissner C. Source: Acta Neuropathologica. 1998 March; 95(3): 280-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9542593&dopt=Abstract

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Enzyme-linked immunoassay for respiratory syncytial virus is not predictive of bronchiolitis in sudden infant death syndrome. Author(s): Parham DM, Cheng R, Schutze GE, Dilday B, Nelson R, Erickson S, Kokes C, Peretti F, Sturner WQ. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 1998 September-October; 1(5): 375-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9688761&dopt=Abstract

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Epidemiological investigation of sudden infant death syndrome infants-recommendations for future studies. Author(s): Blair P, Fleming P. Source: Child: Care, Health and Development. 2002 September; 28 Suppl 1: 49-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515441&dopt=Abstract

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Epidemiology of intrathoracic petechial hemorrhages in sudden infant death syndrome. Author(s): Becroft DM, Thompson JM, Mitchell EA. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 1998 May-June; 1(3): 200-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10463279&dopt=Abstract

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Epidemiology of sudden infant death syndrome (SIDS) in the Tyrol before and after an intervention campaign. Author(s): Kiechl-Kohlendorfer U, Peglow UP, Kiechl S, Oberaigner W, Sperl W. Source: Wiener Klinische Wochenschrift. 2001 January 15; 113(1-2): 27-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11233464&dopt=Abstract

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Epidemiology of sudden infant death syndrome in Japan. Author(s): Watanabe N, Yotsukura M, Kadoi N, Yashiro K, Sakanoue M, Nishida H. Source: Acta Paediatr Jpn. 1994 June; 36(3): 329-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8091991&dopt=Abstract

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Estimation of mean nuclear volume of neocortical neurons in sudden infant death syndrome cases using the nucleator estimator technique. Author(s): Ansari T, Sibbons PD, Howard CV. Source: Biology of the Neonate. 2001 July; 80(1): 48-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11474149&dopt=Abstract

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Ethnic differences in incidence of sudden infant death syndrome in Birmingham. Author(s): Kyle D, Sunderland R, Stonehouse M, Cummins C, Ross O. Source: Archives of Disease in Childhood. 1990 August; 65(8): 830-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2400217&dopt=Abstract

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Ethnic differences in the incidence of the sudden infant death syndrome (SIDS) in Victoria, Australia 1985-1989. Author(s): Kilkenny M, Lumley J. Source: Paediatric and Perinatal Epidemiology. 1994 January; 8(1): 27-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8153016&dopt=Abstract

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Ethnicity and the aetiology of sudden infant death syndrome. Author(s): Davies DP, Gantley M. Source: Archives of Disease in Childhood. 1994 April; 70(4): 349-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8185373&dopt=Abstract

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Ethnicity and the sudden infant death syndrome: important clues from anthropology. Author(s): Mckenna JJ, Fleming PJ. Source: Archives of Disease in Childhood. 1994 May; 70(5): 450. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8017974&dopt=Abstract

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Evidence for a genetic component in sudden infant death syndrome. Author(s): Gordon AE, MacKenzie DA, El Ahmer OR, Al Madani OM, Braun JM, Weir DM, Busuttil A, Blackwell CC. Source: Child: Care, Health and Development. 2002 September; 28 Suppl 1: 27-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515435&dopt=Abstract

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Exposure of piglet coronary arterial muscle cells to low concentrations of Mg2+ found in blood of ischemic heart disease patients result in rapid elevation of cytosolic Ca2+: relevance to sudden infant death syndrome. Author(s): Altura BM, Zhang A, Altura BT. Source: European Journal of Pharmacology. 1997 November 5; 338(2): R7-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9456006&dopt=Abstract

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Exposure to cigarette smoke, a major risk factor for sudden infant death syndrome: effects of cigarette smoke on inflammatory responses to viral infection and bacterial toxins. Author(s): Raza MW, Essery SD, Elton RA, Weir DM, Busuttil A, Blackwell C. Source: Fems Immunology and Medical Microbiology. 1999 August 1; 25(1-2): 145-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10443503&dopt=Abstract

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Facial structure in the sudden infant death syndrome: case-control study. Author(s): Rees K, Wright A, Keeling JW, Douglas NJ. Source: Bmj (Clinical Research Ed.). 1998 July 18; 317(7152): 179-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9665897&dopt=Abstract

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Factors enhancing adherence of toxigenic Staphylococcus aureus to epithelial cells and their possible role in sudden infant death syndrome. Author(s): Saadi AT, Blackwell CC, Raza MW, James VS, Stewart J, Elton RA, Weir DM. Source: Epidemiology and Infection. 1993 June; 110(3): 507-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8519316&dopt=Abstract

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Factors potentiating the risk of sudden infant death syndrome associated with the prone position. Author(s): Ponsonby AL, Dwyer T, Gibbons LE, Cochrane JA, Wang YG. Source: The New England Journal of Medicine. 1993 August 5; 329(6): 377-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8326970&dopt=Abstract

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Familial predisposition and cosegregation analysis of adult obstructive sleep apnea and the sudden infant death syndrome. Author(s): Gislason T, Johannsson JH, Haraldsson A, Olafsdottir BR, Jonsdottir H, Kong A, Frigge ML, Jonsdottir GM, Hakonarson H, Gulcher J, Stefansson K. Source: American Journal of Respiratory and Critical Care Medicine. 2002 September 15; 166(6): 833-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12231493&dopt=Abstract

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Fatal child abuse and sudden infant death syndrome (SIDS): a critical diagnostic decision. Author(s): Beeber B, Cunningham N. Source: Pediatrics. 1994 March; 93(3): 539-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8115231&dopt=Abstract

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Fatal child abuse and sudden infant death syndrome: a critical diagnostic decision. Author(s): Reece RM. Source: Pediatrics. 1993 February; 91(2): 423-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8424022&dopt=Abstract

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Febrile convulsions and sudden infant death syndrome. Author(s): Vestergaard M, Basso O, Henriksen TB, Ostergaard J, Olsen J. Source: Archives of Disease in Childhood. 2002 February; 86(2): 125-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11827907&dopt=Abstract

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Fetal behaviour and the sudden infant death syndrome (SIDS). Author(s): Smoleniec J, James D. Source: Archives of Disease in Childhood. Fetal and Neonatal Edition. 1995 May; 72(3): F168-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7796231&dopt=Abstract

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Fetal growth retardation in sudden infant death syndrome (SIDS) babies and their siblings. Author(s): Oyen N, Skjaerven R, Little RE, Wilcox AJ. Source: American Journal of Epidemiology. 1995 July 1; 142(1): 84-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7785678&dopt=Abstract

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Fetal hemoglobin and sudden infant death syndrome. Author(s): Gilbert-Barness E, Kenison K, Carver J. Source: Archives of Pathology & Laboratory Medicine. 1993 February; 117(2): 177-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7678955&dopt=Abstract

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Fetal hemoglobin levels in sudden infant death syndrome. Author(s): Perry GW, Vargas-Cuba R, Vertes RP. Source: Archives of Pathology & Laboratory Medicine. 1997 October; 121(10): 1048-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9341583&dopt=Abstract

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Fetal hemoglobin synthesis determined by gamma-mRNA/gamma-mRNA + betamRNA quantitation in infants at risk for sudden infant death syndrome being monitored at home for apnea. Author(s): Bard H, Cote A, Praud JP, Infante-Rivard C, Gagnon C. Source: Pediatrics. 2003 October; 112(4): E285. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14523213&dopt=Abstract

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Finding the failure mechanism in Sudden Infant Death Syndrome. Author(s): Harper RM, Bandler R. Source: Nature Medicine. 1998 February; 4(2): 157-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9461186&dopt=Abstract

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Findings in child deaths registered as sudden infant death syndrome (SIDS) in Madison, Wisconsin. Author(s): Emery JL, Chandra S, Gilbert-Barness EF. Source: Pediatr Pathol. 1988; 8(2): 171-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3045783&dopt=Abstract

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Foundation is helping carers to reduce risk of sudden infant death syndrome. Author(s): Deri-Bowen A. Source: Bmj (Clinical Research Ed.). 2001 February 24; 322(7284): 491. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11222433&dopt=Abstract

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Frequency of 985A-to-G mutation in medium-chain acyl-CoA dehydrogenase gene among patients with sudden infant death syndrome, Reye syndrome, severe motor and intellectual disabilities and healthy newborns in Japan. Author(s): Nagao M. Source: Acta Paediatr Jpn. 1996 August; 38(4): 304-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8840534&dopt=Abstract

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From epidemiology to physiology and pathology: apnea and arousal deficient theories in sudden infant death syndrome (SIDS)--with particular reference to hypoxic brainstem gliosis. Author(s): Sawaguchi T, Franco P, Kato I, Shimizu S, Kadhim H, Groswasser J, Sottiaux M, Togari H, Kobayashi M, Takashima S, Nishida H, Sawaguchi A, Kahn A. Source: Forensic Science International. 2002 September 14; 130 Suppl: S21-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12350297&dopt=Abstract

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From physiology to pathology: arousal deficiency theory in sudden infant death syndrome (SIDS)--with reference to apoptosis and neuronal plasticity. Author(s): Sawaguchi T, Franco P, Kato I, Shimizu S, Kadhim H, Groswasser J, Sottiaux M, Togari H, Kobayashi M, Takashima S, Nishida H, Sawaguchi A, Kahn A. Source: Forensic Science International. 2002 September 14; 130 Suppl: S37-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12350299&dopt=Abstract

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Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome. Author(s): Holgert H, Hokfelt T, Hertzberg T, Lagercrantz H. Source: Proceedings of the National Academy of Sciences of the United States of America. 1995 August 1; 92(16): 7575-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7638233&dopt=Abstract

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Fungal volatilization of arsenic and antimony and the sudden infant death syndrome. Author(s): Pearce RB, Callow ME, Macaskie LE. Source: Fems Microbiology Letters. 1998 January 15; 158(2): 261-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9465397&dopt=Abstract

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Gastric secretion in infants. Application to the study of sudden infant death syndrome and apparently life-threatening events. Author(s): Mouterde O, Dacher JN, Basuyau JP, Mallet E. Source: Biology of the Neonate. 1992; 62(1): 15-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1391271&dopt=Abstract

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Gastroesophageal reflux and sudden infant death syndrome. Author(s): Byard RW, Moore L. Source: Pediatr Pathol. 1993 January-February; 13(1): 53-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8474951&dopt=Abstract

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Gastroesophageal reflux, as measured by 24-hour pH monitoring, in 509 healthy infants screened for risk of sudden infant death syndrome. Author(s): Vandenplas Y, Goyvaerts H, Helven R, Sacre L. Source: Pediatrics. 1991 October; 88(4): 834-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1896295&dopt=Abstract

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Gastro-oesophageal reflux in near-miss sudden infant death syndrome or suspected recurrent aspiration. Author(s): MacFadyen UM, Hendry GM, Simpson H. Source: Archives of Disease in Childhood. 1983 February; 58(2): 87-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6830303&dopt=Abstract

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Gender and the sudden infant death syndrome. New Zealand Cot Death Study Group. Author(s): Mitchell EA, Stewart AW. Source: Acta Paediatrica (Oslo, Norway : 1992). 1997 August; 86(8): 854-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9307167&dopt=Abstract

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Gender differences in parental psychological distress following perinatal death or sudden infant death syndrome. Author(s): Vance JC, Boyle FM, Najman JM, Thearle MJ. Source: The British Journal of Psychiatry; the Journal of Mental Science. 1995 December; 167(6): 806-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8829751&dopt=Abstract

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Generalized view of the origins of the sudden infant death syndrome. Author(s): Vorontsov IM, Kelmanson IA. Source: Medical Hypotheses. 1990 November; 33(3): 187-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2292983&dopt=Abstract

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Geophysical variables and behavior: LXXXII. A strong association between sudden infant death syndrome and increments of global geomagnetic activity--possible support for the melatonin hypothesis. Author(s): O'Connor RP, Persinger MA. Source: Percept Mot Skills. 1997 April; 84(2): 395-402. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9106826&dopt=Abstract

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Glomerulosclerosis in the sudden infant death syndrome. Author(s): Valdes-Dapena M, Hoffman HJ, Froelich C, Requeira O. Source: Pediatr Pathol. 1990; 10(1-2): 273-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2315230&dopt=Abstract

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Gluconeogenic enzymes in fibroblasts from infants dying of the sudden infant death syndrome (SIDS). Author(s): Sumbilla CM, Zielke HR, Krause BL, Ozand PT. Source: European Journal of Pediatrics. 1983 June-July; 140(3): 276-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6628449&dopt=Abstract

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Grief intervention and sudden infant death syndrome. Author(s): Lowman J. Source: American Journal of Community Psychology. 1979 December; 7(6): 665-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=517467&dopt=Abstract

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Growth and the sudden infant death syndrome. Author(s): Williams SM, Scragg R, Mitchell EA, Taylor BJ. Source: Acta Paediatrica (Oslo, Norway : 1992). 1996 November; 85(11): 1284-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8955453&dopt=Abstract

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Guidance on preventing sudden infant death syndrome. Author(s): Kenyon S. Source: Community Nurse. 2000 October; 6(9): S9-10. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11982157&dopt=Abstract

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Has changing diagnostic preference been responsible for the recent fall in incidence of sudden infant death syndrome in South Australia? Author(s): Byard RW, Beal SM. Source: Journal of Paediatrics and Child Health. 1995 June; 31(3): 197-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7669379&dopt=Abstract

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Hazards in the epidemiological study of sudden infant death syndrome. Author(s): Meadow SR. Source: Archives of Disease in Childhood. 2003 May; 88(5): 460-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716730&dopt=Abstract

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Heart rate variability in infants subsequently suffering sudden infant death syndrome (SIDS). Author(s): Antila KJ, Valimaki IA, Makela M, Tuominen J, Wilson AJ, Southall DP. Source: Early Human Development. 1990 May; 22(2): 57-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2364905&dopt=Abstract

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Heart weight in infants--a comparison between sudden infant death syndrome and other causes of death. Author(s): Rasten-Almqvist P, Eksborg S, Rajs J. Source: Acta Paediatrica (Oslo, Norway : 1992). 2000 September; 89(9): 1062-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11071085&dopt=Abstract

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Heavy caffeine consumption in pregnancy, smoking, and sudden infant death syndrome. Author(s): Leviton A. Source: Archives of Disease in Childhood. 1998 September; 79(3): 291. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9875035&dopt=Abstract

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Heavy caffeine intake in pregnancy and sudden infant death syndrome. New Zealand Cot Death Study Group. Author(s): Ford RP, Schluter PJ, Mitchell EA, Taylor BJ, Scragg R, Stewart AW. Source: Archives of Disease in Childhood. 1998 January; 78(1): 9-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9534669&dopt=Abstract

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Helicobacter pylori is not the cause of sudden infant death syndrome (SIDS). Author(s): Ho GY, Windsor HM, Snowball B, Marshall BJ. Source: The American Journal of Gastroenterology. 2001 December; 96(12): 3288-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11774938&dopt=Abstract

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High incidence of sudden infant death syndrome among northern Indians and Alaska natives compared with southwestern Indians: possible role of smoking. Author(s): Bulterys M. Source: Journal of Community Health. 1990 June; 15(3): 185-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2365840&dopt=Abstract

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High postmortem concentrations of hypoxanthine and urate in the vitreous humor of infants are not confined to cases of sudden infant death syndrome. Author(s): Belonje PC, Wilson GR, Siroka SA. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1996 July; 86(7): 827-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8764909&dopt=Abstract

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Histopathological findings of the lung and trachea in sudden infant death syndrome: review of 105 cases autopsied at Dade County Medical Examiner Department. Author(s): Aoki Y. Source: Nippon Hoigaku Zasshi. 1994 June; 48(3): 141-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8065063&dopt=Abstract

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Home apnea monitoring and sudden infant death syndrome. Author(s): Malloy MH, Hoffman HJ. Source: Preventive Medicine. 1996 November-December; 25(6): 645-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8936564&dopt=Abstract

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Home monitoring for infants at high risk for the sudden infant death syndrome. Author(s): Sivan Y, Kornecki A, Baharav A, Glaser N, Spirer Z. Source: Isr J Med Sci. 1997 January; 33(1): 45-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9203517&dopt=Abstract

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Housing and sudden infant death syndrome. The New Zealand Cot Death Study Group. Author(s): Schluter PJ, Ford RP, Mitchell EA, Taylor BJ. Source: N Z Med J. 1997 July 11; 110(1047): 243-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9251707&dopt=Abstract

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How does prone sleeping increase prevalence of sudden infant death syndrome? Author(s): Thach BT. Source: Pediatr Pulmonol Suppl. 1997; 16: 115-6. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9443232&dopt=Abstract

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Human heat shock protein gene polymorphisms and sudden infant death syndrome. Author(s): Rahim RA, Boyd PA, Ainslie Patrick WJ, Burdon RH. Source: Archives of Disease in Childhood. 1996 November; 75(5): 451-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8957963&dopt=Abstract

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Hyperekplexia associated with apnea and sudden infant death syndrome. Author(s): Giacoia GP, Ryan SG. Source: Archives of Pediatrics & Adolescent Medicine. 1994 May; 148(5): 540-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8180653&dopt=Abstract

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Hyperplasia of the aorticopulmonary paraganglia: a new insight into the pathogenesis of sudden infant death syndrome? Author(s): Ramos SG, Matturri L, Biondo B, Ottaviani G, Rossi L. Source: Cardiologia. 1998 September; 43(9): 953-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9859610&dopt=Abstract

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Hyper-releasability of mast cells in family members of infants with sudden infant death syndrome and apparent life-threatening events. Author(s): Gold Y, Goldberg A, Sivan Y. Source: The Journal of Pediatrics. 2000 April; 136(4): 460-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10753243&dopt=Abstract

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Hypoxanthine levels in vitreous humor: a study of influencing factors in sudden infant death syndrome. Author(s): Opdal SH, Rognum TO, Vege A, Saugstad OD. Source: Pediatric Research. 1998 August; 44(2): 192-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9702913&dopt=Abstract

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Hypoxic responses in infants. No known mechanism links hypoxia and sudden infant death syndrome. Author(s): Niermeyer S, Moore LG. Source: Bmj (Clinical Research Ed.). 1998 September 5; 317(7159): 675-6; Author Reply 677-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9758493&dopt=Abstract

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Identification of Pneumocystis carinii in the lungs of infants dying of sudden infant death syndrome. Author(s): Morgan DJ, Vargas SL, Reyes-Mugica M, Walterspiel JN, Carver W, Gigliotti F. Source: The Pediatric Infectious Disease Journal. 2001 March; 20(3): 306-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11303835&dopt=Abstract

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Immune and inflammatory responses in sudden infant death syndrome. Author(s): Forsyth KD. Source: Fems Immunology and Medical Microbiology. 1999 August 1; 25(1-2): 79-83. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10443494&dopt=Abstract

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Immunohistochemical techniques improve the diagnosis of myocarditis in cases of suspected sudden infant death syndrome (SIDS). Author(s): Dettmeyer R, Schlamann M, Madea B. Source: Forensic Science International. 1999 November 1; 105(2): 83-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10605078&dopt=Abstract

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Immunological evidence for a bacterial toxin aetiology in sudden infant death syndrome. Author(s): Siarakas S, Brown AJ, Murrell WG. Source: Fems Immunology and Medical Microbiology. 1999 August 1; 25(1-2): 37-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10443490&dopt=Abstract

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Incidence and geographical distribution of sudden infant death syndrome in relation to content of nitrate in drinking water and groundwater levels. Author(s): George M, Wiklund L, Aastrup M, Pousette J, Thunholm B, Saldeen T, Wernroth L, Zaren B, Holmberg L. Source: European Journal of Clinical Investigation. 2001 December; 31(12): 1083-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11903496&dopt=Abstract

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Increase of pulmonary density of macrophages in sudden infant death syndrome. Author(s): Lorin de la Grandmaison G, Dorandeu A, Carton M, Patey A, Durigon M. Source: Forensic Science International. 1999 October 11; 104(2-3): 179-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10581724&dopt=Abstract

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Increased facial temperature as an early warning in Sudden Infant Death Syndrome. Author(s): Russell MJ, Vink R. Source: Medical Hypotheses. 2001 July; 57(1): 61-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11421627&dopt=Abstract

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Infant medication and sudden infant death syndrome. Author(s): Walker AM, Romieu I. Source: American Journal of Preventive Medicine. 1988; 4(2 Suppl): 29-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3275177&dopt=Abstract

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Infant sleeping position and the risk of sudden infant death syndrome in California, 1997-2000. Author(s): Li DK, Petitti DB, Willinger M, McMahon R, Odouli R, Vu H, Hoffman HJ. Source: American Journal of Epidemiology. 2003 March 1; 157(5): 446-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12615609&dopt=Abstract

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Infant stress and sleep deprivation as an aetiological basis for the sudden infant death syndrome. Author(s): Simpson JM. Source: Early Human Development. 2001 February; 61(1): 1-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11172974&dopt=Abstract

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Infant with an apparent life-threatening event and possible risk for sudden infant death syndrome. Author(s): Kahn A, Rebuffat E, Sottiaux M, Blum D. Source: Padiatr Padol. 1988; 23(4): 293-306. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3071768&dopt=Abstract

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Inflammatory responses in sudden infant death syndrome -- past and present views. Author(s): Vege A, Rognum TO. Source: Fems Immunology and Medical Microbiology. 1999 August 1; 25(1-2): 67-78. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10443493&dopt=Abstract

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Inspired CO(2) and O(2) in sleeping infants rebreathing from bedding: relevance for sudden infant death syndrome. Author(s): Patel AL, Harris K, Thach BT. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 2001 December; 91(6): 2537-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11717216&dopt=Abstract

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Intra-alveolar haemorrhage in sudden infant death syndrome: a cause for concern? Author(s): Yukawa N, Carter N, Rutty G, Green MA. Source: Journal of Clinical Pathology. 1999 August; 52(8): 581-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10645227&dopt=Abstract

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Intra-alveolar haemorrhage in sudden infant death syndrome: a cause for concern? Author(s): Berry PJ. Source: Journal of Clinical Pathology. 1999 August; 52(8): 553-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10645223&dopt=Abstract

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Intrathoracic petechiae in sudden infant death syndrome: relationship to face position when found. Author(s): Krous HF, Nadeau JM, Silva PD, Blackbourne BD. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 2001 March-April; 4(2): 160-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11178632&dopt=Abstract

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Intrathoracic petechial hemorrhages: a clue to the mechanism of death in sudden infant death syndrome? Author(s): Beckwith JB. Source: Annals of the New York Academy of Sciences. 1988; 533: 37-47. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3048177&dopt=Abstract

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Is sudden infant death syndrome associated with Helicobacter pylori infection in children? Author(s): Elitsur Y, Btriest W, Sabet Z, Neace C, Jiang C, Thomas E. Source: Helicobacter. 2000 December; 5(4): 227-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179988&dopt=Abstract

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Is sudden infant death syndrome still more common in very low birthweight infants in the 1990s? Author(s): Sowter B, Doyle LW, Morley CJ, Altmann A, Halliday J. Source: The Medical Journal of Australia. 1999 October 18; 171(8): 411-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10590743&dopt=Abstract

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Is the G985A allelic variant of medium-chain acyl-CoA dehydrogenase a risk factor for sudden infant death syndrome? A pooled analysis. Author(s): Wang SS, Fernhoff PM, Khoury MJ. Source: Pediatrics. 2000 May; 105(5): 1175-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10836898&dopt=Abstract

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JAMA patient page. Sudden infant death syndrome. Author(s): Parmet S, Lynm C, Glass RM. Source: Jama : the Journal of the American Medical Association. 2002 December 4; 288(21): 2772. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12460105&dopt=Abstract

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Labor and delivery events and risk of sudden infant death syndrome (SIDS) Author(s): Buck GM, Michalek AM, Kramer AA, Batt RE. Source: American Journal of Epidemiology. 1991 May 1; 133(9): 900-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2028979&dopt=Abstract

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Laryngospasm and diaphragmatic arrest in immature dogs after laryngeal acid exposure: a possible model for sudden infant death syndrome. Author(s): Duke SG, Postma GN, McGuirt WF Jr, Ririe D, Averill DB, Koufman JA. Source: The Annals of Otology, Rhinology, and Laryngology. 2001 August; 110(8): 72933. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11510729&dopt=Abstract

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Lessons from sudden infant death syndrome. Author(s): Kearney PJ. Source: Ir J Med Sci. 2000 January-March; 169(1): 17-8. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10846850&dopt=Abstract

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Lethal challenge of gnotobiotic weanling rats with bacterial isolates from cases of sudden infant death syndrome (SIDS). Author(s): Lee S, Barson AJ, Drucker DB, Morris JA, Telford DR. Source: Journal of Clinical Pathology. 1987 December; 40(12): 1393-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3323245&dopt=Abstract

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Lethal synergistic action of toxins of bacteria isolated from sudden infant death syndrome. Author(s): Drucker DB, Aluyi HS, Morris JA, Telford DR, Gibbs A. Source: Journal of Clinical Pathology. 1992 September; 45(9): 799-801. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1401211&dopt=Abstract

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Lethal synergy between toxins of staphylococci and enterobacteria: implications for sudden infant death syndrome. Author(s): Sayers NM, Drucker DB, Morris JA, Telford DR. Source: Journal of Clinical Pathology. 1995 October; 48(10): 929-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8537492&dopt=Abstract

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Life events, social support and the risk of sudden infant death syndrome. Author(s): Ford RP, Hassall IB, Mitchell EA, Scragg R, Taylor BJ, Allen EM, Stewart AW. Source: Journal of Child Psychology and Psychiatry, and Allied Disciplines. 1996 October; 37(7): 835-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8923226&dopt=Abstract

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Light is recognized best through darkness: mast cells and Sudden Infant Death Syndrome. Author(s): Schwartz LB. Source: Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology. 2001 November; 31(11): 1657-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11696039&dopt=Abstract

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Lipid-containing cells in the brain in sudden infant death syndrome. Author(s): Esiri MM, Urry P, Keeling J. Source: Developmental Medicine and Child Neurology. 1990 April; 32(4): 319-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2332122&dopt=Abstract

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Liver fatty acids and the sudden infant death syndrome. Author(s): Fogerty AC, Ford GL, Willcox ME, Clancy SL. Source: The American Journal of Clinical Nutrition. 1984 February; 39(2): 201-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6230001&dopt=Abstract

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Liver iron concentrations in sudden infant death syndrome. Author(s): Moore CA, Raha-Chowdhury R, Fagan DG, Worwood M. Source: Archives of Disease in Childhood. 1994 April; 70(4): 295-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8185362&dopt=Abstract

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Living at high altitude and risk of sudden infant death syndrome. Author(s): Kohlendorfer U, Kiechl S, Sperl W. Source: Archives of Disease in Childhood. 1998 December; 79(6): 506-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10210996&dopt=Abstract

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Location of smoking and the sudden infant death syndrome (SIDS). Author(s): Mitchell EA, Scragg L, Clements M. Source: Aust N Z J Med. 1995 April; 25(2): 155-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7605299&dopt=Abstract

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Loss of neonatal hypoxia tolerance after prenatal nicotine exposure: implications for sudden infant death syndrome. Author(s): Slotkin TA, Lappi SE, McCook EC, Lorber BA, Seidler FJ. Source: Brain Research Bulletin. 1995; 38(1): 69-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7552377&dopt=Abstract

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Lung development: number of terminal bronchiolar duct endings and gas exchange surface area in victims of sudden infant death syndrome. Author(s): Beech DJ, Sibbons PD, Howard CV, van Velzen D. Source: Pediatric Pulmonology. 2001 May; 31(5): 339-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11340679&dopt=Abstract

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Lung immunoglobulins in the sudden infant death syndrome. Author(s): Matthews TG, Fox GP. Source: Bmj (Clinical Research Ed.). 1989 February 25; 298(6672): 522. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2495093&dopt=Abstract

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Lung immunoglobulins in the sudden infant death syndrome. Author(s): Forsyth KD, Weeks SC, Koh L, Skinner J, Bradley J. Source: Bmj (Clinical Research Ed.). 1989 January 7; 298(6665): 23-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2492843&dopt=Abstract

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Lung surfactant and sudden infant death syndrome. Author(s): Morley C, Hill C, Brown B. Source: Annals of the New York Academy of Sciences. 1988; 533: 289-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3421631&dopt=Abstract

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Lung tissue concentrations of nicotine in sudden infant death syndrome (SIDS). Author(s): McMartin KI, Platt MS, Hackman R, Klein J, Smialek JE, Vigorito R, Koren G. Source: The Journal of Pediatrics. 2002 February; 140(2): 205-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11865272&dopt=Abstract

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Lympho-monocytic enteroviral myocarditis: traditional, immunohistological and molecularpathological methods for diagnosis in a case of suspected sudden infant death syndrome (SIDS). Author(s): Dettmeyer R, Kandolf R, Schmidt P, Schlamann M, Madea B. Source: Forensic Science International. 2001 June 1; 119(1): 141-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11348811&dopt=Abstract

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Magnesium deficit and sudden infant death syndrome (SIDS): SIDS due to magnesium deficiency and SIDS due to various forms of magnesium depletion: possible importance of the chronopathological form. Author(s): Durlach J, Pages N, Bac P, Bara M, Guiet-Bara A. Source: Magnes Res. 2002 December; 15(3-4): 269-78. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635883&dopt=Abstract

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Malignant hyperpyrexia and sudden infant death syndrome. Author(s): Ellis FR, Halsall PJ, Harriman DG. Source: British Journal of Anaesthesia. 1988 January; 60(1): 28-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3337790&dopt=Abstract

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Maternal and paternal recreational drug use and sudden infant death syndrome. Author(s): Klonoff-Cohen H, Lam-Kruglick P. Source: Archives of Pediatrics & Adolescent Medicine. 2001 July; 155(7): 765-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11434841&dopt=Abstract

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Maternal awareness of sudden infant death syndrome in North Queensland, Australia: an analysis of infant care practices. Author(s): Douglas TA, Buettner PG, Whitehall J. Source: Journal of Paediatrics and Child Health. 2001 October; 37(5): 441-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11885706&dopt=Abstract

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Mechanisms for abnormal apnea of possible relevance to the sudden infant death syndrome. Author(s): Southall DP, Talbert DG. Source: Annals of the New York Academy of Sciences. 1988; 533: 329-49. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3048174&dopt=Abstract

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Medial smooth muscle thickness in small pulmonary arteries in sudden infant death syndrome revisited. Author(s): Krous HF, Floyd CW, Nadeau JM, Silva PD, Blackbourne BD, Langston C. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 2002 July-August; 5(4): 375-85. Epub 2002 May 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12016526&dopt=Abstract

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Melatonin concentrations in the sudden infant death syndrome. Author(s): Sturner WQ, Lynch HJ, Deng MH, Gleason RE, Wurtman RJ. Source: Forensic Science International. 1990 March; 45(1-2): 171-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2335331&dopt=Abstract

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Models of mystery: physician and patient perceptions of sudden infant death syndrome. Author(s): Wright AL. Source: Social Science & Medicine (1982). 1988; 26(6): 587-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3363400&dopt=Abstract

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Molecular biology in cerebral cortex of sudden infant death syndrome. Author(s): Sawaguchi T, Takashima S, Ito M, Sawaguchi A. Source: Forensic Science International. 2002 September 14; 130 Suppl: S60-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12350302&dopt=Abstract

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Molecular diagnosis in a child with sudden infant death syndrome. Author(s): Schwartz PJ, Priori SG, Bloise R, Napolitano C, Ronchetti E, Piccinini A, Goj C, Breithardt G, Schulze-Bahr E, Wedekind H, Nastoli J. Source: Lancet. 2001 October 20; 358(9290): 1342-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11684219&dopt=Abstract

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Monolateral hypoplasia of the motor vagal nuclei in a case of sudden infant death syndrome. Author(s): Macchi V, Snenghi R, De Caro R, Parenti A. Source: Journal of Anatomy. 2002 February; 200(Pt 2): 195-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11895117&dopt=Abstract

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Motility and arousal in near miss sudden infant death syndrome. Author(s): Coons S, Guilleminault C. Source: The Journal of Pediatrics. 1985 November; 107(5): 728-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4056972&dopt=Abstract

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Myocarditis and sudden infant death syndrome. Author(s): Rasten-Almqvist P, Eksborg S, Rajs J. Source: Apmis : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica. 2002 June; 110(6): 469-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12193208&dopt=Abstract

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Nasal and intrapulmonary haemorrhage in sudden infant death syndrome. Author(s): Becroft DM, Thompson JM, Mitchell EA. Source: Archives of Disease in Childhood. 2001 August; 85(2): 116-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11466185&dopt=Abstract

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Near-miss sudden infant death syndrome in eight infants with sleep apnea-related cardiac arrhythmias. Author(s): Guilleminault C, Ariagno R, Coons S, Winkle R, Korobkin R, Baldwin R, Souquet M. Source: Pediatrics. 1985 August; 76(2): 236-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4022698&dopt=Abstract

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Neck extension and rotation in sudden infant death syndrome and other natural infant deaths. Author(s): Krous HF, Nadeau JM, Silva PD, Blackbourne BD. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 2001 March-April; 4(2): 154-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11178631&dopt=Abstract

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Negative effect of a short interpregnancy interval on birth weight following loss of an infant to sudden infant death syndrome. Author(s): Spiers PS, Onstad L, Guntheroth WG. Source: American Journal of Epidemiology. 1996 June 1; 143(11): 1137-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8633603&dopt=Abstract

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Neuronal apoptosis in sudden infant death syndrome. Author(s): Waters KA, Meehan B, Huang JQ, Gravel RA, Michaud J, Cote A. Source: Pediatric Research. 1999 February; 45(2): 166-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10022585&dopt=Abstract

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Neuronal development in the medullary reticular formation in sudden infant death syndrome and premature infants. Author(s): Takashima S, Mito T, Becker LE. Source: Neuropediatrics. 1985 May; 16(2): 76-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4010894&dopt=Abstract

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Newborn acoustic cry characteristics of infants subsequently dying of sudden infant death syndrome. Author(s): Corwin MJ, Lester BM, Sepkoski C, Peucker M, Kayne H, Golub HL. Source: Pediatrics. 1995 July; 96(1 Pt 1): 73-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7596727&dopt=Abstract

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Nicotine, serotonin, and sudden infant death syndrome. Author(s): Nattie E, Kinney H. Source: American Journal of Respiratory and Critical Care Medicine. 2002 December 15; 166(12 Pt 1): 1530-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12471066&dopt=Abstract

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Nighttime child care: inadequate sudden infant death syndrome risk factor knowledge, practice, and policies. Author(s): Moon RY, Weese-Mayer DE, Silvestri JM. Source: Pediatrics. 2003 April; 111(4 Pt 1): 795-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671114&dopt=Abstract

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NMDA receptor 1 expression in the brainstem of human infants and its relevance to the sudden infant death syndrome (SIDS). Author(s): Machaalani R, Waters KA. Source: Journal of Neuropathology and Experimental Neurology. 2003 October; 62(10): 1076-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14575242&dopt=Abstract

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Objective measurements of nicotine exposure in victims of sudden infant death syndrome and in other unexpected child deaths. Author(s): Milerad J, Vege A, Opdal SH, Rognum TO. Source: The Journal of Pediatrics. 1998 August; 133(2): 232-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9709711&dopt=Abstract

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Obstructive sleep apnea in infants: relation to family history of sudden infant death syndrome, apparent life-threatening events, and obstructive sleep apnea. Author(s): McNamara F, Sullivan CE. Source: The Journal of Pediatrics. 2000 March; 136(3): 318-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10700687&dopt=Abstract

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On listening to parents: the sudden infant death syndrome over 25 years. Author(s): Tonkin S. Source: Pediatrics. 1996 June; 97(6 Pt 1): 896-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8657533&dopt=Abstract

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Ondine's curse and sudden infant death syndrome. Author(s): Long KJ. Source: Pediatric Emergency Care. 1992 February; 8(1): 61-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1603697&dopt=Abstract

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One more thought on sudden infant death syndrome. Author(s): Albers S, Levy HL. Source: Pediatrics. 2001 April; 107(4): 809. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11380009&dopt=Abstract

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Ontogenesis of CYP2C-dependent arachidonic acid metabolism in the human liver: relationship with sudden infant death syndrome. Author(s): Treluyer JM, Benech H, Colin I, Pruvost A, Cheron G, Cresteil T. Source: Pediatric Research. 2000 May; 47(5): 677-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10813596&dopt=Abstract

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Opioid peptides: a role in sudden infant death syndrome? Author(s): McMillen IC. Source: Aust Paediatr J. 1986; 22 Suppl 1: 75-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2947558&dopt=Abstract

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Organ weights in sudden infant death syndrome. Author(s): Siebert JR, Haas JE. Source: Pediatr Pathol. 1994 November-December; 14(6): 973-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7855017&dopt=Abstract

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Overview of sudden infant death syndrome in Japan. Author(s): Nishida H. Source: Acta Paediatr Jpn. 1994 June; 36(3): 301-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8091984&dopt=Abstract

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Oxidative stress in sudden infant death syndrome. Author(s): Huggle S, Hunsaker JC 3rd, Coyne CM, Sparks DL. Source: Journal of Child Neurology. 1996 November; 11(6): 433-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9120219&dopt=Abstract

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Pacifier use and sudden infant death syndrome: should health professionals recommend pacifier use based on present knowledge? Author(s): Zotter H, Kerbl R, Kurz R, Muller W. Source: Wiener Klinische Wochenschrift. 2002 September 30; 114(17-18): 791-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416286&dopt=Abstract

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Pathological considerations of sudden infant death syndrome. Author(s): Krous HF. Source: Pediatrician. 1988; 15(4): 231-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3068662&dopt=Abstract

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Patterns of symptoms in siblings of sudden infant death syndrome infants. Author(s): Wailoo M, Thompson JR, Waite AJ, Coombs RC, Jackson JA. Source: Child: Care, Health and Development. 2002 September; 28 Suppl 1: 19-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515433&dopt=Abstract

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PCR-based diagnosis of enterovirus and parvovirus B19 in paraffin-embedded heart tissue of children with suspected sudden infant death syndrome. Author(s): Baasner A, Dettmeyer R, Graebe M, Rissland J, Madea B. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2003 October; 83(10): 1451-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14563946&dopt=Abstract

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Perinatal epidemiological characteristics of the sudden infant death syndrome in an Irish population. Author(s): Matthews TG, O'Brien SJ. Source: Ir Med J. 1985 September; 78(9): 251-3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4055325&dopt=Abstract

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Polymorphisms in genes involved in glucose metabolism in cases of sudden infant death syndrome. Author(s): Burchell A, Forsyth L, Hume R. Source: Child: Care, Health and Development. 2002 September; 28 Suppl 1: 37-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515438&dopt=Abstract

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Population trends in sudden infant death syndrome. Author(s): Ponsonby AL, Dwyer T, Cochrane J. Source: Semin Perinatol. 2002 August; 26(4): 296-305. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12211620&dopt=Abstract

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Prenatal and intrapartum events and sudden infant death syndrome. Author(s): Klonoff-Cohen HS, Srinivasan IP, Edelstein SL. Source: Paediatric and Perinatal Epidemiology. 2002 January; 16(1): 82-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11856458&dopt=Abstract

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Prepregnancy body mass index and sudden infant death syndrome. Author(s): Wisborg K, Vesterggard M, Kristensen J, Kesmodel U. Source: Epidemiology (Cambridge, Mass.). 2003 September; 14(5): 630. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14501281&dopt=Abstract

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Pressure volume characteristics of the lungs in sudden infant death syndrome. Author(s): Southall DP, Talbert DG. Source: Archives of Disease in Childhood. 1985 November; 60(11): 1104-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4073941&dopt=Abstract

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QT interval measurements before sudden infant death syndrome. Author(s): Southall DP, Arrowsmith WA, Stebbens V, Alexander JR. Source: Archives of Disease in Childhood. 1986 April; 61(4): 327-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3707181&dopt=Abstract

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QTc and R-R intervals in victims of the sudden infant death syndrome. Author(s): Weinstein SL, Steinschneider A. Source: Am J Dis Child. 1985 October; 139(10): 987-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4036903&dopt=Abstract

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Quantitation of medullary astrogliosis in sudden infant death syndrome. Author(s): Bruce K, Becker LE. Source: Pediatric Neurosurgery. 1991-92; 17(2): 74-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1815732&dopt=Abstract

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Quantitative neuropathological analysis of sudden infant death syndrome. Author(s): Ansari T, Sibbons PD, Parsons A, Rossi ML. Source: Child: Care, Health and Development. 2002 September; 28 Suppl 1: 3-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515429&dopt=Abstract

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Re: Intra-alveolar haemorrhage in sudden infant death syndrome: a cause for concern? Author(s): Batman P. Source: Journal of Clinical Pathology. 2000 June; 53(6): 484. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10911810&dopt=Abstract

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Reducing the incidence of sudden infant death syndrome in the Delta region of Mississippi: a three-pronged approach. Author(s): Kum-Nji P, Mangrem CL, Wells PJ. Source: Southern Medical Journal. 2001 July; 94(7): 704-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11531178&dopt=Abstract

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Relationship between arousal reaction and autonomic nervous system in the sudden infant death syndrome. Author(s): Sawaguchi T, Franco P, Groswasser J, Kahn A. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 2001 June; 22(2): 213-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11394765&dopt=Abstract

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Renal developmental delay expressed by reduced glomerular number and its association with growth retardation in victims of sudden infant death syndrome and in “normal” infants. Author(s): Beech DJ, Sibbons PD, Howard CV, van Velzen D. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 2000 September-October; 3(5): 450-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10890929&dopt=Abstract

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Retrognathism and the sudden infant death syndrome. Author(s): Rosenthal RL. Source: J Pedod. 1990 Winter; 14(2): 61-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2374082&dopt=Abstract

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Review of risk factors for sudden infant death syndrome. Author(s): Sullivan FM, Barlow SM. Source: Paediatric and Perinatal Epidemiology. 2001 April; 15(2): 144-200. Review. Erratum In: Paediatr Perinat Epidemiol 2002 January; 16(1): 96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11383580&dopt=Abstract

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Risk factors for sudden infant death syndrome among northern plains Indians. Author(s): Iyasu S, Randall LL, Welty TK, Hsia J, Kinney HC, Mandell F, McClain M, Randall B, Habbe D, Wilson H, Willinger M. Source: Jama : the Journal of the American Medical Association. 2002 December 4; 288(21): 2717-23. Erratum In: Jama. 2003 January 15; 289(3): 303. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12460095&dopt=Abstract

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Risk factors for sudden infant death syndrome: changes associated with sleep position recommendations. Author(s): Paris CA, Remler R, Daling JR. Source: The Journal of Pediatrics. 2001 December; 139(6): 771-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11743500&dopt=Abstract

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Risk of sudden infant death syndrome and week of gestation of term birth. Author(s): Smith GC, Pell JP, Dobbie R. Source: Pediatrics. 2003 June; 111(6 Pt 1): 1367-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12777554&dopt=Abstract

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Role of apnea in the sudden infant death syndrome: a personal view. Author(s): Southall DP. Source: Pediatrics. 1988 January; 81(1): 73-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3275935&dopt=Abstract

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Sleep environment and the risk of sudden infant death syndrome in an urban population: the Chicago Infant Mortality Study. Author(s): Hauck FR, Herman SM, Donovan M, Iyasu S, Merrick Moore C, Donoghue E, Kirschner RH, Willinger M. Source: Pediatrics. 2003 May; 111(5 Part 2): 1207-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728140&dopt=Abstract

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Sudden infant death syndrome (SIDS) or cot death: a review. Author(s): Ogbu CN. Source: West Afr J Med. 2003 January-March; 22(1): 88-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769316&dopt=Abstract

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Sudden infant death syndrome and psychiatric disorders. Author(s): Howard LM, Hannam S. Source: The British Journal of Psychiatry; the Journal of Mental Science. 2003 May; 182: 379-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724238&dopt=Abstract

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Sudden infant death syndrome and social deprivation: assessing epidemiological factors after post-matching for deprivation. Author(s): Fleming PJ, Blair PS, Ward Platt M, Tripp J, Smith IJ; CESDI SUDI Research Group. Source: Paediatric and Perinatal Epidemiology. 2003 July; 17(3): 272-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839539&dopt=Abstract

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Sudden infant death syndrome. Author(s): Creery D, Mikrogianakis A. Source: American Family Physician. 2003 October 1; 68(7): 1375-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14567492&dopt=Abstract

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Sudden infant death syndrome: association with a promoter polymorphism of the serotonin transporter gene. Author(s): Weese-Mayer DE, Berry-Kravis EM, Maher BS, Silvestri JM, Curran ME, Marazita ML. Source: American Journal of Medical Genetics. 2003 March 15; 117A(3): 268-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12599191&dopt=Abstract

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Sudden infant death syndrome: bed sharing with mothers who smoke. Author(s): James C, Klenka H, Manning D. Source: Archives of Disease in Childhood. 2003 February; 88(2): 112-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538308&dopt=Abstract

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Sudden infant death syndrome: need for simple definition but detailed diagnostic criteria. Author(s): Rognum TO. Source: Archives of Pediatrics & Adolescent Medicine. 2003 March; 157(3): 293. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12622684&dopt=Abstract

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Sudden infant death syndrome: overview and update. Author(s): Byard RW, Krous HF. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 2003 March-April; 6(2): 112-27. Epub 2003 January 21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532258&dopt=Abstract

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Sudden infant death syndrome--a defect in circulatory control? Author(s): Matthews T. Source: Child: Care, Health and Development. 2002 September; 28 Suppl 1: 41-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515439&dopt=Abstract

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Temperament ratings do not predict arousability in normal infants and infants at increased risk of sudden infant death syndrome. Author(s): Parslow PM, Horne RS, Ferens D, Bandopadhayay P, Mitchell K, Watts AM, Adamson TM. Source: Journal of Developmental and Behavioral Pediatrics : Jdbp. 2002 October; 23(5): 365-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12394525&dopt=Abstract

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The apparent impact of gestational magnesium (Mg) deficiency on the sudden infant death syndrome (SIDS). Author(s): Caddell JL. Source: Magnes Res. 2001 December; 14(4): 291-303. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11794637&dopt=Abstract

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The contribution of prone sleeping position to the racial disparity in sudden infant death syndrome: the Chicago Infant Mortality Study. Author(s): Hauck FR, Moore CM, Herman SM, Donovan M, Kalelkar M, Christoffel KK, Hoffman HJ, Rowley D. Source: Pediatrics. 2002 October; 110(4): 772-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12359794&dopt=Abstract

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The epidemiology of sudden infant death syndrome. Author(s): Platt MJ, Pharoah PO. Source: Archives of Disease in Childhood. 2003 January; 88(1): 27-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495955&dopt=Abstract

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The role of bacterial toxins in sudden infant death syndrome (SIDS). Author(s): Blackwell CC, Gordon AE, James VS, MacKenzie DA, Mogensen-Buchanan M, El Ahmer OR, Al Madani OM, Toro K, Csukas Z, Sotonyi P, Weir DM, Busuttil A. Source: International Journal of Medical Microbiology : Ijmm. 2002 February; 291(6-7): 561-70. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11892683&dopt=Abstract

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The significance of ante- and perinatal periods for formation of risk of sudden infant death syndrome. Author(s): Aryayev N, Kukushkin V, Nepomyashcha V. Source: Ginekol Pol. 2001 December; 72(12): 931-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11883247&dopt=Abstract

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The sudden infant death syndrome and cardio-respiratory control in Irish infants. Author(s): Matthews TG, O'Brien S. Source: Ir Med J. 1985 December; 78(12): 347-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4086253&dopt=Abstract

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The triple risk hypotheses in sudden infant death syndrome. Author(s): Guntheroth WG, Spiers PS. Source: Pediatrics. 2002 November; 110(5): E64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415070&dopt=Abstract

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Toxicologic analysis in cases of possible sudden infant death syndrome: a worthwhile exercise? Author(s): Langlois NE, Ellis PS, Little D, Hulewicz B. Source: The American Journal of Forensic Medicine and Pathology : Official Publication of the National Association of Medical Examiners. 2002 June; 23(2): 162-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12040261&dopt=Abstract

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Trends in postneonatal aspiration deaths and reclassification of sudden infant death syndrome: impact of the “Back to Sleep” program. Author(s): Malloy MH. Source: Pediatrics. 2002 April; 109(4): 661-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11927712&dopt=Abstract

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Understanding and preventing sudden infant death syndrome. Author(s): Fleming PJ. Source: Current Opinion in Pediatrics. 1994 April; 6(2): 158-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8032395&dopt=Abstract

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Unexpected infant death: occult cardiac disease and sudden infant death syndromehow much of an overlap is there? Author(s): Byard RW. Source: The Journal of Pediatrics. 2002 September; 141(3): 303-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12219047&dopt=Abstract

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Unexplained stillbirths and sudden infant death syndrome. Author(s): Walsh S, Mortimer G. Source: Medical Hypotheses. 1995 July; 45(1): 73-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8524185&dopt=Abstract

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Unraveling the mysteries of sudden infant death syndrome. Author(s): Brooks JG. Source: Current Opinion in Pediatrics. 1993 June; 5(3): 266-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8374644&dopt=Abstract

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Unsafe sleep practices and an analysis of bedsharing among infants dying suddenly and unexpectedly: results of a four-year, population-based, death-scene investigation study of sudden infant death syndrome and related deaths. Author(s): Kemp JS, Unger B, Wilkins D, Psara RM, Ledbetter TL, Graham MA, Case M, Thach BT. Source: Pediatrics. 2000 September; 106(3): E41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10969125&dopt=Abstract

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Updates on attention deficit hyperactivity disorder, child abuse and neglect, and sudden infant death syndrome. Author(s): Daley KC. Source: Current Opinion in Pediatrics. 2003 April; 15(2): 216-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640282&dopt=Abstract

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Upper airway resistance in infants at risk for sudden infant death syndrome. Author(s): Guilleminault C, Stoohs R, Skrobal A, Labanowski M, Simmons J. Source: The Journal of Pediatrics. 1993 June; 122(6): 881-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8501563&dopt=Abstract

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Up-regulated epithelial expression of HLA-DR and secretory component in salivary glands: reflection of mucosal immunostimulation in sudden infant death syndrome. Author(s): Thrane PS, Rognum TO, Brandtzaeg P. Source: Pediatric Research. 1994 May; 35(5): 625-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8065849&dopt=Abstract

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Use of duvets and the risk of sudden infant death syndrome. Author(s): Mitchell EA, Williams SM, Taylor BJ. Source: Archives of Disease in Childhood. 1999 August; 81(2): 117-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10490515&dopt=Abstract

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Used infant mattresses and sudden infant death syndrome in Scotland: case-control study. Author(s): Tappin D, Brooke H, Ecob R, Gibson A. Source: Bmj (Clinical Research Ed.). 2002 November 2; 325(7371): 1007. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12411359&dopt=Abstract

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Vagal nerve complex in normal development and sudden infant death syndrome. Author(s): Becker LE, Zhang W. Source: The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques. 1996 February; 23(1): 24-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8673958&dopt=Abstract

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Vagal overactivity: a risk factor of sudden infant death syndrome? Author(s): Shojaei-Brosseau T, Bonaiti-Pellie C, Lyonnet S, Feingold J, Lucet V. Source: Archives of Disease in Childhood. 2003 January; 88(1): 88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495979&dopt=Abstract

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Variations in acromial ossification simulating infant abuse in victims of sudden infant death syndrome. Author(s): Curto TL. Source: The Journal of Emergency Medicine. 1992 March-April; 10(2): 206. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1607628&dopt=Abstract

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Vascular endothelial growth factor in the cerebrospinal fluid of infants who died of sudden infant death syndrome: evidence for antecedent hypoxia. Author(s): Jones KL, Krous HF, Nadeau J, Blackbourne B, Zielke HR, Gozal D. Source: Pediatrics. 2003 February; 111(2): 358-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563064&dopt=Abstract

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Ventilatory pattern following diphtheria-tetanus-pertussis immunization in infants at risk for sudden infant death syndrome. Author(s): Keens TG, Ward SL, Gates EP, Andree DI, Hart LD. Source: Am J Dis Child. 1985 October; 139(10): 991-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3876024&dopt=Abstract

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Vertebral artery compression resulting from head movement: a possible cause of the sudden infant death syndrome. Author(s): Pamphlett R, Raisanen J, Kum-Jew S. Source: Pediatrics. 1999 February; 103(2): 460-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9925842&dopt=Abstract

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Virulence factors associated with strains of Escherichia coli from cases of sudden infant death syndrome (SIDS). Author(s): Bettelheim KA, Chang BJ, Elliott SJ, Gunzburg ST, Pearce JL. Source: Comparative Immunology, Microbiology and Infectious Diseases. 1995 June; 18(3): 179-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7554819&dopt=Abstract

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Vitamin A and sudden infant death syndrome in Scandinavia 1992-1995. Author(s): Alm B, Wennergren G, Norvenius SG, Skjaerven R, Lagercrantz H, HelwegLarsen K, Irgens LM; Nordic Epidemiological SIDS Study. Source: Acta Paediatrica (Oslo, Norway : 1992). 2003; 92(2): 162-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12710640&dopt=Abstract

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Vocal cord basement membrane in non-sudden infant death syndrome cases. Author(s): Castro EC, Cesar Peres L. Source: Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society. 1999 September-October; 2(5): 440-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10441621&dopt=Abstract

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Vulnerability of the infant brain stem to ischemia: a possible cause of sudden infant death syndrome. Author(s): Pamphlett R, Murray N. Source: Journal of Child Neurology. 1996 May; 11(3): 181-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8734017&dopt=Abstract

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Water fluoridation and the sudden infant death syndrome. Author(s): Dick AE, Ford RP, Schluter PJ, Mitchell EA, Taylor BJ, Williams SM, Stewart AW, Becroft DM, Thompson JM, Scragg R, Hassall IB, Barry DM, Allen EM. Source: N Z Med J. 1999 August 13; 112(1093): 286-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10493424&dopt=Abstract

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Weather and the risk of sudden infant death syndrome: the effect of wind. Author(s): Macey PM, Schluter PJ, Ford RP. Source: Journal of Epidemiology and Community Health. 2000 May; 54(5): 333-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10814652&dopt=Abstract

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Weather temperatures and sudden infant death syndrome: a regional study over 22 years in New Zealand. Author(s): Schluter PJ, Ford RP, Brown J, Ryan AP. Source: Journal of Epidemiology and Community Health. 1998 January; 52(1): 27-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9604038&dopt=Abstract

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Weight gain and sudden infant death syndrome: changes in weight z scores may identify infants at increased risk. Author(s): Blair PS, Nadin P, Cole TJ, Fleming PJ, Smith IJ, Platt MW, Berry PJ, Golding J. Source: Archives of Disease in Childhood. 2000 June; 82(6): 462-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10833177&dopt=Abstract

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Well health care and the sudden infant death syndrome. Author(s): Ford RP, Mitchell EA, Taylor BJ. Source: Journal of Paediatrics and Child Health. 1994 April; 30(2): 140-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8198848&dopt=Abstract

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What are the national rates for sudden infant death syndrome for Aboriginal and Torres Strait Islander infants? Author(s): Read AW. Source: Journal of Paediatrics and Child Health. 2002 April; 38(2): 122-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12030990&dopt=Abstract

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Why does maternal smoke exposure increase the risk of sudden infant death syndrome? Author(s): Sundell H. Source: Acta Paediatrica (Oslo, Norway : 1992). 2001 July; 90(7): 718-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11519971&dopt=Abstract

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Why is smoking a risk factor for sudden infant death syndrome? Author(s): Gordon AE, El Ahmer OR, Chan R, Al Madani OM, Braun JM, Weir DM, Busuttil A, Blackwell CC. Source: Child: Care, Health and Development. 2002 September; 28 Suppl 1: 23-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515434&dopt=Abstract

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Why the prone position is a risk factor for sudden infant death syndrome. Author(s): Jeffery HE, Megevand A, Page H. Source: Pediatrics. 1999 August; 104(2 Pt 1): 263-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10429005&dopt=Abstract

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CHAPTER 2. NUTRITION AND SUDDEN INFANT DEATH SYNDROME Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and sudden infant death syndrome.

Finding Nutrition Studies on Sudden Infant Death Syndrome 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 “sudden infant death syndrome” (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 “sudden infant death syndrome” (or a synonym): •

A triple-risk model for the sudden infant death syndrome (SIDS) and the apparent life-threatening episode (ALTE): the stressed magnesium deficient weanling rat. Author(s): Department of Pediatrics, Thomas Jefferson University, Philadelphia, PA 19107-5083, USA. Source: Caddell, J L Magnes-Res. 2001 September; 14(3): 227-38 0953-1424

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Caffeine and alcohol as risk factors for sudden infant death syndrome. Nordic Epidemiological SIDS Study. Author(s): Department of Paediatrics, Sahlgrenska University Hospital/Ostra, S-416 85 Goteborg, Sweden. Source: Alm, B Wennergren, G Norvenius, G Skjaerven, R Oyen, N Helweg Larsen, K Lagercrantz, H Irgens, L M Arch-Dis-Child. 1999 August; 81(2): 107-11 0003-9888

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Control of breathing by endogenous opioid peptides: possible involvement in sudden infant death syndrome. Author(s): Laboratoire de Physiologie Nerveuse, C.N.R.S., Gif-sur-Yvette, France. Source: Morin Surun, M P Boudinot, E Fournie Zaluski, M C Champagnat, J Roques, B P Denavit Saubie, M Neurochem-Int. 1992 January; 20(1): 103-7 0197-0186

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Could exogenous melatonin prevent sudden infant death syndrome? Author(s): Department of Pathology, Houston Medical Center, Warner Robins, GA 31093, USA. Source: Maurizi, C P Med-Hypotheses. 1997 November; 49(5): 425-7 0306-9877

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Effects of hypomagnesemia on reactivity of bovine and ovine platelets: possible relevance to infantile apnea and sudden infant death syndrome. Author(s): Department of Animal Science, University of Tennessee, Knoxville 379011071. Source: Miller, J K Schneider, M D Ramsey, N White, P K Bell, M C J-Am-Coll-Nutr. 1990 February; 9(1): 58-64 0731-5724

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Fungal volatilization of arsenic and antimony and the sudden infant death syndrome. Author(s): School of Biological Sciences, University of Birmingham, Edgbaston, UK. Source: Pearce, R B Callow, M E Macaskie, L E FEMS-Microbiol-Lett. 1998 January 15; 158(2): 261-5 0378-1097

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Heavy caffeine intake in pregnancy and sudden infant death syndrome. Author(s): Community Paediatric Unit, Community Child and Family Service, PO Box 25-265, Christchurch (New Zealand) Source: Ford, R.P.K. Schluter, P.J. Mitchell E.A. Taylor, B.J. Scragg, R. Stewart, A.W. Archives-of-Disease-in-Childhood (United Kingdom). (1998). volume 78(1) page 9-13. caffeine pregnancy death infants coffee mankind tea

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Impaired cardiac function during postnatal hypoxia in rats exposed to nicotine prenatally: implications for perinatal morbidity and mortality, and for sudden infant death syndrome. Author(s): Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710, USA. [email protected] Source: Slotkin, T A Saleh, J L McCook, E C Seidler, F J Teratology. 1997 March; 55(3): 177-84 0040-3709

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Increased density of somatostatin binding sites in respiratory nuclei of the brainstem in sudden infant death syndrome. Author(s): European Institute for Peptide Research (IFRMP no. 23), INSERM U 413, UA CNRS, University of Rouen, Mont-Saint-Aignan, France. Source: Carpentier, V Vaudry, H Mallet, E Laquerriere, A Leroux, P Neuroscience. 1998 September; 86(1): 159-66 0306-4522

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Inherited metabolic diseases in the sudden infant death syndrome. Author(s): Department of Clinical Chemistry, Southmead Hospital, Westbury-on-Trym, Bristol. Source: Holton, J B Allen, J T Green, C A Partington, S Gilbert, R E Berry, P J Arch-DisChild. 1991 November; 66(11): 1315-7 0003-9888

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Liver fatty acids and the sudden infant death syndrome [Dihomo-gama-linolenic acid]. Source: Fogerty, A.C. Ford, G.L. Willcox, M.E. Clancy, S.L. Am-J-Clin-Nutr. Bethesda : American Society for Clinical Nutrition. February 1984. volume 39 c (2) page 201-208. 0002-9165

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Loss of neonatal hypoxia tolerance after prenatal nicotine exposure: implications for sudden infant death syndrome. Author(s): Department of Pharmacology, Duke University Medical Center, Durham, NC 27710, USA. Source: Slotkin, T A Lappi, S E McCook, E C Lorber, B A Seidler, F J Brain-Res-Bull. 1995; 38(1): 69-75 0361-9230

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Magnesium and thermoregulation. I. Newborn and infant. Is sudden infant death syndrome a magnesium-dependent disease of the transition from chemical to physical thermoregulation? Author(s): SDRM, Hopital St. Vincent-de-Paul, Paris, France. Source: Durlach, J Durlach, V Rayssiguier, Y Ricquier, D Goubern, M Bertin, R Bara, M Guiet Bara, A Olive, G Mettey, R Magnes-Res. 1991 Sep-December; 4(3-4): 137-52 09531424

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Medium-chain acyl-CoA dehydrogenase deficiency does not correlate with apparent life-threatening events and the sudden infant death syndrome: results from phenylpropionate loading tests and DNA analysis. Author(s): Department of Paediatrics, University of Berne, Switzerland. Source: Penzien, J M Molz, G Wiesmann, U N Colombo, J P Buhlmann, R Wermuth, B Eur-J-Pediatr. 1994 May; 153(5): 352-7 0340-6199

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Melatonin increases cyclic guanosine monophosphate: biochemical effects mediated by porphyrins, calcium and nitric oxide. Relationships to infant colic and the Sudden Infant Death Syndrome. Source: Weissbluth, M Med-Hypotheses. 1994 June; 42(6): 390-2 0306-9877

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Methylxanthine treatment in infants at risk for sudden infant death syndrome. Author(s): Department of Pediatrics, Children's Memorial Hospital, Northwestern University Medical School, Chicago, Illinois 60614. Source: Hunt, C E Brouillette, R T Ann-N-Y-Acad-Sci. 1988; 533119-26 0077-8923

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Ontogenesis of CYP2C-dependent arachidonic acid metabolism in the human liver: relationship with sudden infant death syndrome. Author(s): INSERM U 75, Universite Rene Descartes, Paris, France. Source: Treluyer, J M Benech, H Colin, I Pruvost, A Cheron, G Cresteil, T Pediatr-Res. 2000 May; 47(5): 677-83 0031-3998

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Opioid peptides from milk as a possible cause of sudden infant death syndrome. Author(s): Department of Anesthesiology, New York University Medical Center, NY 10016. Source: Ramabadran, K Bansinath, M Med-Hypotheses. 1988 November; 27(3): 181-7 0306-9877

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Recent advances in sudden infant death syndrome: possible autonomic dysfunction of the airways in infants at risk. Author(s): Pediatric Sleep Unit, University Children's Hospital, Free University of Brussels, Belgium. Source: Kahn, A Rebuffat, E Sottiaux, M Muller, M F Lung. 1990; 168 Suppl920-4 03412040

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Selenium and glutathione peroxidase in mothers experiencing sudden infant death syndrome. Source: Valentine, J. Faraji, B. Akashi, K. Trace elements in man and animals 6 / edited by Lucille S. Hurley,. [et al.]. New York : Plenum Press, c1988. page 13-14. ISBN: 0306430045

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Structural changes in lungs of magnesium-deficient weanling rats dying spontaneously or after spontaneous recovery from the seizure-shock episode. Possible methods for sudden infant death syndromes. Author(s): Section of Disorders of Carbohydrate Metabolism, National Institute of Child Health and Human Development, Bethesda, Md. Source: Caddell, J L Blanchette Mackie, E J Magnesium. 1988; 7(4): 195-209 0252-1156

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Sudden infant death syndrome (SIDS) and disordered blood flow. Source: Reid, G M Tervit, H Med-Hypotheses. 1991 November; 36(3): 295-9 0306-9877

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The apparent impact of gestational magnesium (Mg) deficiency on the sudden infant death syndrome (SIDS). Author(s): Department of Pediatrics, Thomas Jefferson University, Philadelphia, PA 19107-5083, USA. Source: Caddell, J L Magnes-Res. 2001 December; 14(4): 291-303 0953-1424

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The iodine-selenium connection: its possible roles in intelligence, cretinism, sudden infant death syndrome, breast cancer and multiple sclerosis. Author(s): Department of Geography, University of Victoria, British Columbia, Canada. Source: Foster, H D Med-Hypotheses. 1993 January; 40(1): 61-5 0306-9877

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The vitamin E and selenium status of infants and the sudden infant death syndrome. Source: Rhead, W.J. Cary, E.E. Allaway, W.H. Saltzstein, S.L. Schrauzer, G.N. Bioinorganic-Chem. New York, N.Y. : Elsevier Science Publishing. 1972. volume 1 (4) page 289-294. 0162-0134

Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •

healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0

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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov

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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov

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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/

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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/

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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/

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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/

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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/

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

AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats

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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html

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

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

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

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

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

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

The following is a specific Web list relating to sudden infant death syndrome; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •

Minerals Selenium Source: Integrative Medicine Communications; www.drkoop.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND SUDDEN INFANT DEATH SYNDROME Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to sudden infant death syndrome. 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 sudden infant death syndrome 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 “sudden infant death syndrome” (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 sudden infant death syndrome: •

ABR in pediatric audiology. Author(s): Mjoen S. Source: Scand Audiol Suppl. 1981; 13: 141-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6944771&dopt=Abstract

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Age- and dietary-related distributions of hepatic arachidonic and docosahexaenoic acid in early infancy. Author(s): Farquharson J, Jamieson EC, Logan RW, Patrick WJ, Howatson AG, Cockburn F. Source: Pediatric Research. 1995 September; 38(3): 361-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7494660&dopt=Abstract

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An animal model for airway sensory deprivation producing obstructive apnea with postmortem findings of sudden infant death syndrome. Author(s): Abu-Osba YK, Mathew OP, Thach BT. Source: Pediatrics. 1981 December; 68(6): 796-801. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7322715&dopt=Abstract

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An enigma in swaddling clothes: pastoral response to sudden infant death. Author(s): Hawkins DG. Source: Bull Am Protestant Hosp Assoc. 1977; 41(2): 83-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10304631&dopt=Abstract

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Arrhythmogenic right ventricular cardiomyopathy and sudden cardiac death in young Koreans. Author(s): Cho Y, Park T, Yang DH, Park HS, Chae J, Chae SC, Jun JE, Kwak JS, Park WH. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2003 November; 67(11): 925-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14578598&dopt=Abstract

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Auditory arousal thresholds of normal and near-miss SIDS infants. Author(s): Kahn A, Picard E, Blum D. Source: Developmental Medicine and Child Neurology. 1986 June; 28(3): 299-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3721072&dopt=Abstract

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Bacterial vaccines: old and new, veterinary and medical. Author(s): Walker PD. Source: Vaccine. 1992; 10(14): 977-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1471428&dopt=Abstract

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Bed sharing or iron supplementation as a cause of cot death? Author(s): Holborow PL. Source: N Z Med J. 1992 October 28; 105(944): 436-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1297947&dopt=Abstract

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Bereavement counselling after sudden infant death. Author(s): Woodward S, Pope A, Robson WJ, Hagan O. Source: British Medical Journal (Clinical Research Ed.). 1985 February 2; 290(6465): 3635. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3917822&dopt=Abstract

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Brain ganglioside and glycoprotein sialic acid in breastfed compared with formulafed infants. Author(s): Wang B, McVeagh P, Petocz P, Brand-Miller J.

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Source: The American Journal of Clinical Nutrition. 2003 November; 78(5): 1024-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14594791&dopt=Abstract •

Brainstem auditory evoked potentials in adult and infant sleep apnea syndromes, including sudden infant death syndrome and near-miss for sudden infant death. Author(s): Stockard JJ. Source: Annals of the New York Academy of Sciences. 1982; 388: 443-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6953881&dopt=Abstract

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Bystander cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrest. The Cerebral Resuscitation Study Group. Author(s): Bossaert L, Van Hoeyweghen R. Source: Resuscitation. 1989; 17 Suppl: S55-69; Discussion S199-206. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2551021&dopt=Abstract

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Cardiovascular responses to three simple, provocative tests of autonomic activity in sleeping infants. Author(s): Harrington C, Kirjavainen T, Teng A, Sullivan CE. Source: Journal of Applied Physiology (Bethesda, Md. : 1985). 2001 August; 91(2): 561-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11457766&dopt=Abstract

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Care for bereaved families. Author(s): Fukui S. Source: Acta Paediatr Jpn. 1994 June; 36(3): 304-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8091985&dopt=Abstract

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Child rearing and cultural beliefs and practices amongst Thai mothers in Victoria, Australia: implications for the sudden infant death syndrome. Author(s): Rice PL, Naksook C. Source: Journal of Paediatrics and Child Health. 1998 August; 34(4): 320-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9727170&dopt=Abstract

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Conditioned hyperventilation as a factor in animal, infant, and adult apnea: a theoretical analysis of experimental and clinical data. Author(s): Caldwell WE. Source: Genetic, Social, and General Psychology Monographs. 1986 August; 112(3): 32541. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3770464&dopt=Abstract

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Consumers need to be educated about SIDS. Author(s): Putnam A.

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Source: Mich Med. 1989 June; 88(6): 7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2755361&dopt=Abstract •

Developmental alterations in auditory arousal from sleep in healthy and virusinfected cats. Author(s): Toth LA, Chaudhary MA. Source: Sleep. 1998 March 15; 21(2): 143-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9542798&dopt=Abstract

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Diagnosis of medium-chain acyl-CoA dehydrogenase deficiency in lymphocytes and liver by a gas chromatographic method: the effect of oral riboflavin supplementation. Author(s): Duran M, Cleutjens CB, Ketting D, Dorland L, de Klerk JB, van Sprang FJ, Berger R. Source: Pediatric Research. 1992 January; 31(1): 39-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1594328&dopt=Abstract

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Effect of diet on infant subcutaneous tissue triglyceride fatty acids. Author(s): Farquharson J, Cockburn F, Patrick WA, Jamieson EC, Logan RW. Source: Archives of Disease in Childhood. 1993 November; 69(5): 589-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8257182&dopt=Abstract

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Effect of diet on the fatty acid composition of the major phospholipids of infant cerebral cortex. Author(s): Farquharson J, Jamieson EC, Abbasi KA, Patrick WJ, Logan RW, Cockburn F. Source: Archives of Disease in Childhood. 1995 March; 72(3): 198-203. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7741563&dopt=Abstract

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Evolution of bereavement counselling in sudden infant death syndrome, neonatal death and stillbirth. Author(s): Thearle MJ, Gregory H. Source: Journal of Paediatrics and Child Health. 1992 June; 28(3): 204-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1605968&dopt=Abstract

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Familial neonatal SIDS revealing carnitine-acylcarnitine translocase deficiency. Author(s): Nuoffer JM, de Lonlay P, Costa C, Roe CR, Chamoles N, Brivet M, Saudubray JM. Source: European Journal of Pediatrics. 2000 January-February; 159(1-2): 82-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10653336&dopt=Abstract

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Heart rate changes in response to mild mechanical irritation of the high cervical spinal cord region in infants. Author(s): Koch LE, Koch H, Graumann-Brunt S, Stolle D, Ramirez JM, Saternus KS.

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Source: Forensic Science International. 2002 August 28; 128(3): 168-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12175961&dopt=Abstract •

Hemispheric asymmetry of late auditory evoked response induced by pitch changes in infants: influence of sleep stages. Author(s): Duclaux R, Challamel MJ, Collet L, Roullet-Solignac I, Revol M. Source: Brain Research. 1991 December 6; 566(1-2): 152-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1814532&dopt=Abstract

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High cervical stress and apnoea. Author(s): Koch LE, Biedermann H, Saternus KS. Source: Forensic Science International. 1998 October 12; 97(1): 1-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9854836&dopt=Abstract

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Immunological aspects of human milk. Author(s): Chandra RK. Source: Nutrition Reviews. 1978 September; 36(9): 265-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=362248&dopt=Abstract

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Inadvertent clavicular fractures caused by “chiropractic” manipulations in an infant: an unusual form of pseudoabuse. Author(s): Sperry K, Pfalzgraf R. Source: J Forensic Sci. 1990 September; 35(5): 1211-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2230695&dopt=Abstract

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Liver fatty acids and the sudden infant death syndrome. Author(s): Fogerty AC, Ford GL, Willcox ME, Clancy SL. Source: The American Journal of Clinical Nutrition. 1984 February; 39(2): 201-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6230001&dopt=Abstract

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Modification of sleep respiratory patterns by auditory stimulation: indications of a technique for preventing sudden infant death syndrome? Author(s): Stewart MW, Stewart LA. Source: Sleep. 1991 June; 14(3): 241-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1896725&dopt=Abstract

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Neglected spinal cord, brain stem and musculoskeletal injuries stemming from birth trauma. Author(s): Gottlieb MS.

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Source: Journal of Manipulative and Physiological Therapeutics. 1993 October; 16(8): 537-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8263433&dopt=Abstract •

Nursing: sudden infant death. Author(s): Kelleher JC. Source: Emerg Med Serv. 1976 January-February; 5(1): 64. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10243460&dopt=Abstract

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On new ideas and an U.S. experience. Author(s): Kalokerinos A, Dettman G. Source: Australas Nurses J. 1979 November; 9(1): 22-6. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=119534&dopt=Abstract

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Parents help themselves. Interview by Margaret Atkin. Author(s): Purcell J. Source: Qld Nurse. 1991 May-June; 10(3): 13. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1924835&dopt=Abstract

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Parents' response to sudden infant death syndrome. Author(s): Buschbacher VI, Delcampo RL. Source: Journal of Pediatric Health Care : Official Publication of National Association of Pediatric Nurse Associates & Practitioners. 1987 March-April; 1(2): 85-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3694403&dopt=Abstract

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Structural changes in lungs of magnesium-deficient weanling rats dying spontaneously or after spontaneous recovery from the seizure-shock episode. Possible methods for sudden infant death syndromes. Author(s): Caddell JL, Blanchette-Mackie EJ. Source: Magnesium. 1988; 7(4): 195-209. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3244282&dopt=Abstract

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Sudden infant death syndrome and lipoproteins. Author(s): Reid GM. Source: Medical Hypotheses. 1989 June; 29(2): 77-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2666828&dopt=Abstract

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Sudden infant death syndrome: a literature review with chiropractic implications. Author(s): Banks BD, Beck RW, Columbus M, Gold PM, Kinsinger FS, Lalonde MA.

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Source: Journal of Manipulative and Physiological Therapeutics. 1987 October; 10(5): 246-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3320251&dopt=Abstract •

Sudden infant death syndrome: effect of breast and formula feeding on frontal cortex and brainstem lipid composition. Author(s): Byard RW, Makrides M, Need M, Neumann MA, Gibson RA. Source: Journal of Paediatrics and Child Health. 1995 February; 31(1): 14-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7748681&dopt=Abstract

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Vitamin A and sudden infant death syndrome in Scandinavia 1992-1995. Author(s): Alm B, Wennergren G, Norvenius SG, Skjaerven R, Lagercrantz H, HelwegLarsen K, Irgens LM; Nordic Epidemiological SIDS Study. Source: Acta Paediatrica (Oslo, Norway : 1992). 2003; 92(2): 162-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12710640&dopt=Abstract

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

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

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

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

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

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

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

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

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

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

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

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

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

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

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The following is a specific Web list relating to sudden infant death syndrome; 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 Pregnancy and Postpartum Support Source: Healthnotes, Inc.; www.healthnotes.com Sudden Infant Death Syndrome (SIDS) Source: Integrative Medicine Communications; www.drkoop.com

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Herbs and Supplements Melatonin Source: Integrative Medicine Communications; www.drkoop.com

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

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CHAPTER 4. DISSERTATIONS ON SUDDEN INFANT DEATH SYNDROME Overview In this chapter, we will give you a bibliography on recent dissertations relating to sudden infant death syndrome. 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 “sudden infant death syndrome” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on sudden infant death syndrome, we have not necessarily excluded non-medical dissertations in this bibliography.

Dissertations on Sudden Infant Death Syndrome 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 sudden infant death syndrome. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •

An Examination of Parent Coping in Survivors of Sudden Infant Death Syndrome: Implications for the Education of Health and Human Services Professionals by Aadalen, Sharon Price, PhD from University of Minnesota, 1983, 354 pages http://wwwlib.umi.com/dissertations/fullcit/8318034

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An Investigation of the Seasonality of Sudden Infant Death Syndrome in the United States by Hereward, Mark Courtenay, PhD from University of Pennsylvania, 1990, 343 pages http://wwwlib.umi.com/dissertations/fullcit/9026573

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Development of the Neonatal Rat As a Model for Sudden Infant Death Syndrome: Cardiorespiratory Effects of Ethanol by Stout, Rhett Whitman; PhD from Louisiana State University and Agricultural & Mechanical College, 2003, 158 pages http://wwwlib.umi.com/dissertations/fullcit/3085700

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Real and Artifactual Trends in Sudden Infant Death Syndrome: 1975-1986 (Infant Mortality, Sudden Infant Death Syndrome) by Rutrough, Thyne Sieber, PhD from The University of Michigan, 1991, 273 pages http://wwwlib.umi.com/dissertations/fullcit/9208644

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Sudden Infant Death Syndrome: Hospitals' Dissemination, Practice, Support, and Policies for the 'back to Sleep Campaign' by McCarthy, Cheryl Ann; PhD from Temple University, 2000, 263 pages http://wwwlib.umi.com/dissertations/fullcit/9990338

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The Development and Evaluation of a Slide/sound Presentation on Sudden Infant Death Syndrome (SIDS) by Kapp, Minna Rochelle, EDD from Columbia University Teachers College, 1983, 205 pages http://wwwlib.umi.com/dissertations/fullcit/8403268

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The Development and Testing of a Practice Model with Families Bereaved due to Sudden Infant Death Syndrome by Panzer, Barry Marvin, Dsw from Columbia University, 1989, 221 pages http://wwwlib.umi.com/dissertations/fullcit/9020588

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The Environmental Niche of Aboriginal Infants: Possible Implications for Sudden Infant Death Syndrome by Wilson, C. Elizabeth, PhD from The University of Manitoba (Canada), 1999, 229 pages http://wwwlib.umi.com/dissertations/fullcit/NQ35048

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The Impact of the Death of a Child on the Parent's Marriage: a Case Study of Sudden Infant Death Syndrome and the Parent's Marital Relationship (SIDS) by O'malley, Patrick W., PhD from Texas Woman's University, 1987, 144 pages http://wwwlib.umi.com/dissertations/fullcit/8715006

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When a Young Child Dies: the Interactionist Approach to the Crisis of Sudden Infant Death Syndrome and Its Case Management. by Steinmarc, Paul Leandre, PhD from University of Minnesota, 1979, 800 pages http://wwwlib.umi.com/dissertations/fullcit/7918396

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

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CHAPTER 5. CLINICAL TRIALS AND SUDDEN INFANT DEATH SYNDROME Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning sudden infant death syndrome.

Recent Trials on Sudden Infant Death Syndrome The following is a list of recent trials dedicated to sudden infant death syndrome.8 Further information on a trial is available at the Web site indicated. •

Incidence and Severity of Cardiorespiratory Events in Infants at Increased Epidemiological Risk for Sudden Infant Death Syndrome (SIDS) Condition(s): Sudden Infant Death Syndrome; Apnea Study Status: This study is completed. Sponsor(s): National Institute of Child Health and Human Development (NICHD); Yale University Purpose - Excerpt: Objectives: I. Assess and compare the incidence and severity of cardiorespiratory events documented by home monitoring in infants at increased epidemiological risk for sudden infant death syndrome (SIDS). II. Determine the antecedent medical, demographic, physiologic, and behavioral characteristics that predict the incidence of cardiorespiratory events documented by home monitoring. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004392

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Parental knowledge and beliefs about infant sleep position Condition(s): Sudden Infant Death Syndrome

8

These are listed at www.ClinicalTrials.gov.

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Study Status: This study is completed. Sponsor(s): National Center for Research Resources (NCRR) Purpose - Excerpt: In the United States, Sudden Infant Death Syndrome (SIDS)is the leading cause of death in infants between the ages of 1 and 12 months. The etiology of SIDS is still not clear although a number of risk factors have been identified. Sleeping on the stomach has been identified as a major risk for SIDS. The rates of SIDS have dropped substantially in countries in which the usual sleep position has changed from the stomach to the side or back. Back sleep has been shown to be the most stable and safest position. The American Academy of Pediatrics now recommends the back sleeping position for all healthy infants. Since the American Academy of Pediatrics began advocating the back sleep position, the incidence of SIDS has decreased by more than 40% in this country. However, the decrease has not been uniform across segments of the population. Black infants continue to have a higher rate of SIDS compared with other groups. This discrepancy could be related to infant sleep position practices. Several studies have shown that infants born to low income, minority, inner-city families were more likely to be placed on the stomach to sleep. Education appears to influence choice of sleep position and may explain, at least to some degree, the difference in choice of sleep position among certain groups. We believe that uniform education of parents will influence the sleep position that parents choose for their baby. We will undertake this initial study to document what parents choose to do with their infants regarding sleep position and why they make these choices so that we can improve our educational approach. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005567

Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “sudden infant death syndrome” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •

For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/

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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html

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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/

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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm

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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm

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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm

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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp

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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm

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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/

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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm

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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm

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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm

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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm

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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm

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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials

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CHAPTER 6. PATENTS ON SUDDEN INFANT DEATH SYNDROME Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “sudden infant death syndrome” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on sudden infant death syndrome, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Sudden Infant Death Syndrome By performing a patent search focusing on sudden infant death syndrome, 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 9Adapted from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

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descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on sudden infant death syndrome: •

Apnoea monitor Inventor(s): Thatcher; John B. (3860 Pendiente Cir., Bldg. CD-105, San Diego, CA 92124) Assignee(s): none reported Patent Number: 4,738,266 Date filed: May 9, 1983 Abstract: An apnoea monitor for preventing sudden infant death syndrome (SIDS). The exhaled breath of the infant is collected in a hood. A source of infrared energy emits infrared energy into the hood. So long as the infant is breathing, the carbon dioxide in its breath absorbs a portion of the infrared energy in the hood. Should the infant stop breathing, an infrared detector responds to the resulting increase in infrared energy to activate an alarm so as to enable the attendant personnel to take appropriate life saving action. Excerpt(s): There are an estimated 10,000-15,000 deaths in the United States each year due to sudden infant death syndrome (SIDS), making it the most frequent cause of death in the first year of life. Many hypotheses have been formulated to explain its etiology. Most of the easily recognized post-mortem abnormalities in the victims are in the lungs and they have usually been interpreted as evidence of a sudden catastrophic event in an otherwise normal infant. Years of speculation about the nature of the catastrophic event have been unfruitful because the easily recognized post-mortem abnormalities give few clues to the dynamic events surrounding the deaths. The term "apnoea" is often used in conjunction with SIDS as a symptom as well as a cause. Apnoea may be defined as a pause in the infant's breathing equal to or exceeding six seconds. Short periods of apnoea during sleep are normal during infancy while prolonged periods are abnormal. In 1972 Steinschneider (Pediatrics 50:646-654, 1972) reported that several SIDS victims had prolonged periods of apnoea during sleep before death. In an attempt to combat SIDS, monitoring systems have been proposed in the past which react to any period of apnoea in the sleeping infant. Although some of the indications may be false alarms due to normal periods of apnoea by the infant, in any event, the parents or attending nurses are alerted by the monitors whenever the infant stops breathing, even for a short period. Web site: http://www.delphion.com/details?pn=US04738266__

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Apparatus and method for preventing sudden infant death syndrome Inventor(s): von der Heyde; Christian P. (182 Great Hill Rd. Extension, East Sandwich, MA 02537) Assignee(s): none reported Patent Number: 5,887,304 Date filed: July 10, 1997 Abstract: An apparatus and method for preventing asphyxiation of an infant due to breathing of exhaled carbon dioxide. A mattress with optional mattress pad provides an

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even air flow that removes exhaled carbon dioxide that accumulates at or near the surface of the mattress or mattress pad. The infant may be located anywhere on the surface of the mattress or mattress pad as the even air flow disperses carbon dioxide across the entire surface. In a preferred embodiment, the even air flow is accomplished by forcing air into a cavity, or plenum chamber, in the body of the mattress which air distributes equally to air flow holes on the top surfaces of the mattress and mattress pad. Optional temperature regulating or medicine dispensing devices respectively heat or cool the air flow, or introduce medicine into the air flow. In another embodiment, the mattress is itself a mattress pad. That is, the mattress pad provides an even air flow as described and may be placed on the sleeping surface of a conventional mattress. Excerpt(s): This invention generally relates to apparatuses and methods for preventing sudden infant death syndrome, and more particularly to mattresses and pads that remove exhaled carbon dioxide from the vicinity of a sleeping infant's mouth to prevent asphyxiation. Sudden Infant Death Syndrome (SIDS) claims the lives of thousands of infants in the United States each year. These infants generally appear to be normal and healthy, but succumb without warning in their cribs. The cause of SIDS is not known, and thus there is no certain means of preventing these tragedies. Medical specialists have, however, advanced several theories to explain the onset of SIDS. U.S. Pat. No. 5,483,711 issued to Hargest et al. reviews these theories, provides statistics regarding the impact of SIDS in the United States, and explains the advantage of placing an infant on its stomach for rest or sleep to prevent choking on regurgitated fluids. This advantage may be accentuated in the case of a premature or newborn infant with relatively undeveloped lungs. However, placing the infant on its stomach has certain drawbacks. As noted in Hargest, one theory regarding the cause of SIDS is that an infant sleeping or resting on its stomach, and thus with its mouth near the mattress or mattress pad of its crib, inhales the carbon dioxide products of breathing that have accumulated near the top surface of the mattress or mattress pad resulting in "carbon dioxide poisoning." This result may alternatively be described as suffocation due to an insufficient amount of oxygen in the carbon-dioxide rich air near the infant's mouth. The presence of bedding may contribute to such accumulation and thus contribute to the possibility of suffocation by the infant. As a result, there are reasons to conclude that SIDS may be prevented by avoiding the accumulation of carbon dioxide near the top surface of the mattress or mattress pad of an infant's crib. Known apparatuses for attempting to prevent such accumulation, and in some cases for attempting to provide a fresh flow of air or oxygen, include that of Hargest and also the mattresses disclosed in U.S. Pat. No. 5,546,618 issued to Beedy et al., U.S. Pat. No. 4,536,906 issued to Varndell et al., and U.S. Pat. No. 3,339,216 issued to Ormerod. Web site: http://www.delphion.com/details?pn=US05887304__ •

Assay and method for determining newborn risk for sudden infant death syndrome Inventor(s): Beach; Peter G. (6780 SW. 205th Ct., Portland, OR 97007) Assignee(s): none reported Patent Number: 5,556,759 Date filed: August 2, 1993 Abstract: An assay and method for screening newborns to determine risk of Sudden Infant Syndrome is described. The assay and method is based on the detection of elevated IgM-anti-IgG (MAG) levels in newborns' serum within the first year of birth. In particular, it has been discovered that elevated MAG levels indicate an increased risk of

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Sudden Infant Death Syndrome (SIDS).In a preferred embodiment of the invention, an ELISA is utilized in which a first binding agent having specific affinity for IgM is used to capture and separate IgM antibodies from the newborn's blood sample. A second binding agent having specific affinity for IgG which has been separated from the sample eluant by complexing with MAG, is then used in conjunction with an enzyme conjugate to indirectly determine the amount of MAG in the newborn's blood. The MAG level is then compared to a cut-off which is selected to separate out approximately 4% of the newborns which have the highest MAG levels. These newborns are designated "high risk" and are recommended for more testing and/or monitoring. Excerpt(s): The invention relates to newborn diagnostic screening. In particular, the invention involves an assay and method for determining the level of IgM-anti-IgG ("MAG") in a newborn's blood, and correlating the MAG level with an empirically determined cut-off to determine whether the newborn has an elevated risk of premature death. Approximately five thousand infants under the age of one die in the United States each year for unexplained reasons, their death ultimately being classified as being caused by "Sudden Infant Death Syndrome" ("SIDS"). The cause of SIDS is not known and no methods for identifying those babies that either have SIDS or are at high risk of developing SIDS, have been previously disclosed. Prior investigators have suggested that Sudden Infant Death may be related to elevated immunoglobulin concentrations. Urquhart et al., Sudden Unexplained Death in Infancy and Hyperimmunization, J. Clin. Path.; 24:736-739 (Feb. 24, 1971). Urquhart et al. determined postmortem antibody levels in SIDS cases. Urquhart et al.'s studies showed that antiglobulin antibodies were detected in Sudden Infant Death cases more frequently (56%) than in living control cases (5%). Urquhart et al. suggest that anti-antibodies might participate in fatal anaphylaxis in SIDS cases. However, Urquhart et al. did not suggest any technique for identifying newborns who are at elevated risk for SIDS, where the identification can be made at a time early enough to implement measures to prevent premature death. Web site: http://www.delphion.com/details?pn=US05556759__ •

Breathing monitor articles of wearing apparel Inventor(s): Stephens; David L. (6221 La Tijera Blvd., Los Angeles, CA 90056) Assignee(s): none reported Patent Number: 5,454,376 Date filed: August 16, 1993 Abstract: A breathing monitor article of wearing apparel, adapted for child users in order to monitor breathing conditions of a child user. The apparatus and the method of the invention are particularly adaptable for infant child users in order to prevent conditions such as Sudden Infant Death Syndrome and similar conditions arising from apnea. The article of wearing apparel comprises a shirt or like garment adapted to extend around the chest and/or abdomen portion of the child user and which contains a pocket having a monitor therein. An elastic belt extends about the chest and/or abdomen of the user and particularly, in the region of the user's lungs. A strain gauge is secured to the elastic belt and detects breathing movement through the expansion and contraction of the chest wall. The monitor is electronically operated and constructed so as to generate an alarm signal if there is a cessation of breathing for a minimum predetermined time period. The shirt, or like garment, is also constructed so that when it is secured to the child user, it automatically energizes the monitor, thereby eliminating the necessity of an attendant to the child from turning the monitor on or off.

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Excerpt(s): This invention relates in general to certain new and useful improvements in breathing monitor articles of wearing apparel and more particularly, to an article of wearing apparel which is constructed so as to detect and generate an alarm signal when there is a cessation of breathing of the child user for a minimum predetermined time period. Detection of breathing patterns of children, and particularly infant children, has proved to be a more difficult task than one would initially envision. There has been a long-felt need for an apparatus and a method to monitor infant child breathing conditions in order to ensure that the child does not lapse into a non-breathing state. The syndrome of sudden infant death ("SIDS"), is one which is moderately rare, although not uncommon. In the sudden infant death syndrome, oftentimes for some inexplicable reason, the child stops breathing and since there is usually utter silence, a parent, or other attendant to the child, does not recognize the cessation of breathing until long after the death of the infant child. The same situation exists when an infant child becomes entangled in clothing, blankets or the like and is unable to extricate himself or herself. Here, again, suffocation usually occurs, silently resulting in the death of the infant child. Web site: http://www.delphion.com/details?pn=US05454376__ •

Cervical appliance to ameliorate sleep apneas Inventor(s): Bennett; C. Richard (15 Forest Glen Dr., Pittsburgh, PA 15228), Mundell; Robert D. (542 Lucia Dr., Pittsburgh, PA 15221) Assignee(s): none reported Patent Number: 4,700,697 Date filed: May 9, 1985 Abstract: A cervical appliance for preventing ventral flexion of the head to reduce the possibility of sudden infant death syndrome and/or adult sleep apnea, both of which have common characteristics which are at least partially obviated with the use of the invention. Excerpt(s): A variety of theories have been proposed to explain sudden infant death syndrome (SIDS). SIDS is defined as "the sudden death of an infant or young child which is unexpectd by history, and in which a thorough post-mortem examination fails to reveal an adequate cause for death". While SIDS may occur for different reasons, one attribute of this phenomenon, included in the great majority of the cases described in the literature, is apnea (or respiratoray pause or periodic breathing) which occurs during sleep and is fatal. The autopsy reports describe conditions that are consistent with a condition of hypoxia and/or hypoxemia having existed for some time prior to the fatal apneic episode. It is the apneic character of SIDS which is addressed when "SIDS-risks" infants are placed on a cardiopulmonary monitor or treated with respiratory stimulants. Some adult humans also suffer severe apnea during sleep (adult sleep apnea, or hypersomnia with periodic apnea [HPA]). SIDS and HPA share the fact that they occur during sleep, and that at least part of the apnea occurs without the subject's making any attempt to breathe. This latter condition is called "central apnea" because it appears to be ordered by the central nervous system. HPA oocurs most frequently in overweight males, over 40 years of age, who are given to strident or stentorian snoring. Typically, their obesity causes such individuals to sleep in a supine position. Careful observations have shown that they possess redundancy of tissue in the soft palate and the walls of the oropharynx. Part of this may be due to fatty deposit; part may be due to anatomical variation. During sleep, especially "quiet sleep" or "REM (rapid eye-movement) sleep",

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facial muscles become hypotonic. During the inspiratory phase of the respiratory cycle the walls of the oropharynx and the base of the tongue tend to collapse onto the oropharynx. This is partly due to muscular hypotonia, partly due to negative pressure. The latter may be caused by negative intrathoracic pressure as air is breathed in, or by the Bernoulli effect (in which rapid airflow through a restricted space decreases the pressure). Web site: http://www.delphion.com/details?pn=US04700697__ •

Crib death (SIDS) warning device Inventor(s): Macias; Helene (5333 Russell Ave., Ste. 301, Hollywood, CA 90027-3513), Winke; Angos (5333 Russell Ave., Ste. 301, Hollywood, CA 90027-3513) Assignee(s): none reported Patent Number: 4,851,816 Date filed: February 24, 1987 Abstract: An apparatus for specific fluid detection in prophylactic prognosis of a medical condition known as Sudden Infant Death Syndrome, that in one embodiment features a casing which is removably affixable to a sensor configured for receiving and transmitting the information of manifestation of micturition to an embodied acquisitioning accommodation embracing a variable frequency oscillator, the output of which interconnects with a signal converter conceptualized to transition a switching provision into energizing a built-in alarm system consequential to the signal converter's having sampled and found the oscillator's frequency to be representative of a manifestation of micturition in precursor to a CNS agonal episode derived laryngospasm attack, while in another embodiment, a switching structure provides for the energizing of an alarm configuration that injects its modulation into the signal circuitry of a baby listening device, and in yet another embodiment, provides for the switching on of a code modulator and thereto connected propagation device in a manner for propagating the information of manifestation of micturition to an independent capture accommodation connected to a compatible signal converter that is conceptualized upon such code's acquisition to consequently cause the transition of a switching faculty, the configuration of which, results in a bi-directionally spliced signal flow of which one is directed to initiate the tasking of a multi-ported microprocessor that controls an ACLS arrangement operationally architectured to induce increased negative intrathoracic pressure relief when not cancelled by supervising personnel or the microprocessor itself accessing the receipt of data that is comprised of co-processed signals. Excerpt(s): This invention relates to a system for detecting the moment of micturition in babies. More particularly, this invention relates to a system which will interdict enuresis alarm circuitry incorporated in it or attached to it from being tricked into switching itself on when in fact the sensor striping, screens, clips or stripes used in and with swaddles or latest embodiment the plastic layered disposable diaper is not wet with urine but condensation permeated. An inspection of the numerous art precursive to this invention amply demonstrates that enuresis monitors continue to present a challenge to practitioners in the art. Web site: http://www.delphion.com/details?pn=US04851816__

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Infant blood oxygen monitor and SIDS warning device Inventor(s): Jackson, III; William H. (P.O. Box 4795, Wilmington, NC 28406) Assignee(s): none reported Patent Number: 6,047,201 Date filed: April 2, 1998 Abstract: A device to help a caregiver monitor an infant to discover the onset of a Sudden Infant Death Syndrome event and to intervene to prevent the Sudden Infant Death Syndrome event. A foot and ankle wrap containing rechargeable batteries and a radio transmitter is connected to a toe cap containing a pulse oximeter by adjustable cords. Blood oxygen and pulse readouts from the pulse oximeter are transmitted to a monitor kept by the caregiver. Visible readouts of the blood oxygen and pulse are shown on the monitor for continuous view by the caregiver. The monitor sounds an alarm if the infant's blood oxygen drops to a dangerous level for predetermined period. The time delay prevents false alarms, therefore, provides a greater degree of alertness to the caregiver using the device. When not in use the device is recharged on a stand. Excerpt(s): This invention is a monitoring device to detect warning signs indicative in Sudden Infant Death Syndrome (SIDS) and other respiratory or cardiac conditions threatening to infants. It is designed to minimize false alarms, to be easily used by parents or other caregivers who have no special training, to be portable, affordable, and practical. Sudden Infant Death Syndrome is the term used to designate the death of seemingly healthy infants commonly between the ages of two weeks and one year. Sudden Infant Death Syndrome [usually abbreviated SIDS, sometimes called crib death] is the leading cause of infant deaths up to the age of one year. The exact cause of SIDS has not been determined. It has been suggested that SIDS occurs in healthy infants as the result of the occurrence of a series of unrelated events. Infants who have periods of apnea, changes in skin color, changes in muscle tone, or who sometimes require help in breathing are more likely to die of SIDS. It is sometimes thought that the infant's position in the crib is a factor in SIDS, and various arrangements of pillows around the infant have been proposed to reduce the risk of SIDS. Web site: http://www.delphion.com/details?pn=US06047201__

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Mattress for cribs and basinets for sudden infant death prevention Inventor(s): Mahdavi; Habib (11504 Canton Dr., Studio City, CA 91604) Assignee(s): none reported Patent Number: 5,857,232 Date filed: December 4, 1995 Abstract: The present invention provides a safety device and a method to counter a potential cause of Sudden Infant Death Syndrome. A frame, fit to the dimensions of a crib or bassinet is equipped with an air permeable material that allows for the free flow of fresh air to an infant's mouth and offsets any exhaled carbon dioxide that lingers by the infant's air passages. The material is of a particular elasticity that an infant's weight does not cause the material to collapse on itself, thereby keeping the supply of fresh air retained in the material in place. Excerpt(s): The present invention relates generally to an apparatus for the prevention of sudden infant death syndrome, and more particularly to a mattress for bassinets or

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cribs which provides for a supply of fresh air to an infant's mouth and prevents the infant's asphyxiation from carbon dioxide poisoning. Each year, thousands of infants (aged 2 weeks to 1 year) die from Sudden Infant Death Syndrome (SIDS), a mysterious disorder in which otherwise healthy infants seemingly stop breathing. Although scientific and medical research has uncovered factors which indicate a predisposition to the disorder (i.e., low birth weight, age of mothers) no specific cause has been uncovered. Moreover, there are varied theories put forth by the medical community as to the cause of SIDS. Some theories suggest a neurological disorder in the infants which intercepts the breathing functions while sleeping and leads to the infant's death by asphyxiation. Applicant believes a contributing cause of SIDS is that infants fall victim to asphyxiation from carbon dioxide poisoning. More specifically, infants sleeping face down rebreathe the carbon dioxide in the exhaled air trapped in the air pocket of their bedding near their air passages. Doctors, nurses and medical journals have for years recommended placing an infant on its back for sleeping to avoid this concern. However, many parents and caregivers are reluctant to follow this advice. Some infants prefer sleeping on their stomachs, and do not adjust to the changed position well. Moreover after 5-6 months, most infants can roll themselves over to their preferred sleeping position. Further, many infants have a tendency to regurgitate and parents are concerned their infant may choke on the regurgitated matter. Web site: http://www.delphion.com/details?pn=US05857232__ •

Means of aiding in the prevention of sudden infant death syndrome Inventor(s): Moore; Luana (Miami Beach, FL) Assignee(s): Key Pharmaceuticals, Inc. (Miami, FL) Patent Number: 4,639,455 Date filed: October 2, 1984 Abstract: A means of aiding in the prevention of Sudden Infant Death Syndrome (SIDS) is disclosed. The means comprises administering a pharmaceutically effective amount of the drug 6-methylene-6-desoxy-N-cylopryplymethyl-14hydroxydihydronormorphone to an infant determined to be susceptible to SIDS. The drug is preferably administered bi-daily via the GI tract. The drug attaches to the nerve receptor sites responsible for the actuation of respiration thus blocking the attachment of endogenous endorphins which, if present in high levels, prevents such actuation resulting in apnea and SIDS. A suppository containing the drug for use in carrying out the method is also disclosed. Excerpt(s): The present invention relates to the field of means for aiding in the prevention of Sudden Infant Death Syndrome (hereinafter SIDS). More specifically, the invention relates to administering the drug 6-methylene-6-desoxy-Ncyclopropylmethyl-14-hydroxydihydronormorphone to an infant determined to be susceptible to SIDS and to an anal suppository containing such a drug. Sudden Infant Death Syndrome (SIDS), also called "Crib Death", can be defined as the sudden death of any infant which is unexpected according to history and in which a post-mortem fails to demonstrate an adequate cause of death. Although the death might be unexpected according to the infant's history as examined in a conventional manner a SIDS death might have been predictable or at least determined to be more probable with that specific infant due to its history. For example, premature infants, low birth weight infants and those with respiratory distress syndrome are more likely to suffer a SIDS death than other infants. Another group of infants more likely to be susceptible to a

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SIDS death would be the "Near-Miss" infants, i.e. those who have been successfully revived after respiration ceased. A number of other factors are known to be associated with an increased likelihood of suffering a SIDS death. In an attempt to reduce the number of SIDS deaths, attempts have been made to identify those infants who would be more likely to suffer a SIDS death. After identifying such infants, the parents are notified and mechanical devices can be attached to the infant. These mechanical devices monitor the respiration and/or heartbeat of the infant and actuate an alarm when respiration and/or heartbeat ceases. The parents can respond to the alarm and revive the infant. Such devices are advantageous in that they do not require the administration of any drugs to the infant. However, they are undesirable in that they may fail due to mechanical malfunction or an interruption of their power supply. Further, individuals might fail to respond to the alarm or fail to respond fast enough in order to revive the infant. Perhaps most importantly, such devices do nothing to prevent respiratory arrest and respiratory arrest for even a short period of time can of course cause brain damage. Web site: http://www.delphion.com/details?pn=US04639455__ •

Method and apparatus for correlating respiration and heartbeat variability Inventor(s): Nishimura; Toshihiro (Ooita, JP) Assignee(s): Nippon Kayaku Kabushiki Kaisha (Tokyo, JP) Patent Number: 5,105,354 Date filed: January 23, 1989 Abstract: An evaluation method of respiration and heart beat and its apparatus which permits one to forecast sudden infant death syndrome by investigating correlation between respiration and heart beat in the normal state and sleep-apnea of a newborn. Excerpt(s): This invention relates to a method of evaluating data pertaining to respiration and heart beat and an apparatus for evaluating them, especially for forecasting sudden infant death syndrome (SIDS) by investigating the correlation between respiration and heart beat in a normal state and respiratory standstill in sleep. Generally, the data from organisms includes EEG, cardiac electricity, respiration, ocular movement, and EMG. Signal forms of this data are relatively more useful than from EEG etc. It is therefore easier to analyze an R--R interval as a change of peak interval of an ECG wave, chronologically. Considering that respiratory arrhythmia depends upon an efferent impulse from an extension receptor, standstill of the efferent impulse from an extension receptor in respiratory arrest in sleep will have an effect on heart beat. It has been already reported that in Cheyne Stokes respiration during hyperrespiration the increase of heart beat and decrease of blood pressure are observed; during its apnea the decrease of heart beat and increase of blood pressure occur. Web site: http://www.delphion.com/details?pn=US05105354__

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Method and apparatus for improving the respiratory efficiency of an infant Inventor(s): Hale; Theodore M. (39 Celano La., West Islip, NY 11795) Assignee(s): none reported Patent Number: 5,389,037 Date filed: July 15, 1993

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Abstract: A method and apparatus for reducing respiratory abnormalities in infants and the incidence of crib death by providing a flow of room air to a sleeping infant's environment to stimulate breathing. In a preferred embodiment of the invention, room air is delivered into a crib through an air plenum that is removably attached to the vertical bars of a crib and positioned within 1 cm to 20 cm of the infant's mouth, nose, larynx and trachea. The flow of room air from the air plenum safely assists the respiration of an infant with inadequate shallow end tidal volume, decreases rebreathing of expired carbon dioxide from the nose, mouth, oral cavity and trachea, prevents pockets of increasing carbon dioxide from developing within the cushions and beddings surrounding the infant, and decreases the likelihood of overheating and other conditions associated with sudden infant death syndrome, apnea syndromes and hypoventilation. Excerpt(s): The present invention relates to a method and apparatus for providing room oxygen to an infant and removing expired carbon dioxide from the infant's environment by directing a flow of room oxygen to the infant's mouth and nose in a non-intrusive manner. More particularly, the present invention relates to an air plenum assembly that may be permanently or removably mounted to a crib or playpen such that the air flow from the plenum is directed toward the mouth and nose of the child. The present invention is directed toward preventing infant deaths due to prolonged periodic breathing and sudden infant death syndrome. Periodic breathing is a normal phenomenon where an infant's breathing pattern is interrupted by recurrent apneas or absences of breathing. It has been shown in independent studies that an increase in ambient oxygen concentration correlates with a reduction in the incidence of apnea in infants. Kattwinkel, J., Neonatal/Apnea: Pathogenesis and Therapy, 90 J. Pediatric 342 (1977); Hoppen-Brouwers, T., Hodgman, J. E., Harper, R. M., et al., Polygraphic Studies of Normal Infants During the First Six Months of Life: I. V. Incidence of Apnea and Periodic Breathing, 60 Pediatrics 418 (1977). Pharmacological therapies have been used to treat prolonged periodic breathing, but the effect of these therapies remains uncertain. Neil N. Finer, M.D., Keith J. Barrington, M.D., and Barbara Hayes, R.N., Prolonged Periodic Breathing: Significance in Sleep Studies, Pediatrics, Vol. 89, No. 3, pp. 450-52 (March 1992). Web site: http://www.delphion.com/details?pn=US05389037__ •

Method and apparatus for monitoring and treating sudden infant death syndrome Inventor(s): Gliner; Bradford E (Issaquah, WA), Jorgenson; Dawn Billie (Seattle, WA) Assignee(s): Agilent Technologies, Inc. (Palo Alto, CA) Patent Number: 6,208,897 Date filed: April 27, 1999 Abstract: This invention relates generally to a device for monitoring an infant for the onset of sudden infant death syndrome (SIDS), detecting the onset of SIDS and providing immediate treatment. In the broadest sense, the invention includes an apparatus for detecting and treating SIDS. The apparatus comprises a data gatherer for monitoring an infant parameter, a controller for communicating with the data gatherer, an energy source operable to power the data gatherer for monitoring the infant parameter and further operable to provide energy to an energy delivery system which is operable to deliver an electric shock from an energy source to an electrode interface, and an alarm which is activated by the controller for alerting a remote caregiver to the onset of symptoms associated with SIDS. The invention also relates to a method of operating a

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SIDS monitor. The method comprises the steps of monitoring an infant parameter, determining whether the monitored parameter is an acceptable value. If the monitored parameter is an acceptable value, then an alarm is activated to alert a caretaker of the onset of SIDS symptoms, if the monitored parameter is within an acceptable value, then continuing to monitor the infant parameter. Excerpt(s): This invention relates generally to a device for monitoring an infant for the onset of sudden infant death syndrome (SIDS), detecting the onset of SIDS and providing immediate treatment. Treatment could include instructions for administering cardiopulmonary resuscitation (CPR) as well as delivery of a defibrillation pulse from an automatic or semi-automatic external defibrillator (AED). The device may be a SIDS monitor as well as a SIDS trainer, or a SIDS monitor which has the ability to function as a trainer. Because SIDS is identified in situations where no explanation for the death can be found, the potential causes of SIDS has been largely speculative. Potential causes include cardiac disorders, respiratory abnormalities, gastrointestinal diseases, metabolic disorders, injury and child abuse. Many devices have been developed that provide a way to monitor an infant for the onset of SIDS by detecting cessation of movement, cessation of respiration or detection of urination that may accompany agonal movement. Other devices have been developed to prevent SIDS from occuring, such as by providing an oxygenated mattress. The following summarizes a selection of previously patented approaches to SIDS detection and/or prevention. Web site: http://www.delphion.com/details?pn=US06208897__ •

Method and apparatus to prevent positional plagiocephaly in infants Inventor(s): Dixon; Donald L. (Anchorage, KY), Havens; Robert L. (Marysville, IN) Assignee(s): Center for Orthotic & Prosthetic Care, L.L.C. (Louisville, KY) Patent Number: 6,052,849 Date filed: March 18, 1998 Abstract: A cranial suspension apparatus to prevent positional plagiocephaly in an infant by distributing loads on the head of the infant lying in the supine position on a horizontal surface. The infant is placed in the apparatus such that the head of the infant is supported on a flexible porous support material with the tension of the material adjusted to support the head just above or just touching the sleep surface. The flexible porous support material may be a net with an open weave. The apparatus prevents localized pressure on the infant's head in an area contacting a sleep surface when infants are routinely placed in the supine position, which is recommended to avoid sudden infant death syndrome. Excerpt(s): The invention relates to an apparatus and the use of the apparatus to prevent positional plagiocephaly by more evenly distributing loads on the head of an infant lying on a sleep surface in the supine position. Cranial asymmetry (plagiocephaly) and deformations are common in the neonatal period. They may occur from various causes including premature closure of the cranial vault and/or skull base sutures (craniosynostosis), syndromal craniofacial dysostosis, intracranial volume disorders such as hydrocephalus, microcephaly or tumor, metabolic bone disorders such as rickets, and birth trauma such as depressed skull fractures. A subset of patients with plagiocephaly are recognized that do not exhibit pathology of the sutures and do not fall into any of the above categories. These patients are referred to as having plagiocephaly without synostosis (PWS), also known as "positional" or "gestational" plagiocephaly. The

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etiology of cranial asymmetry in PWS has been suggested to result from two possible mechanisms. One proposed mechanism is intrauterine constraint that develops from early descent of the fetal head into the pelvis, effectively placing uneven pressure on one area of the cranium within a confined space. This leads to constraint of one side of the occiput (back of the head) with a compensatory change to the contralateral skull. Another mechanism that can perpetuate the fetal constraint or even lead to the misshapen head is supine positioning of the infant. Once the occiput develops even a mildly flattened area, placing the infant on the back or supine position will perpetuate the deformity. The head will roll to the flattened area by the forces of gravity and, because motor control is lacking in the neonate, the deformity will remain or worsen. This effect is especially illustrated in infants with neuromuscular disorders and hypotonia where deformation of the cranium can be quite profound. This phenomena has been recognized for many years and recommendations for changing the infant's environment with relationship to the crib and placement within the sleeping area are well established. Web site: http://www.delphion.com/details?pn=US06052849__ •

Method for correcting plasma melatonin levels and pharmaceutical formulation comprising melatonin Inventor(s): Zisapel; Nava (Tel Aviv, IL) Assignee(s): Neurim Pharmaceuticals (1991) Ltd. (IL) Patent Number: 5,498,423 Date filed: February 14, 1994 Abstract: In order to correct a melatonin deficiency or distortion in the plasma melatonin level and profile in a human subject, there is administered to a human in which such a deficiency or distortion had been diagnosed, over a predetermined time period including at least part of the nocturnal period, an amount of melatonin in controlledrelease form, such that the melatonin is released according to a profile which, taking into account the existing profile, simulates the profile in plasma of a human having a normal endogenous melatonin plasma profile. The invention also relates to a pharmaceutical controlled-release formulation, which comprises melatonin in combination with at least one pharmaceutical carrier, diluent or coating, the formulation being adapted to release melatonin over a predetermined time period, according to a profile which, taking into account the existing profile, simulates the profile in plasma of a human having a normal endogenous melatonin profile. The method of the invention may be e.g. applied to the prevention of sudden infant death syndrome in infants, and then comprises a preliminary screening step in order to determine the plasma melatonin levels, in order to select infants having a deficient plasma melatonin level. Excerpt(s): The present invention relates to a method for correcting a deficiency or distortion in the plasma melatonin level and profile in a human subject and to a pharmaceutical controlled-release formulation which comprises melatonin. Melatonin is the principal hormone secreted by the pineal gland in all vertebrates. In all mammals studied to date, including humans, a nocturnal rise in the production of melatonin by the pineal gland is evident, regardless of whether the mammals are nocturnal or diurnal, and conversely, melatonin production by the body is acutely suppressed by light. Melatonin is involved in the coordination of photoperiod and physiological processes, e.g. in animals which use changes in the photoperiod to time their thermoregulation, temporal signals to the thermoregulatory system are controlled by the daily rhythm in

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the duration of melatonin during the dark phase. Numerous studies have shown that melatonin has a potent influence on gonadal activity. The timing of melatonin administration has been shown to be crucial for its biological activities. E.g., while in the case of rats whose circadian rhythms are disrupted or arrhythmic in constant light, as well as in the case of rats free running in constant darkness, their rhythms are synchronized by daily melatonin injections, by contrast it has been found that continuous availability of melatonin in circulation, of injection of melatonin in the morning, sometimes prevents gonodal responses to melatonin in the afternoon. The inventor has shown, e.g. in Zisapel et al, Neuroendocrinology 40: 102 (1985), that the inhibition by melatonin of the stimulated release of dopamine from rat hypothalamus, was highest in the early photophase and lowest in the early afternoon. Web site: http://www.delphion.com/details?pn=US05498423__ •

Method for determination of urine components and for preventing sudden infant death syndrome Inventor(s): Laudon; Moshe (Kfar Saba, IL), Zisapel; Nava (Tel Aviv, IL) Assignee(s): Neurim Pharmaceuticals (1991) Ltd. (Tel Aviv, IL) Patent Number: 5,500,225 Date filed: October 19, 1993 Abstract: Non-volatile organic components of interest in the urine of humans using diapers are assayed by carrying out the following sequence of steps at least once and up to as many times as the diapers are changed in a given 24-hour period, namely: removing the outer cover and any extraneous material from a used diaper so as to leave only diaper pulp with absorbed urine, estimating the amount of water in the used diaper, extracting a weighed portion of the diaper pulp with a water-miscible organic solvent, in which the diaper pulp is insoluble, to give an extract containing a component of interest, and determining the amount of the component of interest per unit volume of urine absorbed on the diaper pulp by analyzing an aliquot of the extract. The method may be applied e.g. to the prevention of sudden infant death syndrome in infants, by selecting infants for medication with melatonin where diaper urine indicates a deficiency of its metabolite 6-sulfatoxymelatonin in a 24-hour period. The melatonin may be administered in the form of a pharmaceutical formulation, or in an infant food which is included within the invention. Excerpt(s): The present invention relates to a method for determination of components of urine in diapers, as well as to a method for preventing sudden infant death syndrome (i.e. cot death), which makes use of the results of such determination. In another aspect, the prior patent application (U.S. Ser. No. 07/697,714) relates to a method for correcting a melatonin deficiency or distortion in the plasma melatonin level and profile in a human subject, which comprises administering to a human in which such a deficiency or distortion had been diagnosed, over a time period including at least part of the nocturnal period, an effective plasma melatonin deficiency or distortion correcting amount of melatonin in the form of a pharmaceutical controlled-release formulation defined in the preceding paragraph. (c) administering an effective plasma melatonin deficiency correcting amount of melatonin to the at least one selected infant from step (b), the melatonin being in the form of a pharmaceutical controlled-release formulation defined above. Web site: http://www.delphion.com/details?pn=US05500225__

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Motion monitor useful for sleeping humans Inventor(s): Miller; William (1735 Caminito Ardiente, La Jolla, CA 92037) Assignee(s): none reported Patent Number: 5,796,340 Date filed: August 12, 1996 Abstract: A motion monitor which detects respiration and/or cardiac activity of a human, particularly a sleeping human, has a mattress, for example, an air mattress, for supporting a sleeping human. The mattress has an interior cavity isolated from and at a pressure equal to or greater than ambient atmospheric pressure. A pressure transducer is connected with the interior cavity of the mattress and generates a signal representative of the pressure in the interior cavity. An indication unit is connected to the pressure transducer and presents a signal based on the output of the pressure transducer. This sleep monitor is useful for infants, particularly infants at risk for sudden infant death syndrome (SIDS). Excerpt(s): The present invention relates to motion monitors, particularly sleep monitors useful with children suspected of being at risk for sudden infant death syndrome ("SIDS"). Sleep monitors are used to detect occurrences of apnea (transient cessation of respiration), bradycardia (relatively slow heart action), and tachycardia (relatively rapid heart action) when there is some medical reason to believe that infants (or adults) are at risk for these events. A sleep monitor can also be used with infants who are suspected of being at risk for SIDS. SIDS, which affects one out of every 500 to 600 live births, is the largest single cause of death among infants less than one year of age, and accounts for 6,000 to 10,000 deaths per year in the United States. Conventional sleep monitors measure respiration and heart action by measuring transthoracic impedance and the electrocardiogram (TTI/ECG) and are designed to sound an alarm when apnea, bradycardia or tachycardia is detected and found to persist for more than a predetermined amount of time. The measurements taken by conventional sleep monitors are electrical in nature, and require attaching electrodes to the subject's skin, usually on the chest. Wires from a control box are attached to the electrodes, and a band is wrapped around the chest to keep the wires in place during sleep. The electrodes must be attached each time the subject goes to sleep, and the band, the electrodes and the wires must be removed at the end of each sleep session. Special care must be taken to assure good electrical contact between the electrodes and the skin. Foreign matter on the skin, such as talc, can cause a faulty contact. Motion of the subject during sleep can cause electrical noise at the contacts, can cause the wires to come loose, or can cause the wires to break. In a recent study in which 182 patients were monitored in their sleep, of 30,059 recorded events (i.e., machine-indicated occurrences of apnea and/or bradycardia and/or tachycardia) 91.9% were false alarms. 68.5% of the recorded events were false alarms caused by body motion and/or loose leads, and 23.4% were other machine errors such as interpretation of a low-amplitude respiratory signal as apnea. In addition to the functional problems of using a sleep monitor, there is also the matter of cost. The rental fee for such a machine is several hundred dollars per month. WeeseMayer DE, Morrow AS, Conway LP et al., Assessing clinical significance of apnea exceeding 15 seconds with event recording. J. Pediatrics 117:568, 1990. Also see Nathanson I, O'Donnell J, Commins MF Am Dis Child 143:476. Web site: http://www.delphion.com/details?pn=US05796340__

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Optical monitor for sudden infant death syndrome Inventor(s): Flock; Stephen T. (Mt. Eliza, AU), Marchitto; Kevin S. (Mt. Eliza, AU) Assignee(s): Rocky Mountain Biosystems, Inc. (Golden, CO) Patent Number: 6,492,634 Date filed: May 2, 2001 Abstract: The present invention provides devices and/or methods of monitoring extremely small movements associated with infant breathing and heart rate, therefore monitoring sudden infant death syndrome (SIDS). Provided is a system for monitoring movement of an infant, comprising: a light source which produces radiant energy; an optical device; and an imaging device. Further provided is a method of monitoring movement of an infant, comprising the steps of: producing radiant energy by a light source; coupling said radiant energy into an optical device so as to create a matrix of images; projecting said images into a field of interest; and detecting movement of said infant using an imaging device. Excerpt(s): The present invention relates generally to the field of medical devices. More specifically, the present invention relates to an optical monitor for sudden infant death syndrome. Sudden Infant Death Syndrome (SIDS) is the sudden and unexpected death of an apparently healthy infant, whose death remains unexplained after further medical investigation such as an autopsy. Sudden Infant Death Syndrome is neither a disease, nor can it be a diagnosis for a living baby [1]. SIDS occurs at a rate of approximately 2 per 1,000 live births in the United States and occurs most often (90%) in under six months of age; of these, 18% were preterm infants [2]. One of the events that occurs during Sudden Infant Death Syndrome is a period of apnea (stoppage of breathing) during which it may be possible that the infant may be resuscitated. However, most Sudden Infant Death Syndrome events occur at night when the infant's caregiver is asleep. Since Sudden Infant Death Syndrome is not normally associated with verbal distress, few infants get a chance to be resuscitated. Web site: http://www.delphion.com/details?pn=US06492634__

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Passive apnea monitor Inventor(s): Sullivan; Patrick K. (Honolulu, HI) Assignee(s): Ocean Laboratories, Inc. (Honolulu, HI) Patent Number: 6,375,621 Date filed: December 27, 1994 Abstract: The instrument monitors the acoustic and electromechanical signals of the patient and calculates an energy spectrum periodogram or histogram using time series analysis techniques. The patient lies down on a large piezoelectric film (few microns thick) that has the capability of measuring signals from very high to very low frequencies. The heart and respiration rates as well as obstructive apnea can be observed, detected and measured from the spectral peaks in the resulting energy spectrum. A microcomputing machine provides calculations to determine the energy spectrum and provides for discrimination between noise and a true apnea episode. An alarm calls for assistance in the event of an apnea, including obstructive apnea, or a Sudden Infant Death Syndrome (SIDS) episode.

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Excerpt(s): An interesting application of the proposed technology, to which the invention relates preferably, but not exclusively, is the detection of apnea, the monitoring of biological functions such as heart rate and respiration rates, as well as obstructive apnea, particularly for infants. The invention relates to a system that uses acoustic and electromechanical transducers, such as a piezoelectric film, to measure biological respirative signals over time. Time series analysis techniques are then applied to the measured signals whereby an energy spectrum (periodogram/histogram) is calculated that identifies the rhythmic and pseudo-rhythmic biological functions such as respiration and heart rate and obstructions in the breathing passage (obstructive apnea.). The apnea monitoring instrument offers researchers, clinicians, parents and other people who are involved in child and adult apnea monitoring an inexpensive way to monitor respiration, heart rate and obstructive apnea without the use of restrictive electrical wiring. It makes available a low cost monitoring instrument to be used as a highly reliable tool for researching and monitoring Sudden Infant Death Syndrome (SIDS). Web site: http://www.delphion.com/details?pn=US06375621__ •

Position monitor and alarm apparatus for reducing the possibility of sudden infant death syndrome (SIDS) Inventor(s): Clark, Jr.; Leonard R. (Oreland, PA), Mesibov; Barbara (Mill Neck, NY) Assignee(s): Waterview LLC (East Norwich, NY) Patent Number: 5,914,660 Date filed: March 26, 1998 Abstract: A device for reducing the possibility of sudden infant death syndrome (SIDS) comprises a position-indicating device effectively coupled to a signal-producing circuit and attached to the clothing of the infant. The position-indicating device provides signals varying in response to prone and other positions assumed by the infant during sleep, allowing an associated alarm device to be activated in response to the infant's assuming a SIDS-dangerous prone or side-lying position. In one embodiment, the position of the infant can be determined by an optical sensor interacting with a reflective or other marker adhered to the infant. Gravity or pressure switches may also be used to provide position-responsive signals. A signal generated upon assumption of the SIDSdangerous prone or side-lying positions is transmitted to a remote receiver located proximate the infant's care-giver whereupon an alarm is generated to indicate the need to reposition the infant. A constant low-level or intermittent maintenance signal can be produced to assure the continued and proper operation of the apparatus. An additional awakening alarm can be produced near the sleeping infant to further reduce the likelihood of a SIDS event. Excerpt(s): The present invention relates to an apparatus for continuously monitoring the position assumed by a sleeping infant. More particularly, the invention relates to the provision of an alarm to indicate when the infant has taken a position considered to be conducive to the onset of Sudden Infant Death Syndrome (SIDS). Sudden Infant Death Syndrome (SIDS) has been defined as the "sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and a review of the clinical history." SIDS occurs in all types of families and is generally independent of race and socioeconomic level. It is unexpected and usually occurs in apparently healthy infants from one month to one year of age. Death occurs without warning and is accompanied by no signs of suffering. Five to six thousand infant deaths per year were

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attributed to SIDS during the late eighties and early nineties. The horror of SIDS, also commonly known as "crib death", lies in the thus far unsolved mystery of why a seemingly healthy baby dies suddenly, without warning and without apparent reason. A form of undiagnosed apnea has been suspected; various maternal risk factors, including cigarette smoking during pregnancy, maternal age less than 20 years, poor prenatal care, low weight gain, anemia, drug abuse and a history of sexually transmitted disease and/or urinary tract infection have all been suspected of heightening the likelihood of occurrence; and the presence of soft bedding materials and the breathing of second-hand smoke have also been cited as possible contributing factors. Recent studies at the National Institute of Child Health and Human Development (NICHD) have identified defects in the regions of the brains of SIDS-susceptible infants that control breathing. However, whatever the root cause of SIDS is eventually determined to be, it appears that pro-active parenting can substantially reduce the risk to the newborn. Web site: http://www.delphion.com/details?pn=US05914660__ •

Prevention of sudden infant death Inventor(s): Hedner; Jan (Gothenburg, SE), Pettersson; Anders (Kode, SE) Assignee(s): Diabact AB (SE) Patent Number: 6,083,756 Date filed: May 7, 1998 Abstract: A method for identification of an infant being particularly susceptible to sudden infant death syndrome (SIDS) comprises the determination of an Helicobacter pylori infection in the infant's mother, particularly by detection of antibodies to H. pylori of the IgG type, in a blood sample drawn from the infant's mother or by determination of carbon dioxide formed from urea in the air exhaled from the infant's mother upon oral administration of a challenge dose of urea. Also disclosed is the use of an antibiotic effective against H. pylori for the manufacture of a medicament for administration to mothers and other persons infected by H. pylori and coming into close bodily contact with infants below two years of age, and a method of prevention of SIDS by administration of that antibiotic. Excerpt(s): The present invention relates to the identification of infants with increased risk of sudden death (sudden death syndrome; SIDS), and to methods and means for SIDS prevention. Sudden infant death syndrome (SIDS) occurs in young infants during a narrow time range that peaks at 3 months and extends over about two years from birth. It is relatively common (7,000 deaths in the United States per year). Usually it is defined in the negative: "The sudden death of any infant or young child which is unexpected in history and in which a thorough post-mortem examination fails to demonstrate an adequate cause for death". Several factors identified in epidemiological studies of SIDS are associated with increased susceptibility of infants to infectious diseases, particularly upper respiratory tract infections. The period in which infants are at highest risk roughly corresponds to the period when maternal antibodies in the infant are decreasing while its immature immune system is not able to provide full compensation. The vast majority of SIDS-related deaths occur below the age of two years. Not only are breast-fed infants less vulnerable to infections but also less susceptible to SIDS. Many babies who died from SIDS had mild gastrointestinal tract infection shortly before death; IgA response of their duodenal mucosa was found to be significantly increased (Stoltenberg L et al., Pediatr. Res. 32 (1992) 372-375).

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Web site: http://www.delphion.com/details?pn=US06083756__ •

Respiratory stimulator bed Inventor(s): Totten; Bertram F. (912 Yosemite La., El Dorado Hills, CA 95630) Assignee(s): none reported Patent Number: 4,969,451 Date filed: April 23, 1987 Abstract: Unique crib or bed structure designed and constructed to combat and overcome sudden infant death syndrome by effecting an external and intermittent jarring stimulus to weak, slow and undeveloped body functions in accordance with the age and respiratory rate of an infant or other body reclining upon the crib or bed. In its preferred form in order to effect this intermittent jarring stimulus to a body reclining upon the crib or bed, an electronically controlled cam is positioned beneath the mattress supporting structure of the crib or bed intermittently when rotated to strike the underside of the mattress supporting structure, thereby jarring it in a manner effecting intermittent cycles of upward and downward motions of the mattress supporting structure and a mattress supported thereon, with a momentary pause or rest period between each cycle of cam rotation at which time the cam is completely out of contact with the mattress supporting structure. Excerpt(s): The present invention relates to bio-engineered beds but more particularly to such crib structures wherein its unique construction and best mode of operation is designed to stimulate the respiratory rate of infants while sleeping upon its mattress and thereby overcome the mysterious infant sudden death syndrome. While the known prior art discloses crib structures for moving crib mattresses in a number of ways and directions, none has specifically dwelt with this infant death syndrome, and none discloses a construction and mode of operation which would be effective to overcome it, as has the present invention. The primary object of the present invention is to provide a unique bio-engineered bed or crib structure which, in its best mode of operation is effective to overcome the mysterious infant death syndrome. Web site: http://www.delphion.com/details?pn=US04969451__

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Sleeping pad, beddings and bumpers to improve respiratory efficiency and environmental temperature of an infant and reduce the risks of sudden infant death syndrome (SIDS) and asphyxiation Inventor(s): Koenig; J. Frank (407 Kramer Dr. SE., Vienna, VA 22180) Assignee(s): none reported Patent Number: 6,055,690 Date filed: November 1, 1995 Abstract: Rebreathing carbon dioxide and overheating of the infant are contributing causes of Sudden Infant Death Syndrome (SIDS) and asphyxiation. The characteristics of conventional crib mattresses, beddings and bumper pads contribute to rebreathing of carbon dioxide and overheating of the infant and may be contributing environmental causes of SIDS, asphyxiation, apnea syndromes and hypoventilation. The present invention consists of improved sleeping pads, beddings and bumper pads which reduce

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rebreathing of carbon dioxide and overheating and provide increased crib ventilation to stimulate breathing. Excerpt(s): The present invention relates to apparatus for reducing the risk of sudden infant death syndrome, asphyxiation, apnea syndrome and hypoventilation through the use of improved sleeping pads, beddings and bumper pads within a crib or the like to improve the respiratory efficiency and environmental temperature of an infant. Sudden infant death syndrome (SIDS) is the leading cause of postneonatal infant death in the United States. About 7,000 deaths occur each year from SIDS. In addition, many infants die each year of asphyxiation while in a crib. Prone sleeping is associated with spontaneous face-down sleeping in infants. The face-down position is associated with rebreathing expired gases, including carbon dioxide, and increased carbon dioxide lung pressure in normal infants. In some cases the amount of rebreathed carbon dioxide is sufficient to cause death in normal infants. B. A. Chiodini and B. T. Thach, Impaired ventilation in infants sleeping facedown: Potential significance for sudden infant death syndrome, J. Pediatrics, Vol. 123, 686 (1993); J. S. Kemp and B. T. Thach, Sudden Death in Infants Sleeping on Polystyrene-Filled Cushions, New England Journal of Medicine, Vol. 324, 1858 (1991). In that case the cause of death is asphyxiation, not SIDS. However in SIDS's cases the rebreathing of carbon dioxide, short of asphyxiation, may be a contributing cause of death of the infant. Web site: http://www.delphion.com/details?pn=US06055690__ •

Sudden Infant Death Syndrome (SIDS) monitor and stimulator Inventor(s): Scanlon; Michael (Silver Spring, MD) Assignee(s): The United States of America as represented by the Secretary of the Army (Washington, DC) Patent Number: 5,515,865 Date filed: April 22, 1994 Abstract: A movement and sound monitor and stimulator which is particularly useful for preventing death in human infants from sudden infant death syndrome is disclosed. The movement and sound monitor and stimulator has a base member which may be a fluid-filled sensing pad for supporting the infant or other animate object which is being monitored and a transducer positioned for detecting movement or acoustic activity (e.g., heartbeat, breathing) of the object on the base member to provide an output signal in response to forces applied thereto which are generated by such movement. A circuit is connected to monitor the output signal from the transducer and activates a stimulator which is operable to provide movement to the base member to stimulate movement in the object when output from the transducer to the circuit corresponds to no movement from the object. The transducer may be a pressure transducer in fluid communication with the fluid interior of the sensing pad. In the alternative, a piezo-electric sheet operatively connected to a surface of the sensing pad to detect such movement as well as movement cessation. The circuit may also be connected to an alarm which can provide an audible or visual indication to third parties when there is no movement from the object. Excerpt(s): The present invention relates to a movement monitor suitable for detecting movement and, more particularly, to a movement monitor suitable for monitoring and stimulating/resuscitating a human or other living organism's breathing movement. Sudden Infant Death Syndrome (SIDS) is a medical condition whereby an infant

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suddenly stops breathing, leading to the eventual death of the infant. Although the cause and initial symptoms of SIDS is not completely understood, it is felt that a child can be awakened from the SIDS condition. Unfortunately, many currently available baby monitors are usually only provided with a microphone/transmitter and a receiver/speaker, enabling the parents to monitor baby noises such as crying, coughing, sneezing and sniffling. If the parents do not hear anything, they assume the baby is sleeping, and therefore do not need to check in on the child. Unfortunately, in some tragic situations, the absence of baby noises can be deadly to the child. Web site: http://www.delphion.com/details?pn=US05515865__ •

Sudden infant death syndrome monitor Inventor(s): Kim; Bill H. (702 Doubletree La., Long Beach, CA 90815) Assignee(s): none reported Patent Number: 5,505,199 Date filed: December 1, 1994 Abstract: A sudden infant death syndrome, SIDS, monitor which monitors the infant to determine oxygen desaturation and movement. No alarm indication is produced if movement is detected, a low alarm condition is produced if desaturation occurs while movement is detected and a high condition is produced if desaturation is occurs and no movement is detected. A video monitor is provided to bring the image of the infant into the presence of the caregiver when either alarm is produced. The substantially reduced number of false alarms, due for example to motion artifacts, improves the level of alarm response over the long term that can reasonably be provided by parents and caregivers. Excerpt(s): Sudden infant death syndrome is the medical terminology used to designate the almost inexplicable deaths of seemingly healthy infants. Commonly known as crib death, SIDS is the leading category of infant deaths between the ages of two weeks and one year and account for one-third of all deaths after the new born period. Despite limited information, a scientific consensus suggests that SIDS occurred in healthy infants as a result of the simultaneous occurrence of a series of seemingly unrelated biological events. Infants who have periods of apnea, or difficulty in breathing, sudden skin color change to blue or pale, changes in muscle tone either to limpness or rigidity and who appear to require help in breathing are more likely to die of SIDS. These episodes can occur during sleep, feeding or while awake and are now known as apparent lifethreatening events or ALTEs. Specially designed apnea/bradycardia alarm systems became available for home use in the late 1970s to monitor infant breathing in an attempt to reduce SIDS. Conventional apnea/bradycardia monitors use electrodes attached to the infant's skin. The monitors provide an audible alarm if the baby stops breathing for a pre-determined period of time, or when the heart rate drops below a designated level, to indicate to the parent or guardian that the baby may need assistance in breathing. Conventional home monitors may now also include means for recording the electrocardiogram and respiratory wave form before, during or after the alarm event. Web site: http://www.delphion.com/details?pn=US05505199__

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Sudden infant death syndrome prevention apparatus and method Inventor(s): Hargest; Thomas S. (14 Lockwood Blvd., Apt. 10J., Charleston, SC 29401), Hargest; William M. (8470 Doar Rd., Awendaw, SC 29429) Assignee(s): none reported Patent Number: 5,317,767 Date filed: June 16, 1992 Abstract: A safety pad or mattress such as for use in a crib prevents sudden infant death syndrome by ensuring an oxygenated breathing space beneath the infant. Reticulated foam or other air permeable material is made into the shape of a pad or even a mattress and covered with a fitted open weave fabric covering. An air tube is embedded in the pad or mattress and interconnected with an air pump which circulates fresh, i.e., oxygenated, air in a breathing space formed beneath an infant by the air permeable mattress. The forced air circulation flushes any exhaled carbon dioxide from the breathing space, even when the infant is face down or otherwise in a prone position on the mattress, to prevent carbon dioxide poisoning. The materials of the fabric covering and air permeable mattress permit any fluids regurgitated from the infant to drain away from the infant's face. A relatively tight fit for the fitted covering obviates loose fitting sheets to further prevent potential entanglement and suffocation of a recumbent infant. Excerpt(s): The present invention relates in general to apparatus and method for the prevention of sudden infant death syndrome and in particular to an infant safety pad or mattress and corresponding method for the prevention of infant asphyxiation from carbon dioxide poisoning. Several thousand apparently healthy infants (children under the age of 1 year) die each year in the United States from Sudden Infant Death Syndrome (SIDS). Deaths from SIDS have been estimated at 7,000 to 10,000 per year. See for example Womens Day, volume 55, issue 3, Jan. 7, 1992, pages 38 through 43; and USA Today, volume 117, issue 2626, February 1989, page 11. The occurrence of SIDS in a given family can be particularly devastating emotionally because, in general, there is no warning that the infant is at risk and the parent or care giver has no knowledge of any problem until he or she discovers an unconscious or deceased infant thought to be safely sleeping in its crib. The specific cause of SIDS is generally unknown, which unfortunately leads to the result that heretofore there has generally been no known treatment and generally no means of prevention. Web site: http://www.delphion.com/details?pn=US05317767__

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Vital signs monitor Inventor(s): Cestaro; Victor L. (Farmingville, NY), Sciarra; Michael J. (Southampton, NY) Assignee(s): F. William Carr (Houston, TX) Patent Number: 4,494,553 Date filed: April 1, 1981 Abstract: Provision is made to monitor for vital signs, such as respiratory activity and cardiac activity. The monitoring equipment is mounted by a belt to a person being monitored. Multiple Inductance coils carried by the belt move relative to each other in response to breathing, and the associated mutual inductance changes provide sensory signals to reflect the breathing. Electrical signals indicative of such vital signs are transmitted by radio wave to a central monitor which can monitor the activity of

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numerous persons. A plurality of such patient units including vital signs sensors and transmitters in combination with a single central monitor may be used to monitor multiple patients. The present invention is useful in monitoring to attempt to prevent sudden infant death syndrome, or crib death, and in intensive care units or cardiac units of hospitals and the like. Excerpt(s): The present invention relates to electronic systems for monitoring vital signs, such as respiration and cardiac activity. There have been several types of vital sign monitors to detect interrupted respiration. However, each of these types has suffered from several shortcomings. A first type of monitor was based on detecting the temperature differential between inhaled and exhaled air. Usually, a temperature sensor was mounted near a patient's nose to detect changes in temperature in the air between inhaling and exhaling. However, since a person normally breathes once every five or more seconds, a substantial time delay in seconds lapsed, usually twenty or more, before an abnormal condition was sensed. Another type of monitor utilized a strain gage sensor whose resistance changed as the patient's chest cavity expanded and contracted during breathing. However, for reference reading purposes, the strain gage was required to be applied to the patient's body in a set or fixed state of tension. Usually the strain gage was contained in a bandage or wrap in some manner about the patient's thorax. lf the wrap loosened in any way, however, the readings obtained by the strain gage were no longer accurate. Web site: http://www.delphion.com/details?pn=US04494553__

Patent Applications on Sudden Infant Death Syndrome As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to sudden infant death syndrome: •

Alkylaryl polyether alcohol polymers for treatment and prophylaxis of snoring, sleep apnea, sudden infant death syndrome and for improvement of nasal breathing Inventor(s): Hofmann, Thomas; (Seattle, WA) Correspondence: Hana Verny; Peters, Verny, Jones & Schmitt, Llp; Suite 6; 385 Sherman Avenue; Palo Alto; CA; 94306; US Patent Application Number: 20030053956 Date filed: January 23, 2002 Abstract: A method and composition for treatment and prophylaxis of snoring, sleep apnea or sudden infant death syndrome and for improvement of nasal breathing in mammals by nasal and/or pharyngeal administration of tyloxapol or a related alkylaryl polyether alcohol polymer. A spray, liquid or solid composition comprising from about 0.01 to about 20% (w/v), equivalent to about 100.mu.g/ml to about 200 mg/ml, of tyloxapol or another alkylaryl polyether alcohol polymer alone or in admixture with pharmaceutically acceptable excipients and additives. The composition is administered as a spray, liquid, liquid drops, lozenges or powder suitable for nasal and/or pharyngeal application.

10

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

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Excerpt(s): This application is based on and claims priority of the provisional application Ser. No. 60/264,166 filed on Jan. 24, 2001. The current invention concerns a method and composition for treatment and prophylaxis of snoring, sleep apnea or sudden infant death syndrome and for improvement of nasal breathing in mammals by nasal and/or pharyngeal administration of tyloxapol or a related alkylaryl polyether alcohol polymer. In particular, the present invention provides a spray, liquid or solid composition comprising from about 0.01 to about 20% (w/v), equivalent to about 100.mu.g/ml to about 200 mg/ml, of tyloxapol or another selected alkylaryl polyether alcohol polymer alone, in combination, or in admixture with pharmaceutically acceptable excipients and additives. The composition is administered as a spray, liquid, liquid drops, lozenges or powder suitable for nasal and/or pharyngeal application. Snoring and related sleep apnea are amongst the most troublesome sleeping impairments. Snoring is not only a nuisance for other people, but it has been shown, similarly to sleep apnea, to correlate with increased daytime sleepiness and decreased alertness and work performance. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Computer powered wire(less) ultra-intelligent real-time monitor Inventor(s): Ridley, Alfred Dennis; (Tallahassee, FL) Correspondence: DR. Alfred Dennis Ridley; P.O. Box 12518; Tallahassee; FL; 32317-2518; US Patent Application Number: 20030164762 Date filed: December 2, 2002 Abstract: A device (1)(2) and method to monitor, in real time, one or more variables by an at least 2500 hour water proof sensor/transmitter, not requiring recharge, placed at the source where data are automatically collected and transmitted by wire or wireless means (2A)(2B) to a battery-free computer-powered (2C) receiver connected to a computer, where software continuously analyzes and charts the data. The software auto and cross correlates the variables, continuously updates and displays the data on simple aggregate charts (4A) or decomposes the data and displays them on newly created common cause charts (4B)(4C) of internal systematically related effects and newly created special cause charts (4D)(4E) of external random unrelated effects, including summary data, and creates graduated progressive sound, color, print and world wide, fax, email and telephone alarm signals when the chart values exceed user specified limits, either in terms of actual units (4B)(4D) or standard deviations (4C)(4E), or when any particular pattern occurs. The device helps determine ahead of time, when the source of the monitored variables is functioning abnormally. Advance warning thus obtained, is used to initiate corrective action (3A)(3B)(3C)(3D) so as to prevent failure at the source that is generating the variables. Examples of failure that it helps prevent include but are not limited to, sudden infant death due to sudden infant death syndrome in human babies, heart or respiratory failure in any human being who is either at rest or moving around within a specified area, failure in industrial machines or measuring equipment, manufacturing defects and financial irregularities. Excerpt(s): This application is entitled to the benefit of Provisional Patent Application Ser. No. 60/352,096 filed Jan. 25, 2002. This invention relates to universal electronic data monitoring including their collection, wire or wireless transmission, computer analysis, detection and the classification of abnormalities in the data, where such abnormalities result in automatic alarms that are transmitted to recipients locally or world wide,

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thereby providing a basis for taking corrective action at the source of the data. The prior art U.S. Pat. No. 4,583,524 to Hutchins (1986) shows a instructional system for reviving the victim of a heart attach. U.S. Pat. No. 5,199,439 to Zimmerman et al. (1993) shows the use of a quality control chart for direct and simple monitoring of data. However, the chart is used in a way that is not statistically valid. The reason is as follows. Statistical quality control charts assume that the data on which they are based are independent. That is, each measurement is completely unrelated to all previous measurements. In reality, the measurements are serially related. This is known as autocorrelation. None of these patents employs correlation as part of its analysis. Since correlation analysis is at least one of the requirements to make the charts valid, no valid conclusions can be drawn from the charts that use these patents. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Methods for diagnosing pervasive development disorders, dysautonomia and other neurological conditions Inventor(s): Fallon, Joan M.; (Yonkers, NY) Correspondence: F. Chau & Associates, Llp; Suite 501; 1900 Hempstead Turnpike; East Meadow; NY; 11554; US Patent Application Number: 20020081628 Date filed: November 16, 2001 Abstract: Methods for aiding in the diagnosis of disorders including, but not limited to, PDDs (Pervasive Development Disorders), Dysautonomic disorders, Parkinson's disease and SIDS (Sudden Infant Death Syndrome). In one aspect, a diagnosis method comprises analyzing a stool sample of an individual for the presence of a biological marker (or marker compound) comprising one or more pathogens, which provides an indication of whether the invidual has, or can develop, a disorder including, but not limited to, a PDD, Dysautonomia, Parkinsons disease and SIDS. Preferably, the presence of one or more pathogens is determined using a stool immunoassay to determine the presence of antigens in a stool sample, wherein such antigens are associated with one or more pathogens including, but not limited to, Giardia, Cryptosporidium, E. histolytica, C. difficile, Adenovirus, Rotavirus or H.pylori. Excerpt(s): This application is based on, and claims the benefit of, United States Provisional Application No. 60/249,239, filed on Nov. 16, 2000, which is fully incorporated herein by reference. The present invention generally relates to methods for aiding in the diagnosis of disorders including, but not limited to, PDDs (Pervasive Development Disorders), Dysautonomic disorders, Parkinsons disease and SIDS (Sudden Infant Death Syndrome). More particularly, the invention relates to a diagnosis method comprising analyzing a stool sample of an individual for the presence of a biological marker (or marker compound) comprising one or more pathogens, which provides an indication of whether the invidual has, or can develop, a disorder including, but not limited to, a PDD, a Dysautonomic disorder, Parkinson's disease or SIDS. Currently, extensive research is being conducted to determine associations between gastrointestinal dysfunction and a variety of human disorders that, heretofore, have been of unknown etiology. For example, an association between dysautonomic conditions and gastrointestinal dysfunction has been described in U.S. patent application Ser. No. 09/929,592, filed on Aug. 14, 2001, entitled "Methods For Diagnosing and Treating Dysautonomia and Other Dysautonomic Conditions, which is commonly owned and fully incorporated herein by reference. Further, a relationship

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between gastrointestinal conditions and PDDs such as Autism, ADD (Attention Deficit Disorder) and ADHD (Attention Deficit Hyperactivity Disorder) has been described in detail in U.S. patent application Ser. No. 09/466,559, filed Dec. 17, 1999, entitled "Methods For Treating Pervasive Development Disorders," and U.S. Ser. No. 09/707,395, filed on Nov. 7, 2000, entitled "Methods For Treating Pervasive Development Disorders", both of which are commonly owned and incorporated herein by reference. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Orthomolecular sulpho-adenosylmethionine derivatives with antioxidant properties Inventor(s): Wilburn, Michael D.; (Cedar Hill, TX) Correspondence: Nath & Associates; 1030 15th Street; 6th Floor; Washington; DC; 20005; US Patent Application Number: 20030078231 Date filed: June 22, 2001 Abstract: Orthomolecular Sulpho-Adenosylmethionine derivative compounds, compositions, and their uses for effecting a biological activity in an animal, such as neurochemical activity; liver biology activity; heart and artery function; cartilage, bone and joint health; stomach and/or intestinal lining resistance to ulceration; immune function; cell membrane integrity; and pain and inflammation. The compounds of the present invention are further useful for preventing or treating diseases or conditions; treating viral infections, infectious diseases, leukemia, and obesity; and reducing the risk of Sudden Infant Death Syndrome in an animal. The compounds of the present invention are of formula I: 1A is 0 or N; andX is a reaction product as defined herein. Excerpt(s): The present invention relates to novel compounds and pharmaceutical preparations including the same which are useful in effecting a biological activity in an animal, such as neurochemical activity; liver biology activity; heart and artery function; cartilage, bone and joint health; stomach and/or intestinal lining resistance to ulceration; immune function; cell membrane integrity; and pain and inflammation; in preventing or treating diseases or conditions; in treating viral infections, infectious diseases, leukemia, and obesity; and in reducing the risk of Sudden Infant Death Syndrome. Linus Pauling coined the term "Orthomolecular Medicine" and defined it as: "The preservation of good health and the prevention and treatment of disease by varying the concentrations in the human body of the molecules or substances that are normally present, many of them required for life, such as the vitamins, essential amino acids, essential fats, and minerals." Literally, the term is derived from the Greek "ortho", for correct or right, and "molecule", or "right molecule". When these "right molecules" are out of balance, disorders and disease can result. The Orthomolecular Concomitant Theory of Convergence suggests that the duality of stress and uncontrolled free radical proliferation are major disruptive forces in the delicate balance of life, resulting in disorders, diseases, and premature death. In particular, the free radical theory of aging and disease suggests that excess free radicals can be generated by stress, simple aging, exposure to toxic pollutants in air, water, and foods, as well as cigarette smoke, alcohol, and ionizing radiation. Free radicals may produce oxidative damage to DNA and other cell components which accumulates with age and is suggested to be a major contributor to aging and degenerative diseases. Antioxidants may be used for reducing, eliminating, preventing, and reversing oxidative damage to tissues in an animal. Treatment of disorders and disease by orthomolecular methods is aimed at bringing such natural substances into healthful balance. In a relatively recent phenomenon, traditional

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primary health care practitioners have begun to embrace orthomolecular nutrition as an enhancement to their practices. There are several forces promoting this trend, including consumer demand and the increasing eligibility of alternative health care for medical insurance coverage. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Orthomolecular vitamin E derivatives Inventor(s): Wilburn, Michael D.; (Cedar Hill, TX) Correspondence: Nath & Associates; 1030 15th Street; 6th Floor; Washington; DC; 20005; US Patent Application Number: 20030007961 Date filed: June 22, 2001 Abstract: Orthomolecular Vitamin E derivative compounds, compositions, and their uses for effecting aging and longevity, nerve activity, hematopoiesis and maintenance of blood cells, hepatic activity, nephritic activity, heart and cardiovascular function, pulmonary function, muscular function, cartilage, bone, and joint health, gastrointestinal function, reproductive system function, vision, immune function, cell membrane integrity, and pain and inflammation; preventing or treating diseases or conditions; treating cancers or obesity; and reducing the risk of Sudden Infant Death Syndrome in an animal. The compounds of the present invention are of formula I: 1or a pharmaceutically acceptable salt, ester, or solvate, thereof, wherein:A, B, C, D, and R are as defined herein. Excerpt(s): Linus Pauling coined the term "Orthomolecular Medicine" and defined it as: "The preservation of good health and the prevention and treatment of disease by varying the concentrations in the human body of the molecules or substances that are normally present, many of them required for life, such as the vitamins, essential amino acids, essential fats, and minerals." Literally, the term is derived from the Greek "ortho", for correct or right, and "molecule", or "right molecule". When these "right molecules" are out of balance, disorders and disease can result. The Orthomolecular Concomitant Theory of Convergence suggests that the duality of stress and uncontrolled free radical proliferation are major disruptive forces in the delicate balance of life, resulting in disorders, diseases, and premature death. In particular, the free radical theory of aging and disease suggests that excess free radicals can be generated by simple aging or exposure to toxic pollutants in air, water, and foods, as well as cigarette smoke, alcohol, and ionizing radiation. Free radicals may produce oxidative damage to DNA and other cell components which accumulates with age and is suggested to be a major contributor to aging and degenerative diseases. Antioxidants may be used for reducing, eliminating, preventing, and reversing oxidative damage to tissues in an animal. Treatment of disorders and disease by orthomolecular methods is aimed at bringing such natural substances into healthful balance. In a relatively recent phenomenon, traditional primary health care practitioners have begun to embrace orthomolecular nutrition as an enhancement to their practices. There are several forces promoting this trend, including consumer demand and the increasing eligibility of alternative health care for medical insurance coverage. The National Institutes of Health (NIH) has established the National Center for Complementary and Alternative Medicine (NCCAM) to assist in prioritizing applications for research grants in complementary and alternative medicine (CAM). The NCCAM classification system is divided into seven major categories and includes examples of practices or preparations in each category. The biologically-based therapies

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category includes natural and biologically-based practices, interventions, and products. One subcategory is orthomolecular medicine, which refers to products used as nutritional and food supplements for preventive or therapeutic purposes. The NCCAM classification system lists ascorbic acid, carotenes, tocopherols, folic acid, niacin, niacinamide, pantothenic acid, pyridoxine, riboflavin, thiamine, vitamin A, vitamin D, vitamin K, biotin, choline, s-adenosylmethionine, calcium, magnesium, selenium, potassium, taurine, lysine, tyrosine, gamma-oryzanol, iodine, iron, manganese, molybdenum, boron, silicon, vanadium, co-enzyme Q.sub.10, carnitine, probiotics, glutamine, phenylalanine, glucosamine sulfate, chondroitin sulfate, lipoic acid, amino acids, phosphatidylserine, melatonin, DHEA, inositol, glandular products, fatty acids, and medium chain triglycerides as examples of orthomolecular substances. Other examples of orthomolecular substances include omega-3 fatty acids, lycopene, soy isoflavonoids, tocotrienols, chromium, zinc, and copper. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

PICORNAVIRUSES, VACCINES AND DIAGNOSTIC KITS Inventor(s): NIKLASSON, BO; (STOCKHOLM, SE) Correspondence: James F. Haley, JR., ESQ.; C/o Fish & Neave; 1251 Avenue OF The Americas - 50th Floor; New York; NY; 10020; US Patent Application Number: 20030044960 Date filed: March 11, 1999 Abstract: A new group of picornaviruses is disclosed. The picornaviruses of the invention comprise in the non-coding region of their viral genome a nucleotide sequence which corresponds to cDNA sequence (I) or homologous sequences having at least 75% homology to the SEQ ID NO:1, and they cause mammalian disease. Further aspects of the invention comprise a protein corresponding to a protein of the picornaviruses, antiserum or antibody directed against a protein of the picornaviruses, antigen comprising a protein of the picornaviruses, diagnostic kits, vaccines, use of the picornaviruses in medicaments, particularly for the treatment or prevention of Myocarditis, Cardiomyopathia, Guillain Barr Syndrome, and Diabetes Mellitus, Multiple Sclerosis, Chronic Fatique Syndrome, Myasthenia Gravis, Amyothrophic Lateral Sclerosis, Dermatomyositis, Polymyositis, Spontaneous Abortion, and Sudden Infant Death Syndrome, and methods of treatment of diseases caused by the picornaviruses. 1 SEQ ID NO: 1 (Ljungan 87-012) AGTCTAGTCT TATCTTGTAT GTGTCCTGCA CTGAACTTGT 50 TTCTGTCTCT GGAGTGCTCT ACACTTCAGT AGGGGCTGTA CCCGGGCGGT 100 CCCACTCTTC ACAGGAATCT GCACAGGTGG CTTTCACCTC TGGACAGTGC 150 (I) ATTCCACACC CGCTCCACGG TAGAAGATGA TGTGTGTCTT TGCTTGTGAA 200 AAGCTTGTGA AAATCGTGTG TAGGCGTAGC GGCTACTTGA GTGCCAGCGG 250 ATTACCCCTA GTGGTAACAC TAGC Excerpt(s): The present invention relates to new picornaviruses, proteins expressed by the viruses, antisera and antibodies directed against said viruses, antigens comprising structural proteins of said viruses, diagnostic kits, vaccines, use of said viruses, antisera or antibodies and antigens in medicaments, and methods of treating or preventing diseases caused by said viruses, such as Myocarditis, Cardiomyopathia, Guillain Barr Syndrome, and Diabetes Mellitus, Multiple Sclerosis, Chronic Fatigue Syndrome, Myasthenia Gravis, Amyothrophic Lateral Sclerosis, Dermatomyositis, Polymyositis, Spontaneous Abortion, and Sudden Infant Death Syndrome. Recently, a sudden death

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syndrome among Swedish orienteers has been observed. Of approximately 200 elite orienteers six died in myocarditis during 1989-1992 (1). Orienteering, aiming to find the fastest/shortest way between several checkpoints and often in forested areas, is exceptional with respect to environmental exposure. Thus it has been speculated, that the sudden deaths syndrome among orienteers is caused by a vector borne (rodent or arthropod) infectious agent. It has now been shown in an epidemiological study that the incidence of deaths in myocarditis in northern Sweden tracked the 3-4 year population fluctuations (cycles) of bank voles (Clethrionomys glareolus) with one year time lag. Previously, it has been shown that cardioviruses, with rodents as their natural reservoir, can cause Guillain Barr Syndrome (GBS) in man, Diabetes Mellitus (DM) in mice and myocarditis in several species including non-human primates. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Sleeping pad, bedding and bumpers to improve respiratory efficiency and environmental temperature of an infant and reduce the risks of sudden infant death syndrome (SIDS) and asphyxiation Inventor(s): Koenig, J. Frank; (Vienna, VA) Correspondence: Shlesinger, Arkwright & Garvey Llp; 3000 South Eads Street; Arlington; VA; 22202; US Patent Application Number: 20020178500 Date filed: July 31, 2002 Abstract: Rebreathing carbon dioxide and overheating of the infant are contributing causes of Sudden Infant Death Syndrome (SIDS) and asphyxiation. The characteristics of conventional crib mattresses, bedding and bumper pads contribute to rebreathing of carbon dioxide and overheating of the infant and may be contributing environmental causes of SIDS, asphyxiation, apnea syndromes and hypoventilation. The present invention consists of improved sleeping pads, beddings and bumper pads which reduce rebreathing of carbon dioxide and overheating and provide increased crib ventilation to stimulate breathing. Excerpt(s): This application is a continuation of U.S. application Ser. No. 09/560,139, filed Apr. 28, 2000, which is a continuation-in-part of U.S. application Ser. No. 08/551,319, filed Nov. 1, 1995, and each of which is incorporated herein by reference. The present invention relates to apparatus for reducing the risk of sudden infant death syndrome, asphyxiation, apnea syndrome and hypoventilation through the use of improved sleeping pads, bedding and bumper pads within a crib or the like to improve the respiratory efficiency and environmental temperature of an infant. Sudden infant death syndrome (SIDS) is the leading cause of postneonatal infant death in the United States. About 7,000 deaths occur each year from SIDS. In addition, many infants die each year of asphyxiation while in a crib. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Use of somatostatin receptor agonists in the treatment of human disorders of sleep hypoxia and oxygen deprivation Inventor(s): Young, Charles W.; (New York, NY) Correspondence: Frommer Lawrence & Haug; 745 Fifth Avenue- 10th FL.; New York; NY; 10151; US Patent Application Number: 20030083241 Date filed: October 25, 2002 Abstract: The invention relates to a method of treating diverse human disorders that may arise, in part, out of sleep hypoxia and oxygen deprivation occurring in the context of sleep apnea/hypopnea disturbances. The disorders that may be treated by the invention comprise gastroesophageal reflux disease (GERD), asthma-associated gastroesophageal reflux (GER), GER-associated asthma, asthma, cardiomyopathy, cardioarrhythmia, congestive heart failure, sudden infant death syndrome, and diverse neurologic conditions. The mode of treatment uses somatostatin receptor ligands (SstRLs), particularly somatostatin-receptor agonists. The invention concerns the method of treatment utilizing, and compositions comprising SstRLs and somatostatin receptor agonists, including agonists of the somatostatin receptor types 2 and 5, particularly, the type 2A receptor (SsR-2A), including octreotide and lanreotide. Excerpt(s): The invention relates to a method of using somatostatin receptor agonists to treat diverse human disorders of sleep hypoxia and oxygen deprivation, including but not limited to: 1) gastroesophageal reflux disease (GERD), asthma-associated gastroesophageal reflux (GER), GER-associated asthma, and asthma; 2) obstructive sleep apnea (OSA), and OSA-associated conditions, including GER, asthma, cardiomyopathy, cardioarrhythmia, congestive heart failure, median nerve compression neuropathy (carpal tunnel syndrome) and cognitive impairment; as well as sleep apnea-associated sudden infant death syndrome (SIDS), 3) central sleep apnea (CSA), as well as CSAassociated conditions, including GER, cardiomyopathy, cardioarrhythmia, congestive heart failure, and cognitive impairment; 4) mixed pattern sleep apneas, including but not limited to post-vascular occlusion sleep apnea, dementia-associated sleep apnea, amyotrophic lateral sclerosis-associated sleep apnea, myasthenia gravis-associated sleep apnea, and alcoholism-related sleep apnea; 5) excess calpain-activation disorders in tissues where the injured cell population expresses somatostatin receptors; including, but not limited to the central nervous system, peripheral nerves, heart, liver, kidney, and gastrointestinal tract. Various documents are cited in this text. Citations in the text can be by way of a citation to a document in the reference list, e.g., by way of an author(s) and document year, whereby full citation in the text is to a document that may or may not also be listed in the reference list. There is no admission that any of the various documents cited in this text are prior art as to the present invention. Any document having as an author or inventor person or persons named as an inventor herein is a document that is not by another as to the inventor of entity herein. All documents cited in this text ("herein cited documents") and all documents cited or referenced in herein cited documents are hereby incorporated herein by reference. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Keeping Current In order to stay informed about patents and patent applications dealing with sudden infant death syndrome, 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 “sudden infant death syndrome” (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 sudden infant death syndrome. You can also use this procedure to view pending patent applications concerning sudden infant death syndrome. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 7. SYNDROME

BOOKS ON SUDDEN INFANT DEATH

Overview This chapter provides bibliographic book references relating to sudden infant death syndrome. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on sudden infant death syndrome include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.

Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “sudden infant death syndrome” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on sudden infant death syndrome: •

Sudden Infant Death Syndrome: Trying to Understand the Mystery Source: McLean, VA: National Sudden Infant Death Syndrome Resource Center. February 1994. 56 p. Contact: Available from National SIDS Resource Center, Suite 450, 2070 Chain Bridge Road, Vienna, VA 22182-2536. (703) 821-8955, (703) 821-2098 (Fax), [email protected] (Email), http://www.circsol.com/sids (Website). Free of charge; distribution limited to one per customer. Order No. S106. Summary: Developed as a basic information resource for health professionals, social service personnel, support providers, and families of sudden infant death syndrome (SIDS) infants, this book discusses the basic characteristics of SIDS and its incidence, describes current theories of causation and the research behind them, examines the

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emotional impact of SIDS on families, and describes SIDS research and educational efforts at the Federal level. Chapter 1 provides the definition of SIDS, the most common characteristics of and risk factors for SIDS, the number of SIDS deaths by age for 1988 and 1989, how professionals diagnose SIDS, the importance of autopsies in SIDS cases, and the value of the death certificate. Chapter 2 reviews current theories and research on SIDS in the areas of epidemiology and biomedicine (e.g., fetal predisposition, arousal response, brainstem abnormalities) and on the topics of monitoring, sleep position, and bedding. Chapter 3 examines the impact of SIDS on parents, family, and the community. This chapter covers common grief reactions of parents to the loss of a child; the impact of a SIDS death on siblings, relatives, and child care providers; and the importance of community support for SIDS families. Chapter 4 describes Federal initiatives in SIDS research and services by the National Institute of Child Health and Human Development, the Maternal and Child Health Bureau, the Centers for Disease Control and Prevention, the Food and Drug Administration, the Consumer Product Safety Commission, and other collaborative interagency efforts. Chapter 5 reviews milestones in the history of SIDS dating from 1834 to 1992, including the publication of early medical findings on sudden infant death, the founding of parent and professional organizations, dates of the international SIDS conferences, the passage of significant legislation, and the initiation of major research programs. Appendices include a glossary of terms and a listing of 30 references. •

A Baby Dies a Family Grieves: The Clergy's Response to Sudden Infant Death Syndrome Source: Berkeley, CA: California SIDS Program/CAPHND. June 1991. 16 p. Contact: Available from California Sudden Infant Death Syndrome Program, 5330 Primrose Drive, Suite 231, Fair Oaks, CA 95628-3542. (916) 536-0146, (800) 369-7437 (in CA), (916) 536-0167 (Fax). Free to residents of CA; $1.20 each to residents of other States. Summary: Directed at members of the clergy, this booklet provides basic information about sudden infant death syndrome (SIDS) and discusses the range of emotions families are likely to experience after the sudden loss of an infant. The booklet offers helpful advice to clergy on ways of responding to the family's grief and acknowledging the importance of the baby's life. Clergy can also help the family by explaining the specific religious traditions of the family's faith, helping with funeral arrangements, and providing continuing support to the family after the funeral.

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A Little Friend is Gone: A Book for Kids Dealing With SIDS (Sudden Infant Death Syndrome) Source: Denver, CO: The Colorado SIDS Program, Inc. 1994. 18 p. Contact: Colorado SIDS Program, Inc., 6825 E. Tennessee Avenue, Suite 300, Denver, CO 80224-1631. (303) 320-7771, (800) 332-1018 (in CO), (888) 285-7437 (Nationwide), (303) 322-8775 (Fax). $3.00, postage included. Summary: The goal of this book is to provide day care playmates of sudden infant death syndrome (SIDS) babies with information on SIDS that is geared to their level of understanding and that will help alleviate the fear they may feel following a SIDS death. The book was written for use by day care providers with children who are dealing with a SIDS death. The book tells children how many babies die of SIDS each year; that no one can cause SIDS to happen; that there are many things that SIDS is not (e.g., it is not catching, it cannot be predicted); and that when a baby is found not breathing, it is a very frightening and confusing time. Children are encouraged to talk about the people

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who tried to help the baby and what they did to help, to write down what they remember most about their little friend, to tell the baby's family how they feel about the death, and to send a sympathy card. The first page of the book is a dedication page that children can fill in to dedicate the book to their little day care friend. •

Crib death: Sudden infant death syndrome Source: Rockville, MD: Health Services Administration (DHHS/PHS), Bureau of Community Health Services. 1980. 20 p. Contact: Available from National SIDS Resource Center, Suite 450, 2070 Chain Bridge Road, Vienna, VA 22182-2536. (703) 821-8955, (703) 821- 2098 (Fax), [email protected] (Email), http://www.circsol.com/sids (Web site). Free of charge; distribution limited to one per requestor. Order No. S17, DHHS Publication No. (HSA) 81-5262. Summary: This book provides a very basic description of sudden infant death syndrome (SIDS) in easy-to-understand language. The book presents information on what is known and not known about SIDS, emphasizes that these infants' deaths are no one's fault, explains that everyone will probably react differently to the death, provides suggestions to families for coping with the death, advises parents on how to explain the death to their other children, and reminds parents that no subsequent baby can take the place of the one who died. Printed in large type. The book also is available from the National SIDS Resource Center in Spanish. Chinese, Japanese, Korean, Tagalog, and Vietnamese versions are available from the California SIDS Program, (916) 536-0146.

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Facts and Feelings: Sudden Infant Death Syndrome Source: Sacramento, CA: California SIDS Program. 1990. 16 p. Contact: Available from California Sudden Infant Death Syndrome Program, 5330 Primrose Drive, Suite 231, Fair Oaks, CA 95628-3542. (916) 536- 0146, (800) 369-7437 (in CA), (916) 536-0167 (Fax). Free to residents of CA; $0.78 each for residents of other States. Summary: This booklet is designed especially for families and caregivers who have experienced a sudden infant death syndrome (SIDS) loss. The booklet provides information on what happens in a SIDS death; what causes SIDS; whether anyone is at fault in a SIDS death; whether the baby suffered; whether the baby vomited, choked, or suffocated; whether SIDS is contagious; whether older children can die of SIDS; whether SIDS is caused by DTP shots or child abuse; whether breast feeding helps to prevent SIDS; whether SIDS is hereditary; the feelings experienced by bereaved parents, which are often very different; the effects of the death on surviving siblings; and where families can go to get help and support. The booklet reminds child care providers that they, too, should seek out help and support. Contact information for the California SIDS Program and two national support groups is provided. The booklet also is available in Spanish (MCS000130).

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Helping Children Grieve: Sudden Infant Death Syndrome Source: Sacramento, CA: California SIDS Program. 1993. 8 p. Contact: Available from California Sudden Infant Death Syndrome Program, 5330 Primrose Drive, Suite 231, Fair Oaks, CA 95628-3542. (916) 536-0146, (800) 369-7437 (in CA), (916) 536-0167 (Fax). Free to residents of CA; $0.46 each for residents of other States.

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Summary: This booklet is directed at persons who care for children who have lost a sibling to sudden infant death syndrome (SIDS), including parents, grandparents, childcare providers, clergy, teachers, and other friends and relatives. When a baby dies suddenly with no warning, the whole family must cope with confusing emotions. Surviving siblings need a way to express their feelings, they need help and support, and they need to feel loved and valued. The booklet discusses the types of emotions that children may feel while grieving for an infant sibling who has died, including fear, anger, guilt, and sadness. The booklet also discusses when parents or others should worry about a child's reactions to the death; the importance of everyone talking about the death; what one should and should not say about where the baby went; siblings' participation in the funeral; ways in which siblings can remember the brother or sister who died; and how the level of understanding of death differs with a child's age. The booklet also is available in Spanish (MCS000481). •

Sudden infant death syndrome: A guide for child care providers. Revised edition Source: Salt Lake City, UT: Utah Department of Health. December 1997. 10 p. Contact: Available from Utah Department of Health, Division of Community and Family Health Services, Sudden Infant Death Program, 288 North 1460 West, P.O. Box 142001, Salt Lake City, UT 84114-2001. (801) 538-9970, (800) 826-9662 (UT Baby Hotline), (801) 538-9409 (Fax), [email protected] (E-mail), http://161.119.100.19/ (Web site). Summary: This booklet is intended to help child care providers understand sudden infant death syndrome (SIDS), know what to do in an emergency situation, and know what to do if an infant dies of SIDS while in their care. The following topics are covered: the definition of SIDS; what SIDS is and is not; what causes SIDS; who is at risk for SIDS; what child care providers can do to reduce the risk of SIDS occurring; standards for safe cribs and bedding; the danger of letting an infant sleep on a sofa, waterbed, adult bed, or youth bed; what to do if an infant or child is found not breathing; what to expect if an infant dies and a death investigation is initiated; how to talk to the parents about what happened; emotions that parents are likely to experience after a SIDS death; how to explain the death to other children in the home; common expressions of children's grief; and the ways in which grief may manifest itself in child care workers. The booklet includes a personal narrative written by a child care provider who experienced a SIDS death and a list of emergency numbers for providers in the Salt Lake City, Utah, area.

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Sudden Infant Death Syndrome: Some Facts You Should Know Source: McLean, VA: National Sudden Infant Death Syndrome Resource Center. May 1994. 11 p. Contact: Available from National SIDS Resource Center, Suite 450, 2070 Chain Bridge Road, Vienna, VA 22182-2536. (703) 821-8955, (703) 821-2098 (Fax), [email protected] (Email), http://www.circsol.com/sids (Website). Free of charge; distribution limited to one per customer. Order No. S110. Summary: This booklet provides a brief overview of the facts known to date concerning the causes, characteristics, and consequences of sudden infant death syndrome (SIDS). The booklet covers the following topics: what SIDS is and is not; why finding a cause for SIDS is so problematic; the importance of autopsies in SIDS cases; the infants who are at greatest risk for SIDS; the known risk factors for SIDS; the number of infants who die of SIDS each year; common parental reactions to the sudden, unexpected death of an infant; the effects of a SIDS death on siblings, relatives, and other caregivers; and where

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SIDS families can find peer support. Contact information is given for three organizations that provide SIDS families with information and support. •

Sudden Infant Death Syndrome: Information, Services and Support Source: Rancho Cordova, CA: California SIDS Program. 1999. 9 p. Contact: Available from California SIDS Program, 3164 Gold Camp, Suite 220, Rancho Cordova, CA 95670. (916) 463-0146, (800) 369-7437 (in CA), (916) 463-0167 (Fax), [email protected] (E-mail), http://www.californiasids.com (Web Site). Free to CA residents; $0.50 each plus shipping and handling for residents of other states. Summary: This booklet provides basic information on sudden infant death syndrome (SIDS) and a description of the services the California SIDS Program offers to the residents of that state. The mission of the California SIDS Program is to help reduce the emotional suffering of SIDS families and caregivers, improve the knowledge and skills of people who interact with SIDS families, increase public awareness and knowledge of SIDS, collect and monitor data on SIDS, and encourage medical research. Through its toll-free information line the program provides California residents crisis intervention resources; assistance in identifying local resources for grief counseling and other support services; and referrals to local public health professionals, parent support groups, and trained peer counselors. The California SIDS Program also produces a wide array of educational materials in English and Spanish that are free to all residents and that can be purchased by out-of-state residents for a minimal amount of money. Program staff members conduct training sessions throughout the state for a wide variety of professionals, including emergency department personnel, public health nurses, coroners, medical examiners, pathologists, childcare workers, foster parents, and mortuary professionals. Training sessions also are available to SIDS parents and others who are interested in volunteering as peer counselors and support group facilitators. The program also maintains a roster of speakers for presentations on SIDS within the community, publishes a semi-annual newsletter, and coordinates a conference each October.

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Sudden Infant Death Syndrome (SIDS): What Childcare Providers Should Know. Revised Edition Source: Seattle, WA: SIDS Foundation of Washington. 1996. 4 p. Contact: Available from SIDS Foundation of Washington, 4649 Sunnyside Avenue N., Room 328, Seattle, WA 98103. (206) 548-9290 (Seattle), (509) 456-0505 (Spokane), (800) 533-0376 (WA, ID, OR), (206) 548-9445 (Fax), sids- [email protected] (Email). Summary: This booklet provides child care providers with information about sudden infant death syndrome (SIDS). The booklet covers the following topics: facts about the incidence of SIDS in Washington State; the investigative process that the law requires after every unexplained infant death and questions that investigators will probably ask the provider; some basic facts about SIDS that child care providers should know; causes of death that are not the cause of SIDS (e.g., a contagious illness, choking, suffocation, child abuse); emotions the child care provider may feel after experiencing a SIDS death; how parents may react to the death and to the provider; and how to explain the death to the other children in the child care group. The booklet stresses that there is currently no detection, treatment, or prevention for SIDS and that no one is to blame for a SIDS death. The booklet includes emergency procedures the provider should follow in a suspected SIDS case, a form for recording emergency telephone numbers, and contact information for State chapters of the SIDS Foundation of Washington.

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Sudden Infant Death Syndrome: Role of the Clergy. Revised Edition Source: Seattle, WA: National Sudden Infant Death Syndrome Foundation. 1989. 4 p. Contact: Available from SIDS Foundation of Washington, 4649 Sunnyside Avenue N., Room 328, Seattle, WA 98103. (206) 548-9290 (Seattle), (509) 456-0505 (Spokane), (800) 533-0376 (WA, ID, OR only), (206) 548-9445 (Fax), sids- [email protected] (Email), http://www.zipcon.net/sids-wa (Website). $0.21 each plus shipping and handling. Summary: This booklet provides information to clergy to prepare them for comforting bereaved parents after an infant dies from sudden infant death syndrome (SIDS). The booklet includes a list of facts about SIDS; legal measures that should be taken to help the parents cope effectively with the loss (i.e., conduct a thorough autopsy, use the term 'SIDS' on the death certificate rather than terms that may imply neglect, notify parents of the autopsy findings, offer parents information and counseling about SIDS); and measures that the clergy can take to help the family cope with the loss. These measures are as follows: to be in touch with one's own feelings about death, to convince the family of the blamelessness of SIDS, to act as a family advocate, to make effective use of ritual and ceremony, to provide the family with long-term support, and to make use of available resources. Ten suggested readings are listed.

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What every child-care provider should know about sudden infant death Syndrome Source: St. Louis, MO: Sudden Infant Death Syndrome Resources, Inc. 1993. 6 p. Contact: Available from Sudden Infant Death Syndrome Resources, Inc., 143 Grand Avenue, St. Louis, MO 63122. (314) 822-2323, (800) 421-3511 (Nationwide), (314) 8222098 (Fax), [email protected] (E-mail), http://www.crn.org/sids (Web site). Copies up to 100 are free of charge; $10.00 shipping and handling is charged for each group of 100 copies. Summary: This booklet, part of the SIDS Building Blocks Program, presents information on sudden infant death syndrome for child care providers. The booklet lists the services that Sudden Infant Death Syndrome Resources, Inc., in St. Louis, Missouri, provides to families, caregivers, and professionals who have experienced a SIDS death; describes the emergency procedures that child care providers should follow if they find an infant unresponsive; provides basic facts about SIDS; discusses causes of death (i.e., contagious illness, child abuse, choking) that are not related to SIDS; describes infant care practices that child care providers should adopt to reduce the risk for SIDS (e.g., nonsmoking environment, back sleep position, use of a safe crib and bedding); describes the reactions that providers are likely to experience after a SIDS death; and outlines the ways in which Sudden Infant Death Syndrome Resources, Inc., can help providers survive a SIDS death.

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 “sudden infant death syndrome” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “sudden infant death

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syndrome” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “sudden infant death syndrome” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

Babies sleep safest on their backs a resource kit for reducing the risk of Sudden Infant Death Syndrome (SIDS) in African American communities (SuDoc HE 20.9202:B 11/KIT) by U.S. Dept of Health and Human Services; ISBN: B000114N2Y; http://www.amazon.com/exec/obidos/ASIN/B000114N2Y/icongroupinterna

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Back to sleep : reduce the risk of sudden infant death syndrome (SIDS) (SuDoc HE 20.2:SL 2/998) by U.S. Dept of Health and Human Services; ISBN: B00010YVUO; http://www.amazon.com/exec/obidos/ASIN/B00010YVUO/icongroupinterna

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Control of Breathing During Development: Apnea of the Newborn and Sudden Infant Death Syndrome: Colloquium Nancy-Pone-A-Mousson, France September 7 by Charlotte Catz, et al (1994); ISBN: 3805559755; http://www.amazon.com/exec/obidos/ASIN/3805559755/icongroupinterna

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Cot Deaths: Coping with Sudden Infant Death Syndrome (Survival Handbooks) by Jacquelynn Luben; ISBN: 0719912644; http://www.amazon.com/exec/obidos/ASIN/0719912644/icongroupinterna

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Crib Death: The Sudden Infant Death Syndrome by Warren G. Guntheroth; ISBN: 0879936185; http://www.amazon.com/exec/obidos/ASIN/0879936185/icongroupinterna

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From cells to selves : targeting Sudden Infant Death Syndrome (SIDS) : a strategic plan (SuDoc HE 20.3352:SU 2/2) by U.S. Dept of Health and Human Services; ISBN: B0001154V8; http://www.amazon.com/exec/obidos/ASIN/B0001154V8/icongroupinterna

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Histopathology for the Sudden Infant Death Syndrome by Valdes-Daperna, ValdezDepena (1993); ISBN: 1881041050; http://www.amazon.com/exec/obidos/ASIN/1881041050/icongroupinterna

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Mothers Bereaved by Stillbirth, Neonatal Death or Sudden Infant Death Syndrome by M.Frances Boyle; ISBN: 1859721494; http://www.amazon.com/exec/obidos/ASIN/1859721494/icongroupinterna

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Pludselig spµdbarnsd²d i Norden : resultater fra det nordiske studie 1990-1996 af pludselig og uforklarlig spµdbarnsd²d krybbed²d/vugged²d = Sudden infant death in the Nordic countries : results of the Nordic study of sudden infant death syndrome, 1990-1996; ISBN: 9289301163; http://www.amazon.com/exec/obidos/ASIN/9289301163/icongroupinterna

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Proceedings of the Second Sudden Infant Death Syndrome Family International Conference: Sids - What Does the Future Hold? by C. McMillan (Editor); ISBN: 0916859525; http://www.amazon.com/exec/obidos/ASIN/0916859525/icongroupinterna

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Sids: A Parent's Guide to Understanding and Preventing Sudden Infant Death Syndrome by William Sears; ISBN: 0316779539; http://www.amazon.com/exec/obidos/ASIN/0316779539/icongroupinterna

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Sudden Infant Death Syndrome (1988); ISBN: 3805548923; http://www.amazon.com/exec/obidos/ASIN/3805548923/icongroupinterna

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Sudden Infant Death Syndrome by Tyson J. Tildon, et al; ISBN: 0126910502; http://www.amazon.com/exec/obidos/ASIN/0126910502/icongroupinterna

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Sudden Infant Death Syndrome by Byard & Krous; ISBN: 0412800004; http://www.amazon.com/exec/obidos/ASIN/0412800004/icongroupinterna

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Sudden Infant Death Syndrome by Jan Culbertson, et al; ISBN: 034049381X; http://www.amazon.com/exec/obidos/ASIN/034049381X/icongroupinterna

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Sudden Infant Death Syndrome (Clinical Series) by Robert D. Walker; ISBN: 0850841402; http://www.amazon.com/exec/obidos/ASIN/0850841402/icongroupinterna

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Sudden Infant Death Syndrome (SIDS) infant death programs : centers : National Sudden Infant Death Syndrome/Infant Death Program Support Center, National Center for Cultural Competence, National Sudden Infant Death Syndrome Resource Center (SuDoc HE 20.9202:IN 3/2) by U.S. Dept of Health and Human Services; ISBN: B000113QYU; http://www.amazon.com/exec/obidos/ASIN/B000113QYU/icongroupinterna

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Sudden Infant Death Syndrome (Sids: Report of the Expert Working Group) by Paul Turner; ISBN: 0113213905; http://www.amazon.com/exec/obidos/ASIN/0113213905/icongroupinterna

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Sudden Infant Death Syndrome: Journal: Pediatrician by Torleiv Rognum (Editor) (1995); ISBN: 8200224198; http://www.amazon.com/exec/obidos/ASIN/8200224198/icongroupinterna

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Sudden Infant Death Syndrome: Medical Aspects and Psychological Management (John Hopkins Series in Contemporary Medicine and Public Health) by Jan L. Culbertson (Editor), et al; ISBN: 0801836794; http://www.amazon.com/exec/obidos/ASIN/0801836794/icongroupinterna

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Sudden Infant Death Syndrome: Problems, Progress and Possibilities by Roger W., MD Byard (Editor), Henry F., MD Krous (Editor) (2001); ISBN: 0340759178; http://www.amazon.com/exec/obidos/ASIN/0340759178/icongroupinterna

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Sudden Infant Death Syndrome: Proceedings. by 2D, sea International Conference on Causes of Sudden Death in Infants; ISBN: 0295950870; http://www.amazon.com/exec/obidos/ASIN/0295950870/icongroupinterna

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Sudden Infant Death Syndrome: Risk Factors and Basic Mechanisms by Ronald M. Harper, Howard J. Hoffman (Editor); ISBN: 0893352489; http://www.amazon.com/exec/obidos/ASIN/0893352489/icongroupinterna

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Sudden Infant Death Syndrome: The Possible Role of "the Fear Paralysis Reflex" by Birger Kaada (Editor), et al; ISBN: 8200182045; http://www.amazon.com/exec/obidos/ASIN/8200182045/icongroupinterna

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Sudden Infant Death Syndrome: Who Can Help and How by Charles Corr (Editor), et al (1991); ISBN: 0826167209; http://www.amazon.com/exec/obidos/ASIN/0826167209/icongroupinterna

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The "Discovery" of Sudden Infant Death Syndrome : Lessons in the Practice of Political Medicine by Abraham B. Bergman (Author) (1986); ISBN: 0275920593; http://www.amazon.com/exec/obidos/ASIN/0275920593/icongroupinterna

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The 2002 Official Patient's Sourcebook on Sudden Infant Death Syndrome by James N. Parker (Editor), Philip M. Parker (Editor) (2002); ISBN: 0597832072; http://www.amazon.com/exec/obidos/ASIN/0597832072/icongroupinterna

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The Best-Kept Secret to Raising a Healthy Child.and the Possible Prevention of Sudden Infant Death Syndrome (SIDS) by Dr. Craig Wehrenberg, Dr. Tracey Mulhall-

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Wehrenberg; ISBN: 0615114857; http://www.amazon.com/exec/obidos/ASIN/0615114857/icongroupinterna •

The Sudden infant death syndrome : cardiac and respiratory mechanisms and interventions; ISBN: 0897664639; http://www.amazon.com/exec/obidos/ASIN/0897664639/icongroupinterna

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The Sudden Infant Death Syndrome: Cardiac and Respiratory Mechanisms and Interventions (Annals of the New York Academy of Sciences, Vol 533) by Peter J. Schwartz, David P. Southall (1988); ISBN: 0897664620; http://www.amazon.com/exec/obidos/ASIN/0897664620/icongroupinterna

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Urea and Non-Protein Nitrogen Metabolism in Infants: With Special Reference to the Sudden Infant Death Syndrome (Sids (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1087) by Mary George (2001); ISBN: 9155451411; http://www.amazon.com/exec/obidos/ASIN/9155451411/icongroupinterna

The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “sudden infant death syndrome” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •

Development of upper respiratory anatomy and function: implications for sudden infant death syndrome Author: Bosma, James F.; Year: 1974; Washington: For sale by the Supt. of Docs., U. S. Govt. Print. Off., 1975

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Magnitude of sudden infant death syndrome in Hawaii Author: Burch, Thomas A.,; Year: 1972; Honolulu: Research and Statistics Office, Dept. of Health, State of Hawaii, 1976

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Research Planning Workshop on the Sudden Infant Death Syndrome, August 16, 1971, Bethesda, Maryland Author: Hasselmeyer, Eileen G.; Year: 1974; [Bethesda, Md.: U. S. Dept. of Health, Education, and Welfare, Public Health Service, National Institutes of Health], 1971

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Sudden infant death syndrome: an annotated bibliography for the layman Author: Archuleta, Michael J.; Year: 1972; San Diego, Calif.: Current Bibliography Series, c1975

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Sudden infant death syndrome. Hearing. Ninety-third Congress, first session on H. R. 9585 and H. J. Res. 8. August 2, 1973. Author: United States. Congress. House. Committee on Interstate and Foreign Commerce. Subcommittee on Public Health and Environment.; Year: 1971; Washington, U. S. Govt. Print. Off., 1974

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

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Sudden infant death syndrome; proceedings. Edited by Abraham B. Bergman, J. Bruce Beckwith [and] C. George Ray. Technical editor: Mary D. Keiter. Author: Beckwith, J. Bruce,; Year: 1970; Seattle, Univ. of Washington [c1970]

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Sudden infant death syndrome; selected annotated bibliography, 1960-1971. Author: National Institute of Child Health and Human Development (U.S.). Scientific Publications Section.; Year: 1972; [Bethesda, Md., For sale by the Supt. of Docs., U. S. Govt. Print. Off., Washington, 1972]

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The sudden infant death syndrome. Author: Beckwith, J. Bruce,; Year: 1973; Chicago, Year Book Medical Publishers [c1973]; ISBN: 0815199058 http://www.amazon.com/exec/obidos/ASIN/0815199058/icongroupinterna

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Voluntary family planning services, population research, and sudden infant death syndrome amendments of 1978: report of the Committee on Human Resources, United States Senate, to accompany S. 2522. Author: United States. Congress. Senate. Committee on Human Resources.; Year: 1972; Washington: U. S. Govt. Print. Off., 1978

Chapters on Sudden Infant Death Syndrome In order to find chapters that specifically relate to sudden infant death syndrome, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and sudden infant death syndrome using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “sudden infant death syndrome” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on sudden infant death syndrome: •

Existing Resources Source: in Corr, C.A., Fuller, H., Barnickol, C.A., Corr, D.M. Sudden Infant Death Syndrome: Who Can Help and How. New York: Springer Publishing Co. 1991. 218-239 p. Contact: Available from Springer Publishing Co., 536 Broadway, New York, NY 100123955. (212) 431-4370, (212) 941-7842 (Fax), [email protected] (Email), http://www.libertyweb.com/springer.html (Website). $34.95 plus $4.00 shipping and handling. ISBN 0-8261-6720-9. Summary: This chapter identifies and describes organizations and resources that offer support to families of sudden infant death syndrome (SIDS) victims and training to professionals who come in contact with them. The organizations include those that are devoted to SIDS families and those that support bereaved families no matter how their children died. Print resources are divided into the following categories: SIDS-related literature for scientists and researchers; SIDS-related books for general readers; miscarriage, stillbirth, and neonatal death; parental bereavement; loss, grief, and mourning; and children, adolescents, and death. The audiovisual resources, mainly videotapes, include general introductions to SIDS; videos for training first responders; videos that show parents' reactions to a SIDS death and what they need to cope; and audiovisuals for helping professionals who work with SIDS families. The final section of the chapter summarizes 12 videos appropriate for parents and siblings who have experienced perinatal loss and for the professionals who work with them. Availability

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information for audiotapes and videotapes from four national conferences on SIDS and other fetal/infant death is included.

Directories In addition to the references and resources discussed earlier in this chapter, a number of directories relating to sudden infant death syndrome have been published that consolidate information across various sources. The Combined Health Information Database lists the following, which you may wish to consult in your local medical library:12 •

Pediatric resource guide Source: New York, NY: Pfizer Pediatric Health. 1998. 29 pp. Contact: Available from Pfizer, Inc, 235 East 42nd Street, New York, NY 10017-5755. Summary: Produced in conjunction with Physician's Desk Reference, this booklet is designed to assist physicians in directing patients with special needs to suitable information sources and support groups. It includes contact information and descriptions for support groups in the following categories: advocacy; breastfeeding; child care; children with special needs; injury prevention and safety; maternal and child health information; mental health; multiple births; nutrition; parenting; physical activity; special issues; and sudden infant death syndrome.

•

Directory of Illinois bereavement support groups (for families who have experienced sudden, unexpected infant death). Revised edition Source: Springfield, IL: Illinois Department of Public Health. June 1996. 12 p. Contact: Available from Illinois Department of Public Health, Division of Health Assessment and Screening, Statewide SIDS/Infant Mortality Program, 535 West Jefferson Street, Springfield, IL 62761. (217) 557- 2931, (217) 524-2831 (Fax). Single copies free of charge. Summary: The Illinois Statewide Sudden Infant Death Syndrome (SIDS) Program provides professional counseling services not only to SIDS families but to any family experiencing a sudden, unexpected infant death. In addition to receiving professional counseling, many families also are interested in talking with parents who have suffered a similar loss. This directory was compiled so that families experiencing a sudden, unexpected infant death or a SIDS death could locate a support group in which they might be interested. Although some counties in the state do not have a support group, this directory will help identify the support group most geographically accessible to a particular family. The support groups are organized by county. Each listing includes the name of the support group; the name of a contact person; a telephone number; and for most listings, meeting locations, days, and times. The support groups listed are sponsored by the following: the Statewide SIDS Program; various bereavement organizations, including the SIDS Alliance of Illinois, Inc., SHARE, The Compassionate

12

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

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Friends, Healing Our Lost Dreams, Bereaved Parents of the USA, and Bereavement Services/RTS; and numerous hospitals, medical centers, and churches.

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CHAPTER 8. MULTIMEDIA ON SUDDEN INFANT DEATH SYNDROME Overview In this chapter, we show you how to keep current on multimedia sources of information on sudden infant death syndrome. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.

Video Recordings An excellent source of multimedia information on sudden infant death syndrome is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “sudden infant death syndrome” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “sudden infant death syndrome” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on sudden infant death syndrome: •

A Critical Call: A Videotape About Sudden Infant Death Syndrome for Emergency Medical Technicians Source: Minneapolis, MN: Minnesota Sudden Infant Death Center. 1989. Contact: Available from Minnesota Sudden Infant Death Center, Minneapolis Children's Self Care, 2525 Chicago Avenue South, Minneapolis, MN 55404. (612) 813-6285, (800) 732-3812 (in MN), (612) 813-7344 (Fax). $100.00. Summary: An emergency medical technician (EMT) may be the first person to receive a call that a baby has died. This 21-minute videotape outlines what EMTs should do in response to a sudden infant death syndrome (SIDS) death. The video addresses transporting the victim, making skilled observations while at the scene, and documenting what was observed and done at the scene. The video also illustrates the types of emotional displays the EMT may encounter at the scene and how they should

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be handled. For example, acute grief reactions may affect the family's or caregiver's ability to reason and act. Information also is provided on critical incident stress and how EMTs can overcome it, the roles of physician and medical examiner in a SIDS case, and the differences in responding to infant death in the home or in a child care facility. An instructor's guide accompanies the video. The guide provides basic information about SIDS, reviews the EMT's role in potential SIDS cases, and provides sample case studies to promote discussion among class participants. [Note: This video predates the 1992 announcement by the American Academy of Pediatrics regarding prone sleep position and the 'Back to Sleep' campaign and, therefore, does not discuss the importance of back or side sleep in reducing the risk for SIDS]. •

Back to Sleep. Sudden Infant Death Syndrome: A Video on Helping to Reduce the Risk Source: Bethesda, MD: National Institute of Child Health and Human Development (NIH). 1994. Contact: Available from Back to Sleep, P.O. Box 29111, Washington, DC 20040. (800) 505CRIB. Free of charge. Summary: This videorecording, a product of the national 'Back to Sleep' campaign in the United States, presents parents and child care providers with information on reducing the risk for sudden infant death syndrome (SIDS). The 'Back to Sleep' campaign was initiated in June 1994 to alert new parents and health professionals to sleeping position as a possible risk factor for SIDS. The video also is available in Spanish (MCS000503).

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

After our baby died [motion picture]: a film on sudden infant death syndrome Source: U. S. Bureau of Community Health Services; produced by Peter Rosen Productions; Year: 1975; Format: Motion picture; [Rockville, Md.]: U. S. Department of Health, Education, and Welfare, Public Health Service, Health Services Administration, Bureau of Community Health Services; [Atlanta: for loan by National Medical Audiovisual Center; Washington: forsale by the National Audiovisual Center, 1975]

•

Crib death [sound recording]: a sudden infant death syndrome, a documentary Source: Center for Death Education & Research, University of Minnesota; Year: 1972; Format: Sound recording; Minneapolis: The Center; [Bowie, Md.: for sale by Robert J. Brady Co.], p1972

•

Sudden infant death syndrome [sound recording] Source: ACEP/EDNA, Illinois Chapters; produced by Teach'em; Year: 1976; Format: Sound recording; [Chicago]: The Chapters: [for sale by Teach'em], 1976

•

Sudden infant death syndrome [sound recording]. Year: 1985; Format: Sound recording; Arvada, CO: Contemporary Learning, c1985

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•

Sudden infant death syndrome [videorecording]: apnea, sleep studies and monitoring, when and why Source: presented by the Department of Pediatrics, Emory University, School of Medicine; Year: 1983; Format: Videorecording; Atlanta, Ga.: Emory Medical Television Network, 1983

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CHAPTER 9. PERIODICALS AND NEWS ON SUDDEN INFANT DEATH SYNDROME Overview In this chapter, we suggest a number of news sources and present various periodicals that cover sudden infant death syndrome.

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

Stomach bug linked to sudden infant death syndrome Source: Reuters Health eLine Date: October 24, 2000

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•

H. pylori may be implicated in sudden infant death syndrome Source: Reuters Medical News Date: October 23, 2000

•

Pneumocystis carinii infection linked to sudden infant death syndrome Source: Reuters Medical News Date: January 11, 2000

•

Genetic mutation linked to sudden infant death syndrome Source: Reuters Medical News Date: July 02, 1999

•

Sudden infant death syndrome linked to facial structure Source: Reuters Medical News Date: July 30, 1998 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 “sudden infant death syndrome” (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 “sudden infant death syndrome” (or synonyms). If you know the name of a company that is relevant to sudden infant death syndrome, you can go to any stock trading Web site (such as

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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 “sudden infant death syndrome” (or synonyms).

Newsletters on Sudden Infant Death Syndrome Find newsletters on sudden infant death syndrome using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “sudden infant death syndrome.” Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter.” Type “sudden infant death syndrome” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: •

Back to Sleep: A Newsletter of the Department of Human Resources Sudden Infant Death Syndrome Workgroup Source: Atlanta, GA: Georgia State Dept. of Human Resources. March 1995-. 4 p. Contact: Available from Georgia State Department of Human Resources, Division of Public Health, Family Health Branch/Center for Family Resource Planning and Development, 2600 Skyland Drive, NE, Upper Level, Room 5, Atlanta, GA 30319. (404) 679-0531, (404) 679-0695 TTD, (404) 679-0686 (Fax), [email protected] (Email), http://www.ph.dhr.state.ga.us (Website). Free of charge. Summary: This newsletter is published by the Georgia Department of Human Resources for the benefit of sudden infant death syndrome (SIDS) service providers, administrators, policy makers, and families in the State of Georgia. The newsletter provides its audience with current information on SIDS research and risk factors; updates on State and national initiatives to reduce the risk for SIDS; contact information for organizations, workshops, and other sources of family bereavement support; and up-to-date resources (including the Internet) on SIDS and infant mortality.

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

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•

The Loss of a Multiple to SIDS Source: Our Newsletter. 5(4): 10-11. December 1991. Contact: Available from Center for Loss in Multiple Birth, Inc. (CLIMB), c/o Jean Kollantai, P.O. Box 1064, Palmer, AK 99645. (907) 746-6123 (9 am-1 pm), (907) 274-7029 (Lisa Fleischer). Summary: This newsletter article consists of personal reflections excerpted from the journal of a mother who lost one of her twin daughters to sudden infant death syndrome (SIDS). The article covers a time period of almost 3 years, from the time the author discovered she was pregnant with twins, through the loss of one of the twins, and to the subsequent birth of another child.

Academic Periodicals covering Sudden Infant Death Syndrome Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to sudden infant death syndrome. In addition to these sources, you can search for articles covering sudden infant death syndrome 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 Institute13: •

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

13

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

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•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

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

•

National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm

•

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

•

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

•

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

•

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

•

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

•

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

•

Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm

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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.14 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:15 •

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

•

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

•

NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html

•

Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/

•

Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html

•

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

•

Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/

•

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

•

Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html

•

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

•

MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html

14 Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 15 See http://www.nlm.nih.gov/databases/databases.html.

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•

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

•

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

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

Targeting sudden infant death syndrome (SIDS): A strategic plan Source: Bethesda, MD: National Institute of Child Health and Human Development. 2001. 24 pp. Contact: Available from National Institute of Child Health and Human Development Clearinghouse, P.O. Box 3006, Rockville, MD 20847. Telephone: (800) 370-2943 TTY: (888) 320-6942 / fax: (301) 984-1473 / e-mail: [email protected] / Web site: http://www.nichd.nih.gov/publications/info.htm. Available at no charge; also available from the Web site at no charge. Summary: This report describes a SIDS strategic plan aimed at improving maternal and infant health and at providing researchers with the knowledge and resources needed to illuminate the etiology of SIDS, and, ultimately, eliminate infant death from SIDS. The plan is divided into four sections: (1) etiology and pathogenesis; (2) prognostics and diagnostics; (3) preventive strategies; and (4) health disparities. Each section contains a statement of the problem, background information, and specific recommendations designed to address gaps in the current state of knowledge or intervention activities and to correct deficiencies in the basic scientific infrastructure. The appendix concludes the report with a roster of advisor members of the SIDS strategic plan working group.

•

Nationwide survey of sudden infant death syndrome (SIDS) services: Executive summary Source: [Rochester, NY: School of Medicine and Dentistry, University of Rochester]. 1994. 13 pp. Contact: Available from Librarian, National Center for Education in Maternal and Child Health, 2000 15th Street, North, Suite 701, Arlington, VA 22201-2617. Telephone: (703) 524-7802 / fax: (703) 524- 9335 / e-mail: [email protected] / Web site: http://www.ncemch.org. Photocopy available at no charge. Summary: This report responded to a Congressional mandate to determine the availability and utilization of SIDS support systems. The intended audiences are health care providers, community service providers, and public officials. The report organizes

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survey results by service component: SIDS diagnosis and reporting, availability of SIDS services, and obstacles to availability and utilization of SIDS services. The report concludes with general and specific recommendations for further research and action. [Funded by the Maternal and Child Health Bureau].

The NLM Gateway16 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.17 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “sudden infant death syndrome” (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 5751 181 915 11 4 6862

HSTAT18 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.19 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.20 Simply search by “sudden infant death syndrome” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

16

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

17

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). 18 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 19 20

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 Biologists21 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.22 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.23 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.

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

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

•

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

The Genome Project and Sudden Infant Death Syndrome In the following section, we will discuss databases and references which relate to the Genome Project and sudden infant death syndrome. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).24 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. 21 Adapted 22

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. 23 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process. 24 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.

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To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “sudden infant death syndrome” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for sudden infant death syndrome: •

Sudden Infant Death Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?272120 Genes and Disease (NCBI - Map)

The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then

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select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “sudden infant death syndrome” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database25 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database26 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “sudden infant death syndrome” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).

25 Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 26 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.

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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 sudden infant death syndrome 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 sudden infant death syndrome. 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 sudden infant death syndrome. 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 “sudden infant death syndrome”:

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Guides on sudden infant death syndrome Sudden Infant Death Syndrome http://www.nlm.nih.gov/medlineplus/suddeninfantdeathsyndrome.html

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Other guides African American Health http://www.nlm.nih.gov/medlineplus/africanamericanhealth.html Heart Diseases http://www.nlm.nih.gov/medlineplus/heartdiseases.html Infant and Newborn Care http://www.nlm.nih.gov/medlineplus/infantandnewborncare.html Infant and Toddler Health http://www.nlm.nih.gov/medlineplus/infantandtoddlerhealth.html

Within the health topic page dedicated to sudden infant death syndrome, the following was listed: •

General/Overviews JAMA Patient Page: Sudden Infant Death Syndrome Source: American Medical Association http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZ1I7HB09D&s ub_cat=2001 Questions & Answers on Sudden Infant Death Syndrome (SIDS) Source: Sudden Infant Death Syndrome Alliance http://www.sidsalliance.org/documents/Q_and_A.asp Rock-a-bye Baby. on Their Backs Source: American Medical Association http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZZNDKTIAC &sub_cat=14 SIDS: Sudden and Silent Source: Nemours Foundation http://kidshealth.org/parent/general/sleep/sids.html What is SIDS? Source: National Sudden Infant Death Syndrome Resource Center http://www.sidscenter.org/SIDSFACT.HTM

•

Coping After Sudden Infant Death Syndrome: Facing Anniversaries, Holidays, and Special Events Source: National Sudden Infant Death Syndrome Resource Center http://www.sidscenter.org/FACING.HTM Friends and Relatives: Some Suggestions on How to Help Source: Sudden Infant Death Syndrome Alliance http://www.sidsalliance.org/Documents/Support/Friends_Relatives.asp

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If Your Baby Has Died of SIDS. Source: Sudden Infant Death Syndrome Alliance http://www.sidsalliance.org/Documents/Support/Baby_has_Died_from_SIDS.asp •

Specific Conditions/Aspects Protecting America's Infants - Safe Sleep Practices and the Hazards of the Adult Bed Source: Sudden Infant Death Syndrome Alliance http://www.sidsalliance.org/index/protectamerica.html Safe Sleep for My Grandbaby http://sids-id-psc.org/_documents/pdf/grandparents.pdf Sudden Infant Death Syndrome (SIDS) and Vaccination Source: National Immunization Program http://www.cdc.gov/nip/vacsafe/concerns/SIDS/default.htm Sudden Infant Death Syndrome and the Child Care Provider http://sids-id-psc.org/_documents/pdf/childcare_provider.pdf

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From the National Institutes of Health L.A. Summit Seeks to Reduce SIDS in Western U.S. African American Communities Source: National Institute of Child Health and Human Development http://www.nih.gov/news/pr/mar2003/nichd-13.htm Sudden Infant Death Syndrome Source: National Institute of Child Health and Human Development http://www.nichd.nih.gov/publications/pubs/sidsfact.htm

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Latest News SIDS Research “Flawed;”Clues Ignored Source: 12/09/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_15056 .html

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Organizations American Academy of Pediatrics http://www.aap.org/ National Institute of Child Health and Human Development http://www.nichd.nih.gov/ National SIDS & Infant Death Program Support Center http://sids-id-psc.org/ National Sudden Infant Death Syndrome Resource Center Source: Dept. of Health and Human Services, Maternal and Child Health Bureau http://www.sidscenter.org/ Sudden Infant Death Syndrome (SIDS) Alliance Source: Sudden Infant Death Syndrome Alliance http://www.sidsalliance.org/index/default.asp

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Prevention/Screening Campaign's Resource Kit Seeks to Reduce Incidence of SIDS in African American Communities Source: National Institute of Child Health and Human Development http://www.nichd.nih.gov/new/releases/sids.cfm SIDS Facts: Reducing the Risk of SIDS Source: Sudden Infant Death Syndrome Alliance http://www.sidsalliance.org/documents/Reducing_the_Risk_of_SIDS.asp

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Research Bed Sharing with Siblings, Soft Bedding, Increase SIDS Risk Source: Centers for Disease Control and Prevention, National Institute of Child Health and Human Development http://www.nih.gov/news/pr/may2003/nichd-05.htm Higher SIDS Risk Found in Infants Placed in Unaccustomed Sleeping Position Source: National Institute of Child Health and Human Development, National Institute on Deafness and Other Communication Disorders http://www.nih.gov/news/pr/feb2003/nichd-28.htm Most Definitive Study of Its Kind Shows That Sleeping on the Stomach Increases Infant SIDS Risk Source: Centers for Disease Control and Prevention, National Institute of Child Health and Human Development, National Institute on Deafness and Other Communication Disorders http://www.nih.gov/news/pr/oct2002/nichd-07.htm NICHD-Funded Researchers Uncover Abnormal Brain Pathways in SIDS Victims Source: National Institute of Child Health and Human Development http://www.nichd.nih.gov/new/releases/sidsbrainstem.cfm Study Estimates 20 Percent of SIDS Deaths Occur in Child Care Settings Source: American Academy of Pediatrics http://www.aap.org/advocacy/archives/augsidz.htm Study Raises Questions about Relationship between SIDS and Events Detected by Home Monitors Source: National Institute of Child Health and Human Development http://www.nih.gov/news/pr/may2001/nichd-01.htm Summits Seek to Reduce SIDS Risk in African American Community Source: National Institute of Child Health and Human Development http://www.nih.gov/news/pr/jan2003/nichd-30.htm

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Statistics Infant Mortality Source: National Center for Health Statistics http://www.cdc.gov/nchs/fastats/infmort.htm SIDS Statistics Source: Sudden Infant Death Syndrome Alliance http://www.sidsalliance.org/documents/Back_to_Sleep/Statistics.asp

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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 sudden infant death syndrome. 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: •

Raising Funds to Fight Sudden Infant Death Syndrome Source: Atlanta, GA: American Sudden Infant Death Syndrome Institute. 1995. 4 p. Contact: Available from American Sudden Infant Death Syndrome Institute, 6065 Roswell Road, Suite 876, Atlanta, GA 30328. (404) 843-1030, (800) 232-7437 (Nationwide), (800) 847-7437 (in GA), (404) 843-0577 (Fax), [email protected] (Email), http://www.sids.org (Website). Free of charge. Summary: The American SIDS Institute in Atlanta, Georgia, is dedicated to the prevention of sudden infant death and the promotion of infant health through research, clinical services, family support, and professional education. The institute depends heavily on the financial support of individuals and organizations to achieve its goals. This brochure provides interested persons with a wide variety of ideas for raising funds for SIDS. The ideas include a beautiful baby contest, a canister drive, a car wash, a fun run, a garage sale, money from mall fountains, a walk-a-thon or other marathon event, and requests for memorials. The brochure lists items that the institute can offer fundraisers to assist them in their activities, such as a public service announcement tape, stationery, donation forms, their nonprofit tax ID number, solicitation letters, and brochures. The brochure also includes an event planning checklist and 11 basic facts about SIDS.

•

Volunteering and Raising Funds to Fight Sudden Infant Death Syndrome Source: Atlanta, GA: American Sudden Infant Death Syndrome Institute. 1996. 4 p. Contact: Available from American Sudden Infant Death Syndrome Institute, 6065 Roswell Road, Suite 876, Atlanta, GA 30328. (404) 843-1030, (800) 232-7437 (Nationwide), (800) 847-7437 (in GA), (404) 843-0577 (Fax), [email protected] (Email), http://www.sids.org (Website). Free of charge. Summary: The American Sudden Infant Death Syndrome (SIDS) Institute in Atlanta, Georgia, is dedicated to the prevention of sudden infant death and the promotion of infant health through research, clinical services, family support, and professional education. The institute depends heavily on the financial support of individuals and organizations to achieve its goals. This brochure provides interested persons with a

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wide variety of ideas for raising funds for SIDS. The ideas include a beautiful baby contest, a canister drive, a car wash, a fun run, a garage sale, money from mall fountains, a walk-a-thon or other marathon event, and requests for memorials. The brochure lists items that the institute can offer fund raisers to assist them in their activities, such as a public service announcement tape, stationery, donation forms, their nonprofit tax ID number, solicitation letters, and brochures. The brochure also includes an event planning checklist and 11 basic facts about SIDS. •

Reduce the Risk of Sudden Infant Death Syndrome. Reduciendo el Riesgo del Sindrome de Muerte Infantil Repentina Source: Rancho Cordova, CA: California SIDS Program. 2000. 8 p. Contact: Available from California SIDS Program, 3164 Gold Camp, Suite 220, Rancho Cordova, CA 95670. (916) 463-0146, (800) 369-7437 (in CA), (916) 536-0167 (Fax), [email protected] (E-mail), http://www.californiasids.com (Web Site). Free to CA residents; $0.50 each plus shipping and handling for residents of other states. Summary: This bilingual Spanish-English brochure provides parents and other child care providers with information on reducing the risk of sudden infant death syndrome (SIDS). The brochure states that most SIDS deaths occur by 6 months of age, more boys are victims than girls, and most deaths occur during the fall, winter, and early spring months. SIDS cannot be predicted or prevented, but parents and caregivers are urged to follow certain infant care practices to significantly reduce the risk of SIDS: place your baby to sleep on his or her back; keep the area around your baby smoke-free; make sure your baby sleeps on a firm mattress in a safety-approved crib and not on a waterbed, sheepskin, pillow, or other soft surface; keep fluffy blankets, comforters, stuffed toys, bumper pads, and pillows out of the crib; keep your baby warm, but not hot; receive early and regular prenatal care and do not smoke or use alcohol or drugs while pregnant; and breast feed your baby, if possible. The brochure states that babies who roll over onto their stomachs on their own should not be forced to stay on their back. Parents are urged to talk to their doctor or nurse if they have any questions about their baby's sleep position or health.

•

Sudden Infant Death Syndrome: Information for Coroners and Coroner's Investigators in California Source: Berkeley, CA: California Sudden Infant Death Syndrome Program. June 1992. 8 p. Contact: Available from California Sudden Infant Death Syndrome Program, 5330 Primrose Drive, Suite 231, Fair Oaks, CA 95628-3542. (916) 536-0146, (800) 369-7437 (in CA), (916) 536-0167 (Fax). Free to CA residents; $0.71 per copy for residents of other States. Summary: This booklet provides coroners and their investigators with basic information about sudden infant death syndrome (SIDS) and guidelines for conducting a death scene investigation of a possible SIDS death in California. The first part of the booklet outlines the coroner's responsibilities in a presumptive SIDS death investigation according to California State codes; describes the three types of information the pathologist needs to arrive at a diagnosis of SIDS, and which information is the responsibility of the coroner; and describes a typical SIDS history and typical death scene and autopsy findings. The second part of the booklet provides coroners with six guidelines to follow in dealing with parents or caregivers: explain the purpose of the investigation; treat the baby with kindness and respect; ask open-ended, nonjudgmental

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questions; explain what will happen next; be reassuring; and make sure that both you and the parents know how to contact each other later. Specific information is provided for each guideline. •

Eastern Connecticut Sudden Infant Death Syndrome Network Source: Ledyard, CT: Eastern Connecticut Sudden Infant Death Syndrome Network. December 1993. 2 pp. Contact: Available from Sudden Infant Death Syndrome Network, P.O. Box 520, Ledyard, CT 06339. (860) 892-7042, ext. 551 (Voicemail), (860) 887-7309 (Fax), [email protected] (E-mail), http://sids-network.org (Web site). Summary: This brochure describes the mission and services of the Sudden Infant Death Syndrome Network in Ledyard, CT. The Network is a nonprofit, voluntary agency whose mission is threefold: to eliminate sudden infant death syndrome (SIDS) through the support of SIDS research projects, to provide support for persons who have been touched by the tragedy of SIDS, and to raise public awareness of SIDS through education. The network offers the following services: a website that is accessible worldwide, peer counseling and crisis intervention counseling, monthly support group meetings, referrals to other agencies and professional services, educational programs for health professionals and community service professionals, resource materials on SIDS, public service announcements, and a newsletter. The brochure also includes basic information about SIDS.

•

Sudden Infant Death Syndrome Resources, Inc Source: St. Louis, MO: Sudden Infant Death Syndrome Resources, Inc. 0000. 2 p. Contact: Available from Sudden Infant Death Syndrome Resources, Inc., 143 Grand Avenue, St. Louis, MO 63122. (314) 822-2323, (800) 421-3511 (in MO), (314) 822-2098 (Fax). Summary: This brochure describes the services of Sudden Infant Death Syndrome Resources (SIDS), Inc., a nonprofit organization dedicated to helping people who are affected by Sudden Infant Death Syndrome (SIDS) in Missouri. The organization began as a federally funded project in 1974, and in 1982 the project was awarded a contract by the State to provide SIDS services. Today, the organization offers the following services: family support services, including family counseling, home visits, support groups, peer contact, research update meetings, and a quarterly newsletter; training for health professionals, police, and other emergency workers who are first responders in SIDS cases; community awareness activities; and research support. The brochure includes a list of facts about SIDS.

•

Babies sleep safest on their backs: Reduce the risk of Sudden Infant Death Syndrome (SIDS) Source: Bethesda, MD: National Institute of Child Health and Human Development. 2000. 8 pp. Contact: Available from National Institute of Child Health and Human Development Clearinghouse, P.O. Box 3006, Rockville, MD 20847. Telephone: (800) 370-2943 TTY: (888) 320-6942 / fax: (301) 984-1473 / e-mail: [email protected] / Web site: http://www.nichd.nih.gov/publications/info.htm. Available at no charge.

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Summary: This brochure discusses Sudden Infant Death Syndrome (SIDS) and ways for parents to prevent harm to their infant. Topics include facts about SIDS, why babies should sleep on their backs, ways to lower the risk of SIDS, and other ways parents can keep their baby healthy. Information is provided for contacting the Back to Sleep Campaign for more information. The brochure is available in English and Spanish. •

Sudden infant death syndrome Source: Bethesda, MD: Public Information and Communications Branch, National Institute of Child Health and Human Development, U.S. Department of Health and Human Services. 1997. 4 pp. Contact: Available from National Maternal and Child Health Clearinghouse, 2070 Chain Bridge Road, Suite 450, Vienna, VA 22182-2536. Telephone: (703) 356-1964 or (888) 4344MCH / fax: (703) 821-2098 / e-mail: [email protected] / Web site: http://www.nmchc.org. Available at no charge. Summary: This brochure explains what sudden infant death syndrome (SIDS) is, what the risk factors for it are, what causes it, what might help lower the risk, and how a SIDS baby affects the family. Examples of SIDS counseling and support groups are provided.

•

Sudden Infant Death Syndrome: What Every Young Adult Should Know. Revised Edition Source: Seattle, WA: SIDS Foundation of Washington. January 1996. 2 p. Contact: Available from SIDS Foundation of Washington, 4649 Sunnyside Avenue N., Room 328, Seattle, WA 98103. (206) 548-9290 (Seattle), (509) 456-0505 (Spokane), (800) 533-0376 (WA, ID, OR only), (206) 548-9445 (Fax), sids- [email protected] (Email), http://www.zipcon.net/sids-wa (Website). $0.15 each plus shipping and handling. Summary: This brochure introduces adolescents and young adults to sudden infant death syndrome (SIDS). The brochure is intended to prepare them for the possibility of SIDS occurring in their life, whether they experience it as a family member, babysitter, close friend, or parent. The brochure answers the following questions: What is SIDS?; Why should young adults know about SIDS?; What are the known facts about SIDS?; How can you prepare to face SIDS or another emergency as a babysitter?; What should you know as a new parent to help reduce the risk of SIDS occurring?; When SIDS occurs, what is its impact?; and What can you do to help a parent, sibling, or friend who has experienced a SIDS death?.

•

About Sudden Infant Death Syndrome (SIDS) Source: Camberwell, Australia: National SIDS Council of Australia Ltd. October 1991. 4 p. Contact: Available from National SIDS Council of Australia Ltd., 357 Burwood Road, Hawthorn, VIC 3122 Australia. 011-61-03-9819-9277. Summary: This brochure presents basic information about sudden infant death syndrome (SIDS). The brochure covers the following topics: the definition of SIDS, possible causes, whether the baby smothered or choked on vomit or food, whether the baby suffered, whether SIDS is contagious, whether the death was anyone's fault, why the police are called in SIDS deaths, normal grief reactions, the reactions of other children, having another baby, current research objectives, and sources of information

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and help. Contact information is provided for nine organizations that are located throughout Australia. •

Prevent Sudden Infant Death Syndrome Source: New Brunswick, NJ: New Jersey Sudden Infant Death Syndrome Resource Center. 1996. 2 p. Contact: Available from SIDS Center of New Jersey, 254 Easton Avenue, New Brunswick, NJ 08903. (908) 249-2160, (800) 545-7437 (NJ Hotline), (908) 249-6306 (Fax), [email protected] (Email), http://www2.umdnj.edu/sids/home.htm (Website). Summary: This brochure presents guidelines to parents, relatives, and caregivers of infants for reducing the risk for sudden infant death syndrome (SIDS). The guidelines are as follows: don't smoke and avoid exposure to smoky atmospheres (infants who are exposed to smoke have five times the risk for SIDS as infants who are not exposed to smoke); place infants on their backs to sleep, near the foot of the bed, with blankets or sheets covering no further than the shoulders; make sure the infant sleeps on a firm mattress, never a pillow or a soft surface; do not overheat the infant by bundling him or her with excess bedding and bed clothes; remove the infant's outdoor clothing, including any head covering, upon going indoors into a building, car, train, or bus so the infant can vent excess heat; learn to recognize the signs of a serious illness in the infant (e.g., a high-pitched or weak cry, unresponsiveness and limpness, paleness, grunting while breathing, a lowered intake of fluids, vomiting green fluid, passing blood during bowel movements, or fever); learn to recognize when an infant needs urgent medical attention (i.e., when the infant stops breathing or turns blue, is unresponsive or shows no awareness of what is going on around him or her, has glazed eyes and does not focus on anything, or cannot be awakened); and breastfeed the infant, if possible. The brochure is printed in color. A companion risk-reduction poster also is available.

•

Reduce the Risks of Sudden Infant Death Syndrome Source: Hackensack, NJ: CJ Foundation for SIDS. 1996. Contact: Available from CJ Foundation for SIDS, Don Imus-WFAN Pediatric Center, Hackensack University Medical Center, 30 Prospect Avenue, Hackensack, NJ 07601. (201) 996-5111, (201) 996-5326 (Fax), [email protected] (Email). Free of charge. Summary: This brochure presents parents and child care providers with six steps for reducing the risk for sudden infant death syndrome (SIDS). These steps are as follows: put a healthy infant on his or her back to sleep; do not smoke near the infant; do not let the infant get too hot; put the infant to sleep on a firm mattress; take good care of yourself and the infant; and breast feed the infant, if possible. The brochure stresses that infants should be put to sleep on their backs whether they are being put down for a nap or to bed for the night. If an infant has problems breathing or spits up a lot after feeding, parents should ask their pediatrician about the appropriate sleep position for their child. Basic facts about SIDS are included in the brochure.

•

American Sudden Infant Death Syndrome Institute Source: Atlanta, GA: American Sudden Infant Death Syndrome Institute. 1994. 4 p. Contact: Available from American Sudden Infant Death Syndrome Institute, 6065 Roswell Road, Suite 876, Atlanta, GA 30328. (404) 843-1030, (800) 232-7437 (Nationwide),

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(800) 847-7437 (in GA), (404) 843-0577 (Fax), [email protected] (Email), http://www.sids.org (Website). Free of charge. Summary: This brochure provides a description of the American Sudden Infant Death Syndrome (SIDS) Institute in Atlanta, Georgia, and its activities. The nonprofit organization dedicates itself to a comprehensive national program of research, education, and health care. The Institute encourages collaborative research efforts between members of its staff and investigators from other institutions throughout the country. In terms of health care, the Institute's clinic in Atlanta provides medical services for infants at risk for SIDS, regardless of the family's financial situation. The clinic also provides diagnostic evaluation and a comprehensive program of home monitoring. In the event of a SIDS death, the Institute provides bereavement services to families and friends that include crisis phone counseling, bereavement counseling, and grief literature. The Institute also organizes conferences, workshops, and teaching programs to provide rapid dissemination of the latest research to professional groups, including health care providers, first responders, and researchers. In 1992, the Institute began the SIDS Prevention Campaign to inform both physicians and the general public about research findings that have implications for reducing the incidence of SIDS. •

Facts About Sudden Infant Death Syndrome and Reducing the Risks for SIDS. Revised Edition Source: Baltimore, MD: Sudden Infant Death Syndrome Alliance. 1997. 4 p. Contact: Available from Sudden Infant Death Syndrome Alliance, 1314 Bedford Avenue, Suite 210, Baltimore, MD 21208. (410) 653-8226, (800) 221-7437, (410) 653-8709 (Fax), [email protected] (Email). $0.10 each; $10.00 per packet of 100. Summary: This brochure provides parents and child care providers with basic information on sudden infant death syndrome (SIDS) and recommendations for reducing the risk for SIDS that are based on the latest medical evidence. These recommendations are supported by the Sudden Infant Death Syndrome Alliance, a national not-for-profit voluntary health organization dedicated to the support of SIDS families, education, and research. The brochure recommends that parents and caregivers place their baby on his or her back to sleep but allow the baby supervised awake time on its tummy to promote infant development and prevent head- flattening. Back sleep is preferable to side sleep and wedges are not recommended to keep a baby propped on the side. Research findings show that women who smoke cigarettes during or after pregnancy put their infants at increased risk for SIDS. Parents are advised not to smoke during pregnancy and the first year of the baby's life, and not to allow anyone else to smoke around the baby either. Other recommendations are to use firm, flat bedding; avoid overheating the baby; and take good care of oneself and the baby during pregnancy and infancy. Breastfeeding is good for the baby and is recommended, and parents should follow the recommended schedule for their baby's immunizations. Bedsharing has not been shown to protect against SIDS and may be hazardous under some conditions. The same recommendations for safest sleep conditions apply whether one's baby sleeps alone in a crib or shares a bed with a parent. Though bedsharing may boost breastfeeding and promote the bond between mother and infant, bedsharing with family members other than the parents is not recommended. Parents are encouraged to turn to the SIDS Alliance for help, and to consider becoming a SIDS volunteer, educator, fundraiser, or activist for the Alliance affiliate in their area.

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Back to Sleep. Reduce the Risk of Sudden Infant Death Syndrome (SIDS). Revised Edition Source: Bethesda, MD: National Institute of Child Health and Human Development (NIH). 1997. 2 p. Contact: Available from Back to Sleep, P.O. Box 29111, Washington, DC 20040. (800) 505CRIB. Free of charge. Summary: This brochure, a product of the national 'Back to Sleep' campaign in the United States, presents parents and child care providers with information on reducing the risk for sudden infant death syndrome (SIDS). The 'Back to Sleep' campaign was initiated in June 1994 to alert new parents and health professionals to sleep position as a possible risk factor for SIDS. Research has shown that the greatest risk for SIDS occurs in the prone sleep position. The safest sleep position for healthy babies is the supine position, so pediatricians now recommend that healthy infants be put down to sleep on their backs for nap time and bedtime. The side sleep position does not provide as much protection against SIDS as the back position, but it is still much safer than placing an infant to sleep on his or her stomach. Parents of infants who were born with a birth defect or who have gastrointestinal, respiratory, or heart problems should ask their doctor about which sleep position to use during naps and at night. Other things that parents can do to help reduce the risk for SIDS are as follows: make sure that the baby sleeps on a firm mattress without fluffy blankets or comforters underneath; do not let the baby sleep on a waterbed, sheepskin, pillow, or other soft material; do not place stuffed toys or pillows in the crib; keep the temperature in the baby's room where it feels comfortable to you; do not let anyone smoke around the baby; if the baby seems sick, call your doctor or clinic right away; make sure the baby receives all of his or her shots on time; get early and regular prenatal care; do not smoke or use alcohol or drugs during pregnancy; and breastfeed your baby, if possible. The brochure also is available in Spanish (MCS000501).

•

Sudden Infant Death Syndrome. Revised Edition Source: Seattle, WA: SIDS Foundation of Washington. 1996. 1 p. Contact: Available from SIDS Foundation of Washington, 4649 Sunnyside Avenue, N., Room 438, Seattle, WA 98103. (206) 548-9290 (Seattle), (509) 456-0505 (Spokane), (800) 533-0376 (WA, ID, OR only), (206) 548- 9445 (Fax), [email protected] (Email), http://www.zipcon.net/sids-wa (Website). $0.03 each plus shipping and handling. Summary: This half-page fact sheet presents basic information about sudden infant death syndrome (SIDS). The fact sheet presents the definition of SIDS; its incidence in the United States; the peak age for SIDS and other demographic characteristics; and the fact that SIDS cannot be predicted or prevented, even by a physician. The fact sheet also lists causes of death that are often erroneously thought to be causes of SIDS (e.g., suffocation, child abuse, vomiting, choking), and states that SIDS is not contagious nor does it cause pain or suffering to the infant.

•

California Sudden Infant Death Syndrome Program: Mission Statement; Program Goals and Activities Source: Fair Oaks, CA: California SIDS Program. June 1996. 1 p. Contact: Available from California Sudden Infant Death Syndrome Program, 5330 Primrose Drive, Suite 231, Fair Oaks, CA 95628-3542. (916) 536-0146, (800) 369-7437 (in CA), (916) 536-0167 (Fax).

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Summary: This information sheet describes the mission, goals, and activities of the California Sudden Infant Death Syndrome Program. Following a brief mission statement, specific activities are listed under each of the following program goals: to reduce the emotional suffering that accompanies a SIDS death; to provide SIDS education and training for professionals, paraprofessionals, and parents; to increase public awareness and knowledge of SIDS; and to encourage SIDS research. •

Selected Books on Sudden Infant Death Syndrome Source: McLean, VA: National Sudden Infant Death Syndrome Resource Center. May 1993. 2 p. Contact: Available from National SIDS Resource Center, Suite 450, 2070 Chain Bridge Road, Vienna, VA 22182-2536. (703) 821-8955, (703) 821-2098 (Fax), [email protected] (Email), http://www.circsol.com/sids (Website). Free of charge; distribution limited to one per customer. Order No. S102. Summary: This information sheet lists 13 selected books on sudden infant death syndrome (SIDS) published from 1980 to the present that cover research, the impact of a SIDS death on parents and families, and the role of professionals and others in helping families deal with the loss. Publisher and/or distributor information is listed whenever possible. Three books that are no longer in print are included, as copies may still be available at a medical, university, or public library, or through interlibrary loan arrangements at these institutions.

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Sudden Infant Death Syndrome: The Facts Source: Milwaukee, WI: Wisconsin Sudden Infant Death Center. 1993. 2 p. Contact: Available from Wisconsin Sudden Infant Death Center, Children's Hospital of Wisconsin, P.O. Box 1997, Milwaukee, WI 53201-0997. (414) 266- 2743, (414) 266-2653 (Fax). Order No. 10k TJ93. Summary: This pamphlet, intended for the general public, provides the following information about sudden infant death syndrome (SIDS): a definition, facts about SIDS that are based on research, the characteristics of SIDS victims and the circumstances typically surrounding SIDS deaths, common misconceptions about its cause and prevention, the importance of an autopsy to a SIDS diagnosis, and the chances of recurrence within the same family.

•

When Your Baby Has Died of Sudden Infant Death Syndrome Source: Toronto, Ontario: The Canadian Foundation for the Study of Infant Deaths. 1991. 5 p. Contact: Canadian Foundation for the Study of Infant Deaths, 586 Eglinton Avenue East, Suite 308, Toronto, ON M4P 1P2 Canada. (416) 488-3260, (800) 363-7437, (416) 488-3864 (Fax), [email protected] (Email), http://www.sidscanada.org/sids.html (Website). Summary: This pamphlet, written for the parents of infants who have died from sudden infant death syndrome (SIDS), provides facts about SIDS; identifies common parental reactions to the death of a baby (i.e., guilt, shock, anger, fear); describes the physical symptoms of grief; and discusses the issue of subsequent children. The pamphlet also discusses the unique grief reactions of mothers and fathers, single parents, siblings, and

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grandparents, and advises parents on talking to their other children about the death. The pamphlet also is available in French (MCS000477). •

Reducing the Risk of Sudden Infant Death Syndrome in Canada Source: Toronto, Ontario: The Canadian Foundation for the Study of Infant Deaths. August 1993. 2 pp. Contact: Canadian Foundation for the Study of Infant Deaths, 586 Eglinton Avenue East, Suite 308, Toronto, ON M4P 1P2 Canada. (416) 488-3260, (800) 363-7437, (416) 488-3864 (Fax), [email protected] (E-mail), http://www.sidscanada.org/sids.html (Web site). Summary: This position statement on reducing the risks for sudden infant death syndrome is supported by the Canadian Foundation for the Study of Infant Deaths, the Canadian Institute of Child Health, the Canadian Paediatric Society, and Health Canada. The recommendations include placing healthy infants in the supine or lateral position for sleep, caring for infants in a smoke-free environment, dressing and covering infants in a manner that avoids overheating, and breastfeeding infants whenever possible. The National Guideline Clearinghouse™

The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “sudden infant death syndrome” (or synonyms). The following was recently posted: •

(1) Distinguishing sudden infant death syndrome from child abuse fatalities; (2) Distinguishing sudden infant death syndrome from child abuse fatalities (Addendum) Source: American Academy of Pediatrics - Medical Specialty Society; 2001 February (addendum published 2001 Sep); 5 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2763&nbr=1989&a mp;string=sudden+AND+infant+AND+death+AND+syndrome

•

Apnea, sudden infant death syndrome, and home monitoring Source: American Academy of Pediatrics - Medical Specialty Society; 2003 April; 4 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3732&nbr=2958&a mp;string=sudden+AND+infant+AND+death+AND+syndrome

•

Changing concepts of sudden infant death syndrome: implications for infant sleeping environment and sleep position Source: American Academy of Pediatrics - Medical Specialty Society; 2000 March; 7 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2768&nbr=1994&a mp;string=sudden+AND+infant+AND+death+AND+syndrome

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

Babies Sleep Safest on Their Backs: Reduce the Risk of Sudden Infant Death Syndrome Source: National Institute of Child Health and Human Development, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3179

•

Back to Sleep Campaign Summary: This website offers information for parents and health professionals on sudden infant death syndrome. Some materials are available in Spanish. Source: National Institute of Child Health and Human Development, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=409

•

Frequently Asked Questions and SIDS Research Information Summary: These links focus on a number of issues related to Sudden Infant Death Syndrome: smoking, sleep, sleep apnea, and vaccinations. Source: Sudden Infant Death Syndrome Network, Inc. http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7705

•

healthfinder® just for you: Infants Summary: healthfinder®'s just for you: Infants section features topics such as birth defects, child care, and sudden infant death syndrome (SIDS). Source: U.S. Department of Health and Human Services http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7015

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SIDS Information for New Parents Summary: Here are some important tips for new parents, grandparents and infant caregivers to help reduce the risk of Sudden Infant Death Syndrome and accidental infant deaths. Source: Sudden Infant Death Syndrome Alliance http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7706

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Study Identifies SIDS Risk Factors Among American Indian Infants Summary: A study of Northern Plains Indians found that infants were less likely to die of Sudden Infant Death Syndrome (SIDS) if their mothers received visits from public health nurses before and after giving Source: Indian Health Service http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7136 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 sudden infant death syndrome. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •

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

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

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

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

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

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

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

Associations and Sudden Infant Death Syndrome The following is a list of associations that provide information on and resources relating to sudden infant death syndrome: •

American Sudden Infant Death Syndrome Institute Telephone: (770) 621-1030 Toll-free: (800) 232-7437 Fax: (770) 612-8277 Email: [email protected] Web Site: http://www.sids.org

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Background: The American Sudden Infant Death Syndrome Institute is a not-for-profit organization dedicated to preventing Sudden Infant Death Syndrome (SIDS) and to ensuring that the medical and corporate communities, government agencies, and general public share the sense of urgency in preventing SIDS. Sudden Infant Death Syndrome is characterized by the sudden death of any infant or young child that is unexpected by history and for which no adequate cause of death can be found. The Institution was founded to develop a comprehensive national program of research, clinical care, and education and to focus national attention and resources on the problem of SIDS. Most importantly, the Institute searches aggressively and with a strong sense of urgency for the means to eliminate this disorder. Established in 1983, the organization provides support groups, promotes research, engages in patient and professional education, and offers clinical services. Educational materials include a newsletter entitled 'The Promise,' brochures, and pamphlets. Relevant area(s) of interest: Sudden Infant Death Syndrome •

National Sudden Infant Death Syndrome Resource Center Telephone: (703) 821-8955 Fax: (703) 821-2098 Email: [email protected] Web Site: http://www.circsol.com/sids Background: The National Sudden Infant Death Syndrome (SIDS) Resource Center is a professional for profit health organization that provides information services and technical assistance concerning SIDS and related topics in order to promote understanding of SIDS and to comfort those affected by a SIDS loss. Established in 1981, the Resource Center assists the National Center of Education's Maternal and Child Health Bureau (MCHB) by providing its services to State MCHB-supported projects and State SIDS programs funded through the Maternal and Child Health Block Grant. The Resource Center also offers its services to parents, family members, care providers, counselors, medical and legal professionals, researchers, program planners, policymakers, and the general public. The Resource Center maintains automated databases of SIDS technical literature, public awareness materials, MCHB materials, and organizations concerned with SIDS. The Center also develops and distributes bibliographies of materials on SIDS, fact sheets, and other educational materials, including its 'Information Exchange' newsletter; tracks information and resources on current developments related to SIDS; conducts customized database searches; and refers those making inquiries to State SIDS programs and other regional and national organizations, as appropriate. Relevant area(s) of interest: Sudden Infant Death Syndrome

•

Sudden Infant Death Syndrome Alliance, Inc Telephone: (410) 653-8226 Toll-free: (800) 221-7437 Fax: (410) 653-8709 Email: [email protected] Web Site: http://www.sidsalliance.org Background: The Sudden Infant Death Syndrome Alliance exists to ensure the elimination of sudden infant death syndrome through medical research and education, while providing support to those affected by an infant death. It is a national, non-profit

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voluntary health organization that unites families, caregivers, health professionals and scientists with government, business and community service groups. As a sponsor of the national Back to Sleep Campaign, the SIDS Alliance supplies information on SIDS to nwe and expectant parents and the general public via a nationwide 24-hour, tollfree hotline and its website. It works closely with the National Institute of Child Health and Human Development to advocate for a coordinated research agenda for the nation. Relevant area(s) of interest: Sudden Infant Death Syndrome

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

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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 “sudden infant death syndrome” (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 “sudden infant death syndrome” (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.27

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

Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities 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

27

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)28: •

Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/

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Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)

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Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm

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California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html

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California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html

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California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html

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California: Gateway Health Library (Sutter Gould Medical Foundation)

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California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/

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California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp

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California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html

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California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/

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California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/

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California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/

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California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html

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California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/

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Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/

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Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/

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Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/

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

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•

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

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Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm

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Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html

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Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm

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Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp

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Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/

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Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm

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Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html

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Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/

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Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm

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Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/

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Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/

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Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/

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Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm

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Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html

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Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm

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Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/

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

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

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

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

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

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

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

•

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

•

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

•

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)

•

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

•

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

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

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

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

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

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

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

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

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

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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/

•

Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html

•

On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/

•

Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp

•

Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm

Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on sudden infant death syndrome: •

Basic Guidelines for Sudden Infant Death Syndrome SIDS Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001566.htm Sudden infant death syndrome Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001566.htm

•

Signs & Symptoms for Sudden Infant Death Syndrome Apnea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003069.htm

•

Background Topics for Sudden Infant Death Syndrome Aggravated by Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002227.htm CPR Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000010.htm

198 Sudden Infant Death Syndrome

Incidence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002387.htm Safety Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001931.htm SIDS - support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002202.htm

Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •

Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical

•

MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

•

Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

•

Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

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SUDDEN INFANT DEATH SYNDROME DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Ablation: The removal of an organ by surgery. [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] Accommodation: Adjustment, especially that of the eye for various distances. [EU] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Acoustic: Having to do with sound or hearing. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acyl: Chemical signal used by bacteria to communicate. [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] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH]

200 Sudden Infant Death Syndrome

Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aetiology: Study of the causes of disease. [EU] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the 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] Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Aged, 80 and Over: A person 80 years of age and older. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Airway Obstruction: Any hindrance to the passage of air into and out of the lungs. [NIH] Airway Resistance: Physiologically, the opposition to flow of air caused by the forces of friction. As a part of pulmonary function testing, it is the ratio of driving pressure to the rate of air flow. [NIH] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] 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

Dictionary 201

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] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids, Essential: Amino acids that are not synthesized by the human body in amounts sufficient to carry out physiological functions. They are obtained from dietary foodstuffs. [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] Amniotic Fluid: Amniotic cavity fluid which is produced by the amnion and fetal lungs and kidneys. [NIH] Amphetamines: Analogs or derivatives of amphetamine. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopression, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation. [NIH] 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] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Anaphylactic: Pertaining to anaphylaxis. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaphylaxis: An acute hypersensitivity reaction due to exposure to a previously encountered antigen. The reaction may include rapidly progressing urticaria, respiratory distress, vascular collapse, systemic shock, and death. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU]

202 Sudden Infant Death Syndrome

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] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Ankle: That part of the lower limb directly above the foot. [NIH] Anoxia: Clinical manifestation of respiratory distress consisting of a relatively complete absence of oxygen. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Antecedent: Existing or occurring before in time or order often with consequential effects. [EU]

Anterograde: Moving or extending forward; called also antegrade. [EU] Anthropology: The science devoted to the comparative study of man. [NIH] Antiarrhythmic: An agent that prevents or alleviates cardiac arrhythmia. [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] 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] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH]

Dictionary 203

Antimony: A metallic element that has the atomic symbol Sb, atomic number 51, and atomic weight 121.75. It is used as a metal alloy and as medicinal and poisonous salts. It is toxic and an irritant to the skin and the mucous membranes. [NIH] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] 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] Anus: The opening of the rectum to the outside of the body. [NIH] Apnea: A transient absence of spontaneous respiration. [NIH] Apnoea: Cessation of breathing. [EU] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Aqueous: Having to do with water. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arcuate Nucleus: A nucleus located in the middle hypothalamus in the most ventral part of the third ventricle near the entrance of the infundibular recess. Its small cells are in close contact with the ependyma. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Aromatic: Having a spicy odour. [EU] Arrhythmia: Any variation from the normal rhythm or rate of the heart beat. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Artifacts: Any visible result of a procedure which is caused by the procedure itself and not by the entity being analyzed. Common examples include histological structures introduced by tissue processing, radiographic images of structures that are not naturally present in living tissue, and products of chemical reactions that occur during analysis. [NIH] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aseptic: Free from infection or septic material; sterile. [EU]

204 Sudden Infant Death Syndrome

Aspartate: A synthetic amino acid. [NIH] Asphyxia: A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life. [NIH] Aspiration: The act of inhaling. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] 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] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Audiology: The study of hearing and hearing impairment. [NIH] Auditory: Pertaining to the sense of hearing. [EU] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Autonomic Pathways: Nerves and plexuses of the autonomic nervous system. The central nervous system structures which regulate the autonomic nervous system are not included. [NIH]

Autopsy: Postmortem examination of the body. [NIH] Autoreceptors: Transmitter receptors on or near presynaptic terminals (or varicosities) which are sensitive to the transmitter(s) released by the terminal itself. Receptors for the hormones released by hormone-releasing cells are also included. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron

Dictionary 205

cell body. [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 Physiology: Physiological processes and activities of bacteria. [NIH] Bacterial toxin: A toxic substance, made by bacteria, that can be modified to kill specific tumor cells without harming normal cells. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Baroreflex: A negative feedback system which buffers short-term changes in blood pressure. Increased pressure stretches blood vessels which activates pressoreceptors (baroreceptors) in the vessel walls. The net response of the central nervous system is a reduction of central sympathetic outflow. This reduces blood pressure both by decreasing peripheral vascular resistance and by lowering cardiac output. Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure. [NIH]

Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Base Pair Mismatch: The presence of an uncomplementary base in double-stranded DNA caused by spontaneous deamination of cytosine or adenine, mismatching during homologous recombination, or errors in DNA replication. Multiple, sequential base pair mismatches lead to formation of heteroduplex DNA (nucleic acid heteroduplexes). [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] Bereavement: Refers to the whole process of grieving and mourning and is associated with a deep sense of loss and sadness. [NIH] Beta-Endorphin: A peptide consisting of amino acid sequence 61-91 of the endogenous pituitary hormone beta-lipotropin. The first four amino acids show a common tetrapeptide sequence with methionine- and leucine enkephalin. The compound shows opiate-like activity. Injection of beta-endorphin induces a profound analgesia of the whole body for several hours. This action is reversed after administration of naloxone. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its

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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] Binding agent: A substance that makes a loose mixture stick together. For example, binding agents can be used to make solid pills from loose powders. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Bioengineering: The application of engineering principles to the solution of biological problems, for example, remote-handling devices, life-support systems, controls, and displays. [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] 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] Biotin: Hexahydro-2-oxo-1H-thieno(3,4-d)imidazole-4-pentanoic acid. Growth factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk.The biotin content of cancerous tissue is higher than that of normal tissue. [NIH] Biphasic: Having two phases; having both a sporophytic and a gametophytic phase in the life cycle. [EU] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Body Regions: Anatomical areas of the body. [NIH]

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Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Boron: A trace element with the atomic symbol B, atomic number 5, and atomic weight 10.81. Boron-10, an isotope of boron, is used as a neutron absorber in boron neutron capture therapy. [NIH] Boron Neutron Capture Therapy: A technique for the treatment of neoplasms, especially gliomas and melanomas in which boron-10, an isotope, is introduced into the target cells followed by irradiation with thermal neutrons. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachial: All the nerves from the arm are ripped from the spinal cord. [NIH] Brachial Plexus: The large network of nerve fibers which distributes the innervation of the upper extremity. The brachial plexus extends from the neck into the axilla. In humans, the nerves of the plexus usually originate from the lower cervical and the first thoracic spinal cord segments (C5-C8 and T1), but variations are not uncommon. [NIH] Bradycardia: Excessive slowness in the action of the heart, usually with a heart rate below 60 beats per minute. [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 Hypoxia: Lack of oxygen leading to unconsciousness. [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] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]

Breakdown: A physical, metal, or nervous collapse. [NIH] Breast Feeding: The nursing of an infant at the mother's breast. [NIH] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchioles: The tiny branches of air tubes in the lungs. [NIH] Bronchiolitis: Inflammation of the bronchioles. [NIH] Bronchiseptica: A small, gram-negative, motile bacillus. A normal inhabitant of the

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respiratory tract in man, dogs, and pigs, but is also associated with canine infectious tracheobronchitis and atrophic rhinitis in pigs. [NIH] Bronchopulmonary: Pertaining to the lungs and their air passages; both bronchial and pulmonary. [EU] Bronchopulmonary Dysplasia: A chronic lung disease appearing in certain newborn infants treated for respiratory distress syndrome with mechanical ventilation and elevated concentration of inspired oxygen. [NIH] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]

Cadaver: A dead body, usually a human body. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium Channels: Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue. [NIH] Calpain: Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including neuropeptides, cytoskeletal proteins, proteins from smooth muscle, cardiac muscle, liver, platelets and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. [NIH] Capsid: The outer protein protective shell of a virus, which protects the viral nucleic acid. [NIH]

Carbohydrates: The largest class of organic compounds, including starches, glycogens, cellulose, gums, and simple sugars. Carbohydrates are composed of carbon, hydrogen, and oxygen in a ratio of Cn(H2O)n. [NIH] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogenic: Producing carcinoma. [EU] 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] Cardiac: Having to do with the heart. [NIH]

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Cardiac arrest: A sudden stop of heart function. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] Cardiomyopathy: A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation and closed-chest cardiac massage. [NIH] Cardiopulmonary Resuscitation: The artificial substitution of heart and lung action as indicated for heart arrest resulting from electric shock, drowning, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation and closed-chest cardiac massage. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular Abnormalities: Congenital structural abnormalities of the cardiovascular system. [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [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] Carotid Body: A small cluster of chemoreceptive and supporting cells located near the bifurcation of the internal carotid artery. The carotid body, which is richly supplied with fenestrated capillaries, senses the pH, carbon dioxide, and oxygen concentrations in the blood and plays a crucial role in their homeostatic control. [NIH] Carotid Sinus: The dilated portion of the common carotid artery at its bifurcation into external and internal carotids. It contains baroreceptors which, when stimulated, cause slowing of the heart, vasodilatation, and a fall in blood pressure. [NIH] Carpal Tunnel Syndrome: A median nerve injury inside the carpal tunnel that results in symptoms of pain, numbness, tingling, clumsiness, and a lack of sweating, which can be caused by work with certain hand and wrist postures. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] 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]

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Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Division: The fission of a cell. [NIH] 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 Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Cellobiose: A disaccharide consisting of two glucose units in beta (1-4) glycosidic linkage. Obtained from the partial hydrolysis of cellulose. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] 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] Cerebellar: Pertaining to the cerebellum. [EU] 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] Cerebral Infarction: The formation of an area of necrosis in the cerebrum caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., infarction, anterior cerebral artery), and etiology (e.g., embolic infarction). [NIH]

Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] 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

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the lower, narrow end (the "neck") of the uterus. [NIH] Cervical Plexus: A network of nerve fibers originating in the upper four cervical spinal cord segments. The cervical plexus distributes cutaneous nerves to parts of the neck, shoulders, and back of the head, and motor fibers to muscles of the cervical spinal column, infrahyoid muscles, and the diaphragm. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chest cavity: Space in body surrounding the lungs. [NIH] Chest wall: The ribs and muscles, bones, and joints that make up the area of the body between the neck and the abdomen. [NIH] Child Care: Care of children in the home or institution. [NIH] Chiropractic: A system of treating bodily disorders by manipulation of the spine and other parts, based on the belief that the cause is the abnormal functioning of a nerve. [NIH] Chloral Hydrate: A hypnotic and sedative used in the treatment of insomnia. The safety margin is too narrow for chloral hydrate to be used as a general anesthetic in humans, but it is commonly used for that purpose in animal experiments. It is no longer considered useful as an anti-anxiety medication. [NIH] Chloralose: A derivative of chloral hydrate that was used as a sedative but has been replaced by safer and more effective drugs. Its most common use is as a general anesthetic in animal experiments. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Cholecystokinin: A 33-amino acid peptide secreted by the upper intestinal mucosa and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety. [NIH] 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] Choline: A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chondroitin sulfate: The major glycosaminoglycan (a type of sugar molecule) in cartilage. [NIH]

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Chromaffin Cells: Cells that store epinephrine secretory vesicles. During times of stress, the nervous system signals the vesicles to secrete their hormonal content. Their name derives from their ability to stain a brownish color with chromic salts. Characteristically, they are located in the adrenal medulla and paraganglia (paraganglia, chromaffin) of the sympathetic nervous system. [NIH] Chromaffin System: The cells of the body which stain with chromium salts. They occur along the sympathetic nerves, in the adrenal gland, and in various other organs. [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] Chromic: Catgut sterilized and impregnated with chromium trioxide. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens. [NIH] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Circadian: Repeated more or less daily, i. e. on a 23- to 25-hour cycle. [NIH] Circadian Rhythm: The regular recurrence, in cycles of about 24 hours, of biological processes or activities, such as sensitivity to drugs and stimuli, hormone secretion, sleeping, feeding, etc. This rhythm seems to be set by a 'biological clock' which seems to be set by recurring daylight and darkness. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [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] Coca: Any of several South American shrubs of the Erythroxylon genus (and family) that yield cocaine; the leaves are chewed with alum for CNS stimulation. [NIH]

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Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Colic: Paroxysms of pain. This condition usually occurs in the abdominal region but may occur in other body regions as well. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] 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]

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Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Confounder: A factor of confusion which blurs a specific connection between a disease and a probable causal factor which is being studied. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in body tissues. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constitutional: 1. Affecting the whole constitution of the body; not local. 2. Pertaining to the constitution. [EU] Constriction: The act of constricting. [NIH] Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Contralateral: Having to do with the opposite side of the body. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH]

Convulsions: A general term referring to sudden and often violent motor activity of cerebral or brainstem origin. Convulsions may also occur in the absence of an electrical cerebral discharge (e.g., in response to hypotension). [NIH] 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]

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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] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] 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] 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] Cytoskeletal Proteins: Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible. [NIH]

Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Day Care: Institutional health care of patients during the day. The patients return home at night. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decompression: Decompression external to the body, most often the slow lessening of external pressure on the whole body (especially in caisson workers, deep sea divers, and persons who ascend to great heights) to prevent decompression sickness. It includes also sudden accidental decompression, but not surgical (local) decompression or decompression applied through body openings. [NIH] Defibrillation: The act to arrest the fibrillation of (heart muscle) by applying electric shock across the chest, thus depolarizing the heart cells and allowing normal rhythm to return. [EU] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU]

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Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diaphragm: The musculofibrous partition that separates the thoracic cavity from the abdominal cavity. Contraction of the diaphragm increases the volume of the thoracic cavity aiding inspiration. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Dilatation: The act of dilating. [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] Diphtheria: A localized infection of mucous membranes or skin caused by toxigenic strains of Corynebacterium diphtheriae. It is characterized by the presence of a pseudomembrane at the site of infection. Diphtheria toxin, produced by C. diphtheriae, can cause myocarditis, polyneuritis, and other systemic toxic effects. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH]

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Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Diurnal: Occurring during the day. [EU] Diving: An activity in which the organism plunges into water. It includes scuba and bell diving. Diving as natural behavior of animals goes here, as well as diving in decompression experiments with humans or animals. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dorsum: A plate of bone which forms the posterior boundary of the sella turcica. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Duke: A lamp which produces ultraviolet radiations for certain ophthalmologic therapy. [NIH]

Duodenum: The first part of the small intestine. [NIH] 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] Dynorphins: A class of opioid peptides including dynorphin A, dynorphin B, and smaller

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fragments of these peptides. Dynorphins prefer kappa-opioid receptors (receptors, opioid, kappa) and have been shown to play a role as central nervous system transmitters. [NIH] Dysostosis: Defective bone formation. [NIH] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] 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] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electric shock: A dangerous patho-physiological effect resulting from an electric current passing through the body of a human or animal. [NIH] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrode: Component of the pacing system which is at the distal end of the lead. It is the interface with living cardiac tissue across which the stimulus is transmitted. [NIH] Electroencephalography: Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]

Electrophysiological: Pertaining to electrophysiology, that is a branch of physiology that is concerned with the electric phenomena associated with living bodies and involved in their functional activity. [EU] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH]

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Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endocrine Glands: Ductless glands that secrete substances which are released directly into the circulation and which influence metabolism and other body functions. [NIH] 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] Endorphin: Opioid peptides derived from beta-lipotropin. Endorphin is the most potent naturally occurring analgesic agent. It is present in pituitary, brain, and peripheral tissues. [NIH]

Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Enkephalin: A natural opiate painkiller, in the hypothalamus. [NIH] Enterovirus: A genus of the family Picornaviridae whose members preferentially inhabit the intestinal tract of a variety of hosts. The genus contains many species. Newly described members of human enteroviruses are assigned continuous numbers with the species designated "human enterovirus". [NIH] Enuresis: Involuntary discharge of urine after the age at which urinary control should have been achieved; often used alone with specific reference to involuntary discharge of urine occurring during sleep at night (bed-wetting, nocturnal enuresis). [EU] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]

Environmental tobacco smoke: ETS. Smoke that comes from the burning of a tobacco product and smoke that is exhaled by smokers (second-hand smoke). Inhaling ETS is called involuntary or passive smoking. [NIH] Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Ependyma: A thin membrane that lines the ventricles of the brain and the central canal of the spinal cord. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] 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

220 Sudden Infant Death Syndrome

and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [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]

Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Evoked Potentials: The electric response evoked in the central nervous system by stimulation of sensory receptors or some point on the sensory pathway leading from the receptor to the cortex. The evoked stimulus can be auditory, somatosensory, or visual, although other modalities have been reported. Event-related potentials is sometimes used synonymously with evoked potentials but is often associated with the execution of a motor, cognitive, or psychophysiological task, as well as with the response to a stimulus. [NIH] Excipients: Usually inert substances added to a prescription in order to provide suitable consistency to the dosage form; a binder, matrix, base or diluent in pills, tablets, creams, salves, etc. [NIH] Excitability: Property of a cardiac cell whereby, when the cell is depolarized to a critical level (called threshold), the membrane becomes permeable and a regenerative inward current causes an action potential. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] 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] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Expiration: The act of breathing out, or expelling air from the lungs. [EU] Extracellular: Outside a cell or cells. [EU] 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] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extremity: A limb; an arm or leg (membrum); sometimes applied specifically to a hand or foot. [EU] Facial: Of or pertaining to the face. [EU] Fallopian Tubes: Two long muscular tubes that transport ova from the ovaries to the uterus. They extend from the horn of the uterus to the ovaries and consist of an ampulla, an infundibulum, an isthmus, two ostia, and a pars uterina. The walls of the tubes are composed of three layers: mucosal, muscular, and serosal. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatal Outcome: Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from death, the physiological cessation of life and from mortality, an epidemiological or statistical concept. [NIH] Fathers: Male parents, human or animal. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]

Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] 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] Ferritin: An iron-containing protein complex that is formed by a combination of ferric iron with the protein apoferritin. [NIH] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH] Fetal Alcohol Syndrome: A disorder occurring in children born to alcoholic women who continue to drink heavily during pregnancy. Common abnormalities are growth deficiency (prenatal and postnatal), altered morphogenesis, mental deficiency, and characteristic facies - small eyes and flattened nasal bridge. Fine motor dysfunction and tremulousness are observed in the newborn. [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] Fibrillation: A small, local, involuntary contraction of muscle, invisible under the skin, resulting from spontaneous activation of single muscle cells or muscle fibres. [EU] Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including

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chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibronectins: Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Flaccid: Weak, lax and soft. [EU] Flatus: Gas passed through the rectum. [NIH] Flexion: In gynaecology, a displacement of the uterus in which the organ is bent so far forward or backward that an acute angle forms between the fundus and the cervix. [EU] 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] Fluoridation: The addition of fluorine usually as a fluoride to something, as the adding of a fluoride to drinking water or public water supplies for prevention of tooth decay in children. [NIH] Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride to prevent dental caries. [NIH] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Fourth Ventricle: An irregularly shaped cavity in the rhombencephalon, between the medulla oblongata, the pons, and the isthmus in front, and the cerebellum behind. It is continuous with the central canal of the cord below and with the cerebral aqueduct above, and through its lateral and median apertures it communicates with the subarachnoid space. [NIH]

Friction: Surface resistance to the relative motion of one body against the rubbing, sliding, rolling, or flowing of another with which it is in contact. [NIH] Functional magnetic resonance imaging: A noninvasive tool used to observe functioning in the brain or other organs by detecting changes in chemical composition, blood flow, or both. [NIH]

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Fundus: The larger part of a hollow organ that is farthest away from the organ's opening. The bladder, gallbladder, stomach, uterus, eye, and cavity of the middle ear all have a fundus. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] GABA: The most common inhibitory neurotransmitter in the central nervous system. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma-Endorphin: An endogenous opioid peptide derived from the pro-opiomelanocortin precursor peptide. It differs from alpha-endorphin by one amino acid. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglioside: Protein kinase C's inhibitor which reduces ischemia-related brain damage. [NIH]

Gangrenous: A circumscribed, deep-seated, suppurative inflammation of the subcutaneous tissue of the eyelid discharging pus from several points. [NIH] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gas exchange: Primary function of the lungs; transfer of oxygen from inhaled air into the blood and of carbon dioxide from the blood into the lungs. [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastrin-Releasing Peptide: Neuropeptide and gut hormone that helps regulate gastric acid secretion and motor function. Once released from nerves in the antrum of the stomach, the neuropeptide stimulates release of gastrin from the G cells. [NIH] Gastroesophageal Reflux: Reflux of gastric juice and/or duodenal contents (bile acids, pancreatic juice) into the distal esophagus, commonly due to incompetence of the lower esophageal sphincter. Gastric regurgitation is an extension of this process with entry of fluid into the pharynx or mouth. [NIH] Gastroesophageal Reflux Disease: Flow of the stomach's contents back up into the esophagus. Happens when the muscle between the esophagus and the stomach (the lower

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esophageal sphincter) is weak or relaxes when it shouldn't. May cause esophagitis. Also called esophageal reflux or reflux esophagitis. [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

Genomics: The systematic study of the complete DNA sequences (genome) of organisms. [NIH]

Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Gestational Age: Age of the conceptus. In humans, this may be assessed by medical history, physical examination, early immunologic pregnancy tests, radiography, ultrasonography, and amniotic fluid analysis. [NIH] 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] Gliosis: The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]

Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glottis: The vocal apparatus of the larynx, consisting of the true vocal cords (plica vocalis) and the opening between them (rima glottidis). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamate Decarboxylase: A pyridoxal-phosphate protein that catalyzes the alphadecarboxylation of L-glutamic acid to form gamma-aminobutyric acid and carbon dioxide. The enzyme is found in bacteria and in invertebrate and vertebrate nervous systems. It is the rate-limiting enzyme in determining gaba levels in normal nervous tissues. The brain enzyme also acts on L-cysteate, L-cysteine sulfinate, and L-aspartate. EC 4.1.1.15. [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]

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Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]

Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]

Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycan: A type of long, unbranched polysaccharide molecule. Glycosaminoglycans are major structural components of cartilage and are also found in the cornea of the eye. [NIH] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Government Agencies: Administrative units of government responsible for policy making and management of governmental activities in the U.S. and abroad. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Gravis: Eruption of watery blisters on the skin among those handling animals and animal products. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Guanylate Cyclase: An enzyme that catalyzes the conversion of GTP to 3',5'-cyclic GMP and pyrophosphate. It also acts on ITP and dGTP. (From Enzyme Nomenclature, 1992) EC 4.6.1.2. [NIH] Habitat: An area considered in terms of its environment, particularly as this determines the type and quality of the vegetation the area can carry. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Haematoma: A localized collection of blood, usually clotted, in an organ, space, or tissue, due to a break in the wall of a blood vessel. [EU] Haemorrhage: The escape of blood from the vessels; bleeding. Small haemorrhages are

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classified according to size as petechiae (very small), purpura (up to 1 cm), and ecchymoses (larger). The massive accumulation of blood within a tissue is called a haematoma. [EU] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; 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] Head-Down Tilt: Posture while lying with the head lower than the rest of the body. Extended time in this position is associated with temporary physiologic disturbances. [NIH] Health Policy: Decisions, usually developed by government policymakers, for determining present and future objectives pertaining to the health care system. [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Heart Arrest: Sudden and usually momentary cessation of the heart beat. This sudden cessation may, but not usually, lead to death, sudden, cardiac. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Heat Stroke: A condition characterized by cessation of sweating, hot dry skin, delirium, collapse, and coma and resulting from prolonged exposure to high environmental temperature. [NIH] Hematopoiesis: The development and formation of various types of blood cells. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobin A: Normal adult human hemoglobin. The globin moiety consists of two alpha and two beta chains. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemosiderin: Molecule which can bind large numbers of iron atoms. [NIH] Hemosiderosis: Conditions in which there is a generalized increase in the iron stores of body tissues, particularly of liver and the reticuloendothelial system, without demonstrable

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tissue damage. The name refers to the presence of stainable iron in the tissue in the form of hemosiderin. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]

Hepatic: Refers to the liver. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heteroduplex Analysis: A method of detecting gene mutation by mixing PCR-amplified mutant and wild-type DNA followed by denaturation and reannealing. The resultant products are resolved by gel electrophoresis, with single base substitutions detectable under optimal electrophoretic conditions and gel formulations. Large base pair mismatches may also be analyzed by using electron microscopy to visualize heteroduplex regions. [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] Histology: The study of tissues and cells under a microscope. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homogeneous: Consisting of or composed of similar elements or ingredients; of a uniform quality throughout. [EU] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] 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] Hospice: Institution dedicated to caring for the terminally ill. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [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

228 Sudden Infant Death Syndrome

of brain substance loss from cerebral infarction and other conditions. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hypercapnia: A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood. [NIH] Hyperpnea: Increased ventilation in proportion to increased metabolism. [NIH] Hyperpyrexia: Exceptionally high fever either in comparison of the fever usually accompanying a particular disease or absolutely (as in heat stroke). [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] Hyperthermia: A type of treatment in which body tissue is exposed to high temperatures to damage and kill cancer cells or to make cancer cells more sensitive to the effects of radiation and certain anticancer drugs. [NIH] Hyperventilation: A pulmonary ventilation rate faster than is metabolically necessary for the exchange of gases. It is the result of an increased frequency of breathing, an increased tidal volume, or a combination of both. It causes an excess intake of oxygen and the blowing off of carbon dioxide. [NIH] Hypoplasia: Incomplete development or underdevelopment of an organ or tissue. [EU] Hypotension: Abnormally low blood pressure. [NIH] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [NIH] Hypotonia: A condition of diminished tone of the skeletal muscles; diminished resistance of muscles to passive stretching. [EU] Hypoventilation: A reduction in the amount of air entering the pulmonary alveoli. [NIH] Hypoxanthine: A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway. [NIH] Hypoxemia: Deficient oxygenation of the blood; hypoxia. [EU] Hypoxia: Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood. [EU] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH]

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Imaging procedures: Methods of producing pictures of areas inside the body. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immaturity: The state or quality of being unripe or not fully developed. [EU] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]

effects

of

foreign

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] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incompetence: Physical or mental inadequacy or insufficiency. [EU] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Incubation period: The period of time likely to elapse between exposure to the agent of the disease and the onset of clinical symptoms. [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU]

230 Sudden Infant Death Syndrome

Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant Care: Care of infants in the home or institution. [NIH] Infant Food: Food processed and manufactured for the nutritional health of children in their first year of life. [NIH] Infant Mortality: Perinatal, neonatal, and infant deaths in a given population. [NIH] Infant, Newborn: An infant during the first month after birth. [NIH] Infantile: Pertaining to an infant or to infancy. [EU] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]

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] 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] Inlay: In dentistry, a filling first made to correspond with the form of a dental cavity and then cemented into the cavity. [NIH] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. [NIH] Inotropic: Affecting the force or energy of muscular contractions. [EU] 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] Instillation: . [EU] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Intensive Care: Advanced and highly specialized care provided to medical or surgical

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patients whose conditions are life-threatening and require comprehensive care and constant monitoring. It is usually administered in specially equipped units of a health care facility. [NIH]

Intensive Care Units: Hospital units providing continuous surveillance and care to acutely ill patients. [NIH] Intercostal: Situated between the ribs. [EU] Intercostal Nerves: The ventral rami of the thoracic nerves from segments T1 through T11. The intercostal nerves supply motor and sensory innervation to the thorax and abdomen. The skin and muscles supplied by a given pair are called, respectively, a dermatome and a myotome. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intracranial 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] 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]

Involuntary: Reaction occurring without intention or volition. [NIH] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for channel gating can be a membrane potential, drug, transmitter, cytoplasmic messenger, or a mechanical deformation. Ion channels which are integral parts of ionotropic neurotransmitter receptors are not included. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH]

232 Sudden Infant Death Syndrome

Kainate: Glutamate receptor. [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 Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Laceration: 1. The act of tearing. 2. A torn, ragged, mangled wound. [EU] Lactation: The period of the secretion of milk. [EU] Lag: The time elapsing between application of a stimulus and the resulting reaction. [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] Laryngeal: Having to do with the larynx. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Lentivirus: A genus of the family Retroviridae consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species. [NIH] 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] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Library Services: Services offered to the library user. They include reference and circulation.

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[NIH]

Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] 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] Linkage Disequilibrium: Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone. [NIH] Lip: Either of the two fleshy, full-blooded margins of the mouth. [NIH] Lipid: Fat. [NIH] Lipophilic: Having an affinity for fat; pertaining to or characterized by lipophilia. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [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] Locus Coeruleus: Bluish region in the superior angle of the fourth ventricle floor, corresponding to melanin-like pigmented nerve cells which lie lateral to the pontomesencephalic central gray (griseum centrale). It is also known as nucleus pigmentosus pontis. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Lower Esophageal Sphincter: The muscle between the esophagus and stomach. When a person swallows, this muscle relaxes to let food pass from the esophagus to the stomach. It stays closed at other times to keep stomach contents from flowing back into the esophagus. [NIH]

Lycopene: A red pigment found in tomatoes and some fruits. [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).

234 Sudden Infant Death Syndrome

[NIH]

Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Mannans: Polysaccharides consisting of mannose units. [NIH] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Mastitis: Inflammatory disease of the breast, or mammary gland. [NIH] Median Nerve: A major nerve of the upper extremity. In humans, the fibers of the median nerve originate in the lower cervical and upper thoracic spinal cord (usually C6 to T1), travel via the brachial plexus, and supply sensory and motor innervation to parts of the forearm and hand. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH]

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Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Megaloblastic: A large abnormal red blood cell appearing in the blood in pernicious anaemia. [EU] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells. [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] Mental deficiency: A condition of arrested or incomplete development of mind from inherent causes or induced by disease or injury. [NIH] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mesencephalic: Ipsilateral oculomotor paralysis and contralateral tremor, spasm. or choreic movements of the face and limbs. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Mice Minute Virus: The type species of parvovirus prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [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]

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Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Micturition: The passage of urine; urination. [EU] Miscarriage: Spontaneous expulsion of the products of pregnancy before the middle of the second trimester. [NIH] Miscible: Susceptible of being mixed. [EU] 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] Modulator: A specific inductor that brings out characteristics peculiar to a definite region. [EU]

Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monogenic: A human disease caused by a mutation in a single gene. [NIH] Monophosphate: So called second messenger for neurotransmitters and hormones. [NIH] Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle. [NIH] Morphogenesis: The development of the form of an organ, part of the body, or organism. [NIH]

Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [NIH] Motor nerve: An efferent nerve conveying an impulse that excites muscular contraction. [NIH]

Motor Neurons: Neurons which activate muscle cells. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin

Dictionary 237

filaments slide inward among the myosin filaments. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] 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] Myasthenia: Muscular debility; any constitutional anomaly of muscle. [EU] Mycotoxins: Toxins derived from bacteria or fungi. [NIH] Myelin: The fatty substance that covers and protects nerves. [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] Myofibrils: Highly organized bundles of actin, myosin, and other proteins in the cytoplasm of skeletal and cardiac muscle cells that contract by a sliding filament mechanism. [NIH] Myoglobin: A conjugated protein which is the oxygen-transporting pigment of muscle. It is made up of one globin polypeptide chain and one heme group. [NIH] Myopathy: Any disease of a muscle. [EU] Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors. [NIH] Narcosis: A general and nonspecific reversible depression of neuronal excitability, produced by a number of physical and chemical aspects, usually resulting in stupor. [NIH] Narcotic: 1. Pertaining to or producing narcosis. 2. An agent that produces insensibility or stupor, applied especially to the opioids, i.e. to any natural or synthetic drug that has morphine-like actions. [EU] 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

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swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Needs Assessment: Systematic identification of a population's needs or the assessment of individuals to determine the proper level of services needed. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neonatal period: The first 4 weeks after birth. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephropathy: Disease of the kidneys. [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] Nerve Endings: Specialized terminations of peripheral neurons. Nerve endings include neuroeffector junction(s) by which neurons activate target organs and sensory receptors which transduce information from the various sensory modalities and send it centrally in the nervous system. Presynaptic nerve endings are presynaptic terminals. [NIH] Nerve Growth Factor: Nerve growth factor is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity. [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] Neural Pathways: Neural tracts connecting one part of the nervous system with another. [NIH]

Neuroanatomy: Study of the anatomy of the nervous system as a specialty or discipline. [NIH]

Neuroeffector Junction: The synapse between a neuron (presynaptic) and an effector cell other than another neuron (postsynaptic). Neuroeffector junctions include synapses onto muscles and onto secretory cells. [NIH] Neuroglia: The non-neuronal cells of the nervous system. They are divided into macroglia (astrocytes, oligodendroglia, and schwann cells) and microglia. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the blood-brain and blood-retina barriers, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH]

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Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neuronal Plasticity: The capacity of the nervous system to change its reactivity as the result of successive activations. [NIH] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neurophysiology: The scientific discipline concerned with the physiology of the nervous system. [NIH] Neurosecretory Systems: A system of neurons that has the specialized function to produce and secrete hormones, and that constitutes, in whole or in part, an endocrine organ or system. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotoxin: A substance that is poisonous to nerve tissue. [NIH] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neurotrophins: A nerve growth factor. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Niacin: Water-soluble vitamin of the B complex occurring in various animal and plant tissues. Required by the body for the formation of coenzymes NAD and NADP. Has pellagra-curative, vasodilating, and antilipemic properties. [NIH] Niacinamide: An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and pellagra. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake. [NIH] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] 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

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activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]

Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Obstetrics: A medical-surgical specialty concerned with management and care of women during pregnancy, parturition, and the puerperium. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [EU] Octreotide: A potent, long-acting somatostatin octapeptide analog which has a wide range of physiological actions. It inhibits growth hormone secretion, is effective in the treatment of hormone-secreting tumors from various organs, and has beneficial effects in the management of many pathological states including diabetes mellitus, orthostatic hypertension, hyperinsulinism, hypergastrinemia, and small bowel fistula. [NIH] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Oculomotor: Cranial nerve III. It originate from the lower ventral surface of the midbrain and is classified as a motor nerve. [NIH] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH] Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Ophthalmologic: Pertaining to ophthalmology (= the branch of medicine dealing with the eye). [EU]

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Opioid Peptides: The endogenous peptides with opiate-like activity. The three major classes currently recognized are the enkephalins, the dynorphins, and the endorphins. Each of these families derives from different precursors, proenkephalin, prodynorphin, and proopiomelanocortin, respectively. There are also at least three classes of opioid receptors, but the peptide families do not map to the receptors in a simple way. [NIH] Opium: The air-dried exudate from the unripe seed capsule of the opium poppy, Papaver somniferum, or its variant, P. album. It contains a number of alkaloids, but only a few morphine, codeine, and papaverine - have clinical significance. Opium has been used as an analgesic, antitussive, antidiarrheal, and antispasmodic. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]

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] Oropharynx: Oral part of the pharynx. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Ossification: The formation of bone or of a bony substance; the conversion of fibrous tissue or of cartilage into bone or a bony substance. [EU] 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] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] 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]

Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Oxygenase: Enzyme which breaks down heme, the iron-containing oxygen-carrying constituent of the red blood cells. [NIH] Oxygenation: The process of supplying, treating, or mixing with oxygen. No:1245 oxygenation the process of supplying, treating, or mixing with oxygen. [EU] Oxytocin: A nonapeptide posterior pituitary hormone that causes uterine contractions and stimulates lactation. [NIH] Pacemaker: An object or substance that influences the rate at which a certain phenomenon occurs; often used alone to indicate the natural cardiac pacemaker or an artificial cardiac pacemaker. In biochemistry, a substance whose rate of reaction sets the pace for a series of interrelated reactions. [EU] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate

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and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical antiinflammatory. It is also commonly used as an embedding material in histology. [NIH] Paraganglia, Chromaffin: Small bodies containing chromaffin cells occurring outside of the adrenal medulla, most commonly near the sympathetic ganglia and in organs such as the kidney, liver, heart and gonads. [NIH] Paralysis: Loss of ability to move all or part of the body. [NIH] Parathyroid: 1. Situated beside the thyroid gland. 2. One of the parathyroid glands. 3. A sterile preparation of the water-soluble principle(s) of the parathyroid glands, ad-ministered parenterally as an antihypocalcaemic, especially in the treatment of acute hypoparathyroidism with tetany. [EU] Parathyroid Glands: Two small paired endocrine glands in the region of the thyroid gland. They secrete parathyroid hormone and are concerned with the metabolism of calcium and phosphorus. [NIH] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Particle: A tiny mass of material. [EU] Parturition: The act or process of given birth to a child. [EU] Parvovirus: A genus of the family Parvoviridae, subfamily Parvovirinae, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is mice minute virus. [NIH] Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]

Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

Pelvic: Pertaining to the pelvis. [EU]

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Penicillin: An antibiotic drug used to treat infection. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Pertussis: An acute, highly contagious infection of the respiratory tract, most frequently affecting young children, usually caused by Bordetella pertussis; a similar illness has been associated with infection by B. parapertussis and B. bronchiseptica. It is characterized by a catarrhal stage, beginning after an incubation period of about two weeks, with slight fever, sneezing, running at the nose, and a dry cough. In a week or two the paroxysmal stage begins, with the characteristic paroxysmal cough, consisting of a deep inspiration, followed by a series of quick, short coughs, continuing until the air is expelled from the lungs; the close of the paroxysm is marked by a long-drawn, shrill, whooping inspiration, due to spasmodic closure of the glottis. This stage lasts three to four weeks, after which the convalescent stage begins, in which paroxysms grow less frequent and less violent, and finally cease. Called also whooping cough. [EU] Petechiae: Pinpoint, unraised, round red spots under the skin caused by bleeding. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Pharmaceutical Preparations: Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form. [NIH] 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

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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] 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] Phosphorylase: An enzyme of the transferase class that catalyzes the phosphorylysis of a terminal alpha-1,4-glycosidic bond at the non-reducing end of a glycogen molecule, releasing a glucose 1-phosphate residue. Phosphorylase should be qualified by the natural substance acted upon. EC 2.4.1.1. [NIH] Photoperiod: The time period of daily exposure that an organism receives from daylight or artificial light. It is believed that photoperiodic responses may affect the control of energy balance and thermoregulation. [NIH] Phrenic Nerve: The motor nerve of the diaphragm. The phrenic nerve fibers originate in the cervical spinal column (mostly C4) and travel through the cervical plexus to the diaphragm. [NIH]

Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]

Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pineal Body: A small conical midline body attached to the posterior part of the third ventricle and lying between the superior colliculi, below the splenium of the corpus callosum. [NIH] Pineal gland: A tiny organ located in the cerebrum that produces melatonin. Also called pineal body or pineal organ. [NIH] Pitch: The subjective awareness of the frequency or spectral distribution of a sound. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH]

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Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasticity: In an individual or a population, the capacity for adaptation: a) through gene changes (genetic plasticity) or b) through internal physiological modifications in response to changes of environment (physiological plasticity). [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]

Plethysmograph: An instrument for measuring swelling or expansion of the body or part of it, such as a limb or digit, commonly used for the indirect measurement of blood flow or other displacement of internal fluids. [NIH] Plethysmography: Recording of change in the size of a part as modified by the circulation in it. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Policy Making: The decision process by which individuals, groups or institutions establish policies pertaining to plans, programs or procedures. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] 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] Pontine: A brain region involved in the detection and processing of taste. [NIH] Porphyrins: A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin. [NIH]

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Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Postural: Pertaining to posture or position. [EU] 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] Potassium Channels: Cell membrane glycoproteins selective for potassium ions. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precipitating Factors: Factors associated with the definitive onset of a disease, illness, accident, behavioral response, or course of action. Usually one factor is more important or more obviously recognizable than others, if several are involved, and one may often be regarded as "necessary". Examples include exposure to specific disease; amount or level of an infectious organism, drug, or noxious agent, etc. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] Pregnancy Tests: Tests to determine whether or not an individual is pregnant. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prenatal Care: Care provided the pregnant woman in order to prevent complications, and decrease the incidence of maternal and prenatal mortality. [NIH] Pressoreceptors: Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls. [NIH] Presumptive: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Presynaptic Terminals: The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the

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central and peripheral nervous systems are included. [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] 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] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prone Position: The posture of an individual lying face down. [NIH] Pro-Opiomelanocortin: A precursor protein, MW 30,000, synthesized mainly in the anterior pituitary gland but also found in the hypothalamus, brain, and several peripheral tissues. It incorporates the amino acid sequences of ACTH and beta-lipotropin. These two hormones, in turn, contain the biologically active peptides MSH, corticotropin-like intermediate lobe peptide, alpha-lipotropin, endorphins, and methionine enkephalin. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandins: A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteoglycans: Glycoproteins which have a very high polysaccharide content. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with

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formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Proxy: A person authorized to decide or act for another person, for example, a person having durable power of attorney. [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]

Puerperium: Period from delivery of the placenta until return of the reproductive organs to their normal nonpregnant morphologic state. In humans, the puerperium generally lasts for six to eight weeks. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Alveoli: Small polyhedral outpouchings along the walls of the alveolar sacs, alveolar ducts and terminal bronchioles through the walls of which gas exchange between alveolar air and pulmonary capillary blood takes place. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Ventilation: The total volume of gas per minute inspired or expired measured in liters per minute. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]

Purpura: Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. [NIH] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [NIH] Pyrogenic: Inducing fever. [EU] 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

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sufficiently so as to achieve the status of a taxon. [NIH] Radar: A system using beamed and reflected radio signals to and from an object in such a way that range, bearing, and other characteristics of the object may be determined. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radioactive: Giving off radiation. [NIH] Radiography: Examination of any part of the body for diagnostic purposes by means of roentgen rays, recording the image on a sensitized surface (such as photographic film). [NIH] 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] 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] Raphe Nuclei: Collections of small neurons centrally scattered among many fibers from the level of the trochlear nucleus in the midbrain to the hypoglossal area in the medulla oblongata. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflective: Capable of throwing back light, images, sound waves : reflecting. [EU] Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord. [NIH] Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regurgitation: A backward flowing, as the casting up of undigested food, or the backward

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flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] 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] Reproduction Techniques: Methods pertaining to the generation of new individuals. [NIH] Reproductive system: In women, this system includes the ovaries, the fallopian tubes, the uterus (womb), the cervix, and the vagina (birth canal). The reproductive system in men includes the prostate, the testes, and the penis. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Research Support: Financial support of research activities. [NIH] 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] Respiratory distress syndrome: A lung disease that occurs primarily in premature infants; the newborn must struggle for each breath and blueing of its skin reflects the baby's inability to get enough oxygen. [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Respiratory Muscles: These include the muscles of the diaphragm and the intercostal muscles. [NIH] Respiratory Physiology: Functions and activities of the respiratory tract as a whole or of any of its parts. [NIH] Respiratory syncytial virus: RSV. A virus that causes respiratory infections with cold-like symptoms. [NIH] Respiratory System: The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Reticular: Coarse-fibered, netlike dermis layer. [NIH] Reticular Formation: A region extending from the pons & medulla oblongata through the mesencephalon, characterized by a diversity of neurons of various sizes and shapes, arranged in different aggregations and enmeshed in a complicated fiber network. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal

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combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retrograde: 1. Moving backward or against the usual direction of flow. 2. Degenerating, deteriorating, or catabolic. [EU] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Riboflavin: Nutritional factor found in milk, eggs, malted barley, liver, kidney, heart, and leafy vegetables. The richest natural source is yeast. It occurs in the free form only in the retina of the eye, in whey, and in urine; its principal forms in tissues and cells are as FMN and FAD. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Rickets: A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles, and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. [EU] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Rigor Mortis: Muscular rigidity which develops in the cadaver usually from 4 to 10 hours after death and lasts 3 or 4 days. [NIH] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] 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] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Second Messenger Systems: Systems in which an intracellular signal is generated in response to an intercellular primary messenger such as a hormone or neurotransmitter. They are intermediate signals in cellular processes such as metabolism, secretion,

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contraction, phototransduction, and cell growth. Examples of second messenger systems are the adenyl cyclase-cyclic AMP system, the phosphatidylinositol diphosphate-inositol triphosphate system, and the cyclic GMP system. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Secretory Vesicles: Vesicles derived from the golgi apparatus containing material to be released at the cell surface. [NIH] Sedative: 1. Allaying activity and excitement. 2. An agent that allays excitement. [EU] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] 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] Sensory Deprivation: The absence or restriction of the usual external sensory stimuli to which the individual responds. [NIH] 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] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] 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] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Shivering: Involuntary contraction or twitching of the muscles. It is a physiologic method of heat production in man and other mammals. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral

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upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]

Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Silicon: A trace element that constitutes about 27.6% of the earth's crust in the form of silicon dioxide. It does not occur free in nature. Silicon has the atomic symbol Si, atomic number 14, and atomic weight 28.09. [NIH] Silicon Dioxide: Silica. Transparent, tasteless crystals found in nature as agate, amethyst, chalcedony, cristobalite, flint, sand, quartz, and tridymite. The compound is insoluble in water or acids except hydrofluoric acid. [NIH] Single Parent: A natural, adoptive, or substitute parent of a dependent child, who lives with only one parent. The single parent may live with or visit the child. The concept includes the never-married, as well as the divorced and widowed. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Skull Base: The inferior region of the skull consisting of an internal (cerebral), and an external (basilar) surface. [NIH] Skull Fracture, Depressed: A skull fracture characterized by inward depression of a fragment or section of cranial bone, often compressing the underlying dura mater and brain. Depressed cranial fractures which feature open skin wounds that communicate with skull fragments are referred to as compound depressed skull fractures. [NIH] Skull Fractures: Fractures of the skull which may result from penetrating or nonpenetrating head injuries or rarely bone diseases (see also fractures, spontaneous). skull fractures may be classified by location (e.g., skull fracture, basilar), radiographic appearance (e.g., linear), or based upon cranial integrity (e.g., skull fracture, depressed). [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Sleep Apnea Syndromes: Disorders characterized by multiple cessations of respirations

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during sleep that induce partial arousals and interfere with the maintenance of sleep. Sleep apnea syndromes are divided into central (sleep apena, central), obstructive (sleep apnea, obstructive), and mixed central-obstructive types. [NIH] Sleep Deprivation: The state of being deprived of sleep under experimental conditions, due to life events, or from a wide variety of pathophysiologic causes such as medication effect, chronic illness, psychiatric illness, or sleep disorder. [NIH] Sleep Stages: Periods of sleep manifested by changes in EEG activity and certain behavioral correlates; includes Stage 1: sleep onset, drowsy sleep; Stage 2: light sleep; Stages 3 and 4: delta sleep, light sleep, deep sleep, telencephalic sleep. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Snoring: Rough, noisy breathing during sleep, due to vibration of the uvula and soft palate. [NIH]

Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Cyanide: Na(CN). A highly poisonous compound that is an inhibitor of many metabolic processes and is used as a test reagent for the function of chemoreceptors. It is also used in many industrial processes. [NIH] Solitary Nucleus: Gray matter located in the dorsomedial part of the medulla oblongata associated with the solitary tract. The solitary nucleus receives inputs from most organ systems including the terminations of the facial, glossopharyngeal, and vagus nerves. It is a major coordinator of autonomic nervous system regulation of cardiovascular, respiratory, gustatory, gastrointestinal, and chemoreceptive aspects of homeostasis. The solitary nucleus is also notable for the large number of neurotransmitters which are found therein. [NIH] 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] Somatostatin: A polypeptide hormone produced in the hypothalamus, and other tissues and organs. It inhibits the release of human growth hormone, and also modulates important physiological functions of the kidney, pancreas, and gastrointestinal tract. Somatostatin receptors are widely expressed throughout the body. Somatostatin also acts as a neurotransmitter in the central and peripheral nervous systems. [NIH] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH]

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Spasmodic: Of the nature of a spasm. [EU] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] 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] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] Spike: The activation of synapses causes changes in the permeability of the dendritic membrane leading to changes in the membrane potential. This difference of the potential travels along the axon of the neuron and is called spike. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Spores: The reproductive elements of lower organisms, such as protozoa, fungi, and cryptogamic plants. [NIH] 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] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]

Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between

256 Sudden Infant Death Syndrome

the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] 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] Stupor: Partial or nearly complete unconsciousness, manifested by the subject's responding only to vigorous stimulation. Also, in psychiatry, a disorder marked by reduced responsiveness. [EU] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substrate: A substance upon which an enzyme acts. [EU] Sudden cardiac death: Cardiac arrest caused by an irregular heartbeat. [NIH] Sudden death: Cardiac arrest caused by an irregular heartbeat. The term "death" is somewhat misleading, because some patients survive. [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] Supine: Having the front portion of the body upwards. [NIH] Supine Position: The posture of an individual lying face up. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] 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]

Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic

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nervous system. Called also adrenergic. [EU] Symphysis: A secondary cartilaginous joint. [NIH] Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate through direct electrical connections which are sometimes called electrical synapses; these are not included here but rather in gap junctions. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synaptic Vesicles: Membrane-bound compartments which contain transmitter molecules. Synaptic vesicles are concentrated at presynaptic terminals. They actively sequester transmitter molecules from the cytoplasm. In at least some synapses, transmitter release occurs by fusion of these vesicles with the presynaptic membrane, followed by exocytosis of their contents. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Synostosis: The joining of contiguous and separate bones by osseous tissue. [NIH] Systemic: Affecting the entire body. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Talc: A native magnesium silicate. [NIH] Taurine: 2-Aminoethanesulfonic acid. A conditionally essential nutrient, important during mammalian development. It is present in milk but is isolated mostly from ox bile and strongly conjugates bile acids. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Tetani: Causal agent of tetanus. [NIH] Tetanic: Having the characteristics of, or relating to tetanus. [NIH] Tetanus: A disease caused by tetanospasmin, a powerful protein toxin produced by Clostridium tetani. Tetanus usually occurs after an acute injury, such as a puncture wound

258 Sudden Infant Death Syndrome

or laceration. Generalized tetanus, the most common form, is characterized by tetanic muscular contractions and hyperreflexia. Localized tetanus presents itself as a mild condition with manifestations restricted to muscles near the wound. It may progress to the generalized form. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [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] Thermogenesis: The generation of heat in order to maintain body temperature. The uncoupled oxidation of fatty acids contained within brown adipose tissue and shivering are examples of thermogenesis in mammals. [NIH] Thermoregulation: Heat regulation. [EU] Thiamine: 3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2methylthiazolium chloride. [NIH]

hydroxyethyl)-4-

Third Ventricle: A narrow cleft inferior to the corpus callosum, within the diencephalon, between the paired thalami. Its floor is formed by the hypothalamus, its anterior wall by the lamina terminalis, and its roof by ependyma. It communicates with the fourth ventricle by the cerebral aqueduct, and with the lateral ventricles by the interventricular foramina. [NIH] Thoracic: Having to do with the chest. [NIH] Thoracic Nerves: The twelve spinal nerves on each side of the thorax. They include eleven intercostal nerves and one subcostal nerve. Both sensory and motor, they supply the muscles and skin of the thoracic and abdominal walls. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called 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] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation,

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contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [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] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroid Hormones: Hormones secreted by the thyroid gland. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tidal Volume: The volume of air inspired or expired during each normal, quiet respiratory cycle. Common abbreviations are TV or V with subscript T. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tonic: 1. Producing and restoring the normal tone. 2. Characterized by continuous tension. 3. A term formerly used for a class of medicinal preparations believed to have the power of restoring normal tone to tissue. [EU] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Tracer: A substance (such as a radioisotope) used in imaging procedures. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH]

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Traction: The act of pulling. [NIH] Tractus: A part of some structure, usually that part along which something passes. [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] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Tremor: Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of cerebellar diseases, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of Parkinson disease. [NIH] Trigeminal: Cranial nerve V. It is sensory for the eyeball, the conjunctiva, the eyebrow, the skin of face and scalp, the teeth, the mucous membranes in the mouth and nose, and is motor to the muscles of mastication. [NIH] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods. [NIH] Trophic: Of or pertaining to nutrition. [EU] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] 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] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] Tubulin: A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from sperm flagella, cilia, and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to colchicine, vincristine, and vinblastine. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulceration: 1. The formation or development of an ulcer. 2. An ulcer. [EU] Ultrasonography: The visualization of deep structures of the body by recording the

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reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Urban Population: The inhabitants of a city or town, including metropolitan areas and suburban areas. [NIH] Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urinary tract infection: An illness caused by harmful bacteria growing in the urinary tract. [NIH]

Urinate: To release urine from the bladder to the outside. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterine Contraction: Contraction of the uterine muscle. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Uvula: Uvula palatinae; specifically, the tongue-like process which projects from the middle of the posterior edge of the soft palate. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vagal: Pertaining to the vagus nerve. [EU] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx). [NIH] 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] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular Resistance: An expression of the resistance offered by the systemic arterioles, and to a lesser extent by the capillaries, to the flow of blood. [NIH]

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Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which constriction, pathologic is used. [NIH] Vasodilatation: A state of increased calibre of the blood vessels. [EU] Vasodilator: An agent that widens blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venom: That produced by the poison glands of the mouth and injected by the fangs of poisonous snakes. [NIH] Venous: Of or pertaining to the veins. [EU] Ventilation: 1. In respiratory physiology, the process of exchange of air between the lungs and the ambient air. Pulmonary ventilation (usually measured in litres per minute) refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, in which gas exchange with the blood takes place. 2. In psychiatry, verbalization of one's emotional problems. [EU] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Vertebrae: A bony unit of the segmented spinal column. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Afferents: The sensory fibers innervating the viscera. [NIH] Vitamin A: A substance used in cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Vitreous Humor: The transparent, colorless mass of gel that lies behind the lens and in front of the retina and fills the center of the eyeball. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation

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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] Void: To urinate, empty the bladder. [NIH] Volition: Voluntary activity without external compulsion. [NIH] Voltage-gated: It is opened by the altered charge distribution across the cell membrane. [NIH]

Wakefulness: A state in which there is an enhanced potential for sensitivity and an efficient responsiveness to external stimuli. [NIH] Weight Gain: Increase in body weight over existing weight. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]

Whooping Cough: A respiratory infection caused by Bordetella pertussis and characterized by paroxysmal coughing ending in a prolonged crowing intake of breath. [NIH] Whooping Cough: A respiratory infection caused by Bordetella pertussis and characterized by paroxysmal coughing ending in a prolonged crowing intake of breath. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] 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]

265

INDEX A Abdomen, 114, 199, 207, 211, 231, 233, 242, 255, 258, 261 Abdominal, 199, 213, 216, 242, 258 Ablation, 38, 199 Acceptor, 199, 241 Accommodation, 116, 199 Acetylcholine, 7, 11, 199, 211, 239 Acidosis, 9, 12, 199 Acoustic, 76, 125, 126, 129, 199 Actin, 199, 236, 237 Acyl, 5, 20, 63, 71, 93, 100, 199 Adaptation, 8, 199, 245 Adenine, 22, 199, 205 Adenosine, 15, 22, 199, 208, 228, 244 Adipose Tissue, 199, 258 Adjustment, 199 Adrenal Medulla, 199, 209, 212, 219, 240, 242 Adrenergic, 200, 217, 219, 256 Adverse Effect, 200, 253 Aerobic, 200, 236 Aetiology, 60, 68, 200 Afferent, 30, 38, 45, 200 Affinity, 30, 114, 200, 204, 233, 238, 254 Age Groups, 15, 200 Aged, 80 and Over, 200 Agonist, 15, 31, 200, 217, 237, 239 Airway, 14, 25, 42, 86, 98, 200, 253 Airway Obstruction, 14, 42, 200 Airway Resistance, 86, 200 Alertness, 117, 133, 200, 208 Algorithms, 200, 206 Alkaline, 199, 200, 201, 208 Alkaloid, 200, 213, 236, 239 Alleles, 38, 200, 233 Alpha Particles, 200, 249 Alternative medicine, 158, 200 Alveoli, 201, 262 Amino Acid Sequence, 201, 202, 205, 247 Amino Acids, 135, 136, 201, 205, 239, 240, 243, 245, 247, 256, 261 Amino Acids, Essential, 135, 136, 201 Ammonia, 201, 224, 261 Amniotic Fluid, 201, 224 Amphetamines, 201, 213 Anaerobic, 29, 201 Anaesthesia, 74, 201, 230

Anal, 40, 118, 201, 233 Analgesic, 201, 219, 236, 241 Analog, 201, 240 Analogous, 28, 201, 260 Anaphylactic, 58, 201 Anaphylatoxins, 201, 213 Anaphylaxis, 114, 201 Anatomical, 31, 39, 115, 201, 206, 214, 229, 251 Anemia, 127, 170, 202, 222 Anesthesia, 44, 200, 202 Animal model, 98, 202 Ankle, 117, 202 Anoxia, 6, 23, 202 Antagonism, 16, 202, 208 Antecedent, 10, 87, 107, 202 Anterograde, 22, 202 Anthropology, 60, 202 Antiarrhythmic, 8, 202 Antibacterial, 202, 255 Antibiotic, 127, 202, 243, 255 Antibodies, 114, 127, 137, 202, 203, 226, 229, 234, 245 Antibody, 28, 29, 42, 58, 114, 137, 200, 202, 213, 226, 227, 229, 230, 234, 255 Anticoagulant, 202, 247 Antigen, 137, 200, 201, 202, 203, 213, 227, 228, 229, 230, 234 Antigen-Antibody Complex, 202, 213 Anti-infective, 202, 228, 231 Anti-inflammatory, 202, 242 Antimony, 50, 63, 92, 203 Antioxidant, 135, 203 Antiserum, 137, 203 Anus, 201, 203, 207 Apnoea, 101, 112, 203 Apoptosis, 63, 76, 203 Applicability, 22, 203 Aqueous, 203, 205, 215, 228, 232 Arachidonic Acid, 78, 93, 203, 232, 247 Arcuate Nucleus, 11, 24, 43, 44, 51, 55, 203 Arginine, 201, 203, 239 Aromatic, 203, 244 Arrhythmia, 7, 8, 20, 27, 119, 202, 203 Arterial, 27, 33, 35, 43, 45, 60, 63, 203, 210, 228, 247, 257 Arteries, 9, 74, 203, 206, 214, 235, 259 Artifacts, 130, 203

266 Sudden Infant Death Syndrome

Ascorbic Acid, 137, 203 Aseptic, 203, 241 Aspartate, 14, 204, 224 Asphyxia, 23, 25, 44, 204 Aspiration, 17, 64, 85, 204 Assay, 113, 114, 204, 229 Astrocytes, 204, 224, 238 Ataxia, 169, 170, 204, 227, 258 Atmospheric Pressure, 124, 204 Atrophy, 169, 204 Attenuated, 12, 38, 204 Audiology, 97, 204 Auditory, 98, 99, 100, 101, 204, 220, 261 Autoimmune disease, 204, 236 Autonomic, 11, 18, 19, 28, 30, 36, 38, 43, 55, 81, 94, 99, 199, 204, 240, 243, 254, 256 Autonomic Nervous System, 18, 36, 43, 81, 204, 243, 254, 256 Autonomic Pathways, 38, 204 Autopsy, 47, 115, 125, 126, 146, 178, 184, 204 Autoreceptors, 28, 204 Axons, 204, 243, 246 B Bacteria, 72, 199, 202, 205, 219, 220, 221, 224, 235, 237, 255, 260, 261 Bacterial Physiology, 199, 205 Bacterial toxin, 60, 68, 84, 205 Bacteriophage, 205, 260 Bacterium, 29, 205 Baroreflex, 43, 205 Basal Ganglia, 204, 205, 207 Basal Ganglia Diseases, 204, 205 Base, 19, 116, 129, 199, 205, 216, 220, 227, 232, 257 Base Pair Mismatch, 205, 227 Basement Membrane, 87, 205, 220, 232 Bereavement, 3, 98, 100, 150, 151, 159, 182, 205 Beta-Endorphin, 52, 205 Bile, 205, 206, 223, 233, 257 Bile Acids, 206, 223, 257 Binding agent, 114, 206 Binding Sites, 93, 206 Biochemical, 6, 20, 42, 93, 200, 206, 252 Bioengineering, 41, 164, 206 Biological therapy, 206, 225 Biosynthesis, 203, 206 Biotechnology, 45, 46, 149, 158, 165, 168, 169, 170, 206 Biotin, 137, 206 Biphasic, 44, 206

Bladder, 206, 223, 229, 236, 247, 261, 263 Blood Coagulation, 206, 208, 222, 258 Blood Glucose, 206, 226 Blood Platelets, 206, 252 Blood pressure, 25, 26, 27, 34, 35, 43, 44, 119, 205, 206, 209, 211, 228, 236, 254 Blood vessel, 205, 206, 209, 212, 219, 224, 225, 231, 243, 254, 256, 257, 258, 261, 262 Body Fluids, 206, 217, 254 Body Mass Index, 79, 206, 241 Body Regions, 206, 213 Bone Marrow, 207, 229, 234, 255 Boron, 137, 207 Boron Neutron Capture Therapy, 207 Bowel, 181, 201, 207, 216, 231, 240, 256 Bowel Movement, 181, 207, 216, 256 Brachial, 207, 234 Brachial Plexus, 207, 234 Bradycardia, 36, 43, 124, 130, 207 Bradykinin, 207, 239 Brain Hypoxia, 24, 27, 207, 258 Brain Neoplasms, 207, 227, 258 Brain Stem, 87, 101, 207 Branch, 159, 180, 195, 207, 218, 240, 242, 248, 255, 258 Breakdown, 207, 216, 223 Breast Feeding, 143, 207 Bronchi, 207, 219, 259 Bronchial, 207, 208 Bronchioles, 201, 207, 248 Bronchiolitis, 59, 207 Bronchiseptica, 207, 243 Bronchopulmonary, 36, 208 Bronchopulmonary Dysplasia, 36, 208 Buffers, 205, 208 C Cadaver, 208, 251 Caffeine, 66, 92, 208 Calcium, 6, 7, 23, 33, 35, 93, 137, 208, 213, 242, 253 Calcium Channels, 8, 35, 208 Calpain, 139, 208 Capsid, 19, 208 Carbohydrates, 208, 210 Carcinogenic, 208, 230, 240, 247 Carcinogens, 208, 212, 240 Cardiac arrest, 22, 99, 209, 256 Cardiac Output, 205, 209 Cardiomyopathy, 98, 139, 209 Cardiopulmonary, 7, 11, 19, 30, 39, 99, 115, 121, 209

Index 267

Cardiopulmonary Resuscitation, 99, 121, 209 Cardiorespiratory, 10, 11, 18, 19, 24, 26, 27, 28, 33, 34, 36, 38, 43, 44, 105, 107, 209 Cardiovascular, 10, 20, 25, 27, 30, 32, 43, 99, 136, 208, 209, 232, 252, 254 Cardiovascular Abnormalities, 10, 209 Cardiovascular System, 209 Carnitine, 100, 137, 209 Carotid Body, 7, 12, 24, 38, 45, 209, 211 Carotid Sinus, 35, 209, 246 Carpal Tunnel Syndrome, 139, 209 Case report, 209, 221 Catecholamine, 33, 209, 217 Caudal, 25, 44, 209, 216, 228, 246 Causal, 7, 209, 214, 252, 257 Cause of Death, 13, 36, 108, 112, 118, 124, 129, 188, 209 Cell Death, 203, 210, 238 Cell Division, 169, 205, 210, 225, 235, 236, 244, 247 Cell membrane, 15, 135, 136, 208, 210, 216, 223, 244, 246, 263 Cell Respiration, 210, 236, 250 Cell Survival, 210, 225 Cell Transplantation, 210 Cellobiose, 210 Cellulose, 41, 208, 210, 223, 244 Central Nervous System Infections, 210, 226, 227 Cerebellar, 204, 210, 249, 260 Cerebral, 52, 75, 99, 100, 204, 205, 207, 210, 214, 220, 222, 227, 253, 258 Cerebral hemispheres, 205, 207, 210 Cerebral Infarction, 210, 228 Cerebrospinal, 12, 52, 87, 210, 227 Cerebrospinal fluid, 12, 52, 87, 210, 227 Cerebrum, 210, 244, 260 Cervical, 56, 100, 101, 115, 207, 210, 211, 234, 244 Cervical Plexus, 211, 244 Cervix, 210, 211, 222, 250 Character, 115, 211, 215 Chemoreceptor, 6, 7, 12, 25, 27, 36, 38, 44, 211 Chemotactic Factors, 211, 213 Chest cavity, 132, 211 Chest wall, 114, 211 Child Care, 4, 13, 77, 142, 143, 144, 145, 146, 151, 154, 175, 176, 178, 181, 182, 183, 186, 211 Chiropractic, 101, 102, 211

Chloral Hydrate, 211 Chloralose, 28, 211 Chlorophyll, 211, 223 Cholecystokinin, 11, 211 Cholera, 211, 252 Choline, 11, 137, 211 Cholinergic, 16, 33, 211, 239 Chondroitin sulfate, 137, 211 Chromaffin Cells, 33, 212, 242 Chromaffin System, 212, 219 Chromatin, 203, 212 Chromic, 212 Chromium, 137, 212 Chromosome, 212, 233 Chronic renal, 212, 245 Circadian, 123, 212 Circadian Rhythm, 123, 212 Circulatory system, 212, 219 Citrus, 203, 212 Clamp, 7, 8, 9, 15, 17, 22, 24, 212 Clinical Medicine, 212, 246 Clinical trial, 5, 107, 108, 165, 212, 214, 248, 249 Clone, 8, 212 Cloning, 206, 212 Coca, 212, 213 Cocaine, 9, 212, 213 Coenzyme, 203, 213, 239 Cofactor, 213, 247, 258 Colic, 93, 213 Collagen, 205, 213, 221, 222, 224, 245 Collapse, 116, 117, 201, 207, 213, 226, 253 Complement, 41, 201, 213, 214, 234 Complementary and alternative medicine, 97, 104, 136, 213 Complementary medicine, 97, 214 Computational Biology, 165, 168, 214 Conception, 214, 221, 246 Confounder, 49, 214 Confusion, 214 Congestive heart failure, 139, 214 Conjugated, 28, 214, 237 Conjunctiva, 214, 260 Connective Tissue, 203, 207, 213, 214, 222, 223, 224, 233, 243 Consciousness, 201, 214, 216, 217 Constitutional, 214, 237 Constriction, 214, 231, 262 Constriction, Pathologic, 214, 262 Consumption, 66, 214, 216, 241 Contraindications, ii, 214 Contralateral, 122, 214, 235, 241, 249

268 Sudden Infant Death Syndrome

Controlled study, 41, 214 Convulsions, 61, 214 Coordination, 122, 214, 236 Coronary, 60, 214, 215, 235 Coronary Thrombosis, 215, 235 Cortex, 75, 100, 103, 204, 215, 220, 249 Cortical, 35, 52, 215, 220, 252, 258 Cranial, 41, 121, 215, 226, 231, 240, 243, 253, 260, 261 Craniocerebral Trauma, 205, 215, 226, 227, 258 Curative, 215, 239, 251, 258 Cyclic, 93, 208, 215, 225, 240, 245, 252 Cysteine, 208, 215, 224, 256 Cytoplasm, 203, 210, 215, 237, 257 Cytoskeletal Proteins, 208, 215 Cytoskeleton, 215, 236 D Data Collection, 30, 215 Databases, Bibliographic, 165, 215 Day Care, 142, 215 Deamination, 205, 215, 261 Decarboxylation, 215, 224 Decompression, 215, 217 Defibrillation, 121, 215 Degenerative, 135, 136, 215, 224 Deletion, 203, 216 Dementia, 139, 216 Denaturation, 216, 227 Dendrites, 216, 239 Dendritic, 51, 56, 216, 235, 255 Density, 13, 29, 48, 69, 93, 206, 216, 240, 254 Depolarization, 7, 26, 35, 216, 253 Deprivation, 56, 82, 139, 216 Developed Countries, 36, 216 Diabetes Mellitus, 137, 216, 226, 240 Diagnostic procedure, 111, 158, 216 Diaphragm, 15, 211, 216, 244, 250 Diastolic, 216, 228 Diencephalon, 216, 228, 258 Digestion, 206, 207, 216, 231, 233, 255 Digestive system, 109, 216 Dilatation, 216, 247 Dilation, 207, 216, 227 Diphtheria, 87, 216 Direct, iii, 19, 22, 28, 38, 134, 212, 216, 217, 249, 257 Discrimination, 125, 216 Disparity, 84, 217 Dissociation, 200, 217, 231 Distal, 217, 218, 223, 246, 248

Diuresis, 208, 217 Diurnal, 122, 217 Diving, 42, 217 Dopamine, 123, 213, 217, 244 Dorsal, 43, 217, 246, 255 Dorsum, 217 Drive, ii, vi, 33, 35, 91, 142, 143, 159, 177, 178, 183, 217 Drug Interactions, 217 Drug Tolerance, 217, 259 Duct, 73, 217, 220, 251 Duke, 71, 92, 93, 217 Duodenum, 205, 217, 242, 256 Dyes, 217, 222 Dynorphins, 217, 241 Dysostosis, 121, 218 Dysplasia, 170, 218 Dystrophy, 169, 218 E Effector, 30, 199, 213, 218, 238, 239 Effector cell, 218, 238, 239 Efficacy, 11, 31, 42, 218 Elasticity, 117, 218 Elastin, 213, 218, 221 Elective, 218 Electric shock, 120, 209, 215, 218 Electrocardiogram, 124, 130, 218 Electrode, 7, 120, 218 Electroencephalography, 13, 41, 218 Electrolyte, 218, 246, 254 Electrons, 203, 205, 218, 231, 241, 249 Electrophoresis, 218, 227 Electrophysiological, 27, 218 Embryo, 218, 230, 246, 255 Embryo Transfer, 218, 246 Endocardium, 16, 219 Endocrine Glands, 219, 242 Endocrine System, 7, 219 Endorphin, 205, 219, 223 Endothelial cell, 219, 222, 258 Endothelium, 219, 239 Endothelium-derived, 219, 239 Endotoxin, 58, 219 End-stage renal, 212, 219, 245 Energy balance, 219, 244 Enkephalin, 205, 219, 247 Enterovirus, 79, 219 Enuresis, 116, 219 Environmental Exposure, 20, 138, 219, 240 Environmental Health, 7, 164, 166, 219 Environmental tobacco smoke, 41, 219 Enzymatic, 208, 213, 219, 250

Index 269

Enzyme, 20, 33, 59, 114, 137, 213, 218, 219, 224, 225, 235, 241, 244, 247, 253, 256, 258, 262, 263 Ependyma, 203, 219, 258 Epidemiological, 37, 42, 52, 59, 65, 79, 82, 87, 92, 103, 107, 127, 138, 219, 221 Epinephrine, 200, 212, 217, 219, 240, 260 Epithelial, 56, 61, 86, 220, 227, 232 Epithelial Cells, 56, 61, 220, 227, 232 Epithelium, 205, 219, 220 Erythrocytes, 202, 207, 208, 220, 249 Esophageal, 220, 224 Esophagitis, 220, 224 Esophagus, 216, 220, 223, 233, 243, 249, 256 Essential Tremor, 169, 220 Evoke, 220, 255 Evoked Potentials, 99, 220 Excipients, 132, 133, 220 Excitability, 24, 220, 237 Excitation, 7, 24, 27, 201, 211, 220 Excitatory, 14, 23, 24, 28, 32, 44, 220, 224 Exhaustion, 202, 220 Exocrine, 211, 220, 242 Exogenous, 24, 31, 44, 45, 92, 220 Expiration, 220, 250 Extracellular, 17, 22, 28, 31, 43, 204, 214, 220, 221, 222, 238, 254 Extracellular Matrix, 17, 214, 220, 222 Extracellular Matrix Proteins, 17, 220 Extracellular Space, 220, 221 Extrapyramidal, 217, 221 Extremity, 207, 221, 234 F Facial, 25, 45, 60, 69, 116, 158, 221, 254 Fallopian Tubes, 221, 250 Family Planning, 150, 165, 221 Fat, 199, 203, 207, 221, 233, 236, 240, 241, 256, 260 Fatal Outcome, 25, 221 Fathers, 184, 221 Fatigue, 137, 221, 226 Fatty acids, 19, 55, 72, 93, 100, 101, 137, 221, 225, 247, 258, 259 Feces, 221, 256 Ferritin, 50, 221 Fertilization in Vitro, 221, 246 Fetal Alcohol Syndrome, 40, 221 Fetal Death, 33, 221 Fetus, 19, 48, 221, 246, 255, 261 Fibrillation, 215, 221 Fibroblast Growth Factor, 33, 221

Fibroblasts, 65, 222 Fibronectins, 221, 222 Fibrosis, 170, 222, 251 Fistula, 222, 240 Flaccid, 29, 222 Flatus, 222, 223 Flexion, 115, 222 Fluorescence, 26, 222 Fluorescent Dyes, 26, 222 Fluoridation, 88, 222 Fluorine, 222 Folate, 222 Folic Acid, 137, 222 Forearm, 206, 222, 234 Fourth Ventricle, 222, 233, 258 Friction, 200, 222 Functional magnetic resonance imaging, 35, 222 Fundus, 222, 223 Fungi, 42, 223, 225, 235, 237, 255, 263 Fungus, 41, 223 G GABA, 11, 15, 27, 28, 223, 224, 253 Gallbladder, 199, 211, 216, 223 Gamma-Endorphin, 223 Ganglia, 199, 205, 223, 238, 242, 243, 256 Ganglioside, 98, 223 Gangrenous, 223, 252 Gap Junctions, 223, 257 Gas, 73, 100, 201, 208, 222, 223, 228, 239, 240, 248, 250, 262 Gas exchange, 73, 223, 248, 250, 262 Gastric, 63, 209, 223 Gastric Acid, 223 Gastrin, 16, 223, 227 Gastrin-Releasing Peptide, 16, 223 Gastroesophageal Reflux, 139, 223 Gastroesophageal Reflux Disease, 139, 223 Gastrointestinal, 121, 127, 134, 136, 139, 183, 207, 211, 219, 224, 232, 252, 254, 256 Gastrointestinal tract, 127, 139, 224, 232, 252, 254 Gelatin, 224, 225 Gene, 19, 21, 31, 52, 63, 67, 83, 149, 170, 171, 200, 206, 224, 227, 236, 240, 245 Genomics, 7, 224 Genotype, 9, 224, 244 Gestation, 34, 82, 224, 243, 255 Gestational, 50, 83, 94, 121, 224 Gestational Age, 50, 224 Gland, 122, 199, 212, 224, 233, 234, 242, 244, 247, 252, 255, 259

270 Sudden Infant Death Syndrome

Gliosis, 63, 224 Glomerular, 81, 224 Glomerulus, 224 Glottis, 224, 243 Glucose, 9, 79, 169, 203, 206, 210, 212, 216, 224, 225, 226, 230, 244 Glutamate, 11, 12, 15, 25, 44, 224, 232 Glutamate Decarboxylase, 11, 224 Glutamic Acid, 222, 224 Glutamine, 137, 224 Glutathione Peroxidase, 94, 225, 252 Glycerol, 225, 244 Glycerophospholipids, 225, 244 Glycine, 14, 15, 225 Glycogen, 20, 225, 244 Glycoprotein, 98, 225, 232, 258 Glycosaminoglycan, 211, 225 Goats, 12, 225 Gonad, 225 Gonadal, 123, 225 Governing Board, 40, 225, 246 Government Agencies, 188, 225, 246 Grasses, 222, 225 Gravis, 137, 139, 225 Growth factors, 16, 38, 225 Guanylate Cyclase, 225, 240 H Habitat, 29, 225 Habitual, 211, 225 Haematoma, 225, 226 Haemorrhage, 70, 76, 80, 225 Haplotypes, 20, 226 Haptens, 200, 226 Headache, 208, 226, 227 Head-Down Tilt, 34, 226 Health Policy, 37, 226 Health Services, 25, 143, 144, 154, 226 Heart Arrest, 209, 226 Heart failure, 20, 139, 226 Heartbeat, 119, 129, 226, 256 Heat Stroke, 226, 228 Hematopoiesis, 136, 226 Heme, 24, 226, 237, 241, 245 Hemoglobin, 62, 202, 220, 226, 232, 245 Hemoglobin A, 62, 226, 245 Hemoglobinuria, 169, 226 Hemorrhage, 41, 215, 226, 248, 256 Hemosiderin, 42, 226, 227 Hemosiderosis, 41, 226 Hemostasis, 227, 252 Hepatic, 97, 136, 227 Hepatocytes, 5, 20, 227

Hereditary, 143, 227, 251 Heredity, 224, 227 Heteroduplex Analysis, 7, 227 Heterogeneity, 17, 32, 200, 227 Heterotrophic, 223, 227 Histology, 227, 242 Homeostasis, 9, 15, 28, 227, 254 Homogeneous, 16, 227 Homologous, 11, 14, 24, 44, 137, 200, 205, 227, 257 Hormonal, 204, 212, 227 Hormone, 11, 25, 44, 122, 204, 205, 212, 219, 223, 227, 231, 240, 241, 242, 251, 253, 254, 259 Hospice, 37, 227 Host, 205, 227, 229, 232, 262 Hybrid, 212, 227 Hydrocephalus, 121, 227, 231 Hydrogen, 199, 205, 208, 216, 220, 225, 228, 236, 239, 241, 243, 248 Hydrogen Peroxide, 225, 228 Hydrolysis, 22, 210, 228, 245, 247 Hypercapnia, 11, 25, 26, 30, 31, 43, 44, 228 Hyperpnea, 29, 228 Hyperpyrexia, 74, 228 Hypersensitivity, 201, 228, 232 Hypertension, 10, 228, 231, 240 Hyperthermia, 22, 35, 228 Hyperventilation, 31, 99, 228 Hypoplasia, 51, 75, 228 Hypotension, 214, 228 Hypothalamus, 123, 203, 204, 207, 216, 219, 228, 244, 247, 254, 258 Hypothermia, 22, 228 Hypotonia, 35, 116, 122, 228 Hypoventilation, 12, 27, 32, 35, 38, 39, 44, 120, 128, 129, 138, 228 Hypoxanthine, 66, 68, 228 Hypoxemia, 115, 228 I Id, 95, 103, 175, 185, 187, 194, 196, 228 Idiopathic, 10, 32, 42, 228 Imaging procedures, 229, 259 Imidazole, 206, 229 Immaturity, 36, 51, 229 Immune function, 135, 136, 229 Immune response, 202, 204, 226, 229, 234, 256, 262 Immune Sera, 229 Immune system, 127, 206, 218, 229, 232, 234, 236, 261, 263 Immunity, 229, 240, 260

Index 271

Immunization, 57, 87, 175, 229 Immunoassay, 59, 134, 229 Immunodeficiency, 169, 229 Immunoglobulin, 114, 202, 229 Immunohistochemistry, 16, 32, 229 Immunologic, 211, 224, 229 Immunology, 56, 58, 60, 68, 70, 72, 87, 200, 222, 229 Impairment, 139, 204, 229, 235 In situ, 121, 229 In vitro, 14, 32, 33, 39, 42, 218, 229 In vivo, 23, 32, 39, 42, 229, 258 Incision, 229, 231 Incompetence, 223, 229 Incontinence, 227, 229 Incubation, 229, 232, 243 Incubation period, 229, 232, 243 Indicative, 117, 131, 147, 229, 242, 261 Induction, 33, 46, 230 Infancy, 10, 26, 34, 35, 44, 97, 112, 114, 182, 230, 251 Infant Care, 54, 74, 146, 178, 186, 230 Infant Food, 123, 230 Infant Mortality, 18, 23, 33, 42, 82, 84, 151, 159, 176, 230 Infant, Newborn, 200, 230 Infantile, 20, 58, 92, 230 Infarction, 210, 215, 230, 235 Inflammation, 46, 135, 136, 202, 207, 220, 222, 223, 230, 232, 237, 251 Ingestion, 230, 245 Inhalation, 42, 230, 245 Initiation, 43, 142, 230 Inlay, 230, 250 Innervation, 27, 30, 207, 230, 231, 234 Inositol, 137, 230, 252 Inotropic, 217, 230 Insight, 9, 23, 26, 39, 67, 230 Instillation, 42, 230 Insulator, 230, 236 Intensive Care, 13, 41, 132, 230, 231 Intensive Care Units, 132, 231 Intercostal, 25, 44, 231, 250, 258 Intercostal Nerves, 25, 231, 258 Intermittent, 126, 128, 231 Intestinal, 135, 211, 219, 231, 234 Intestine, 207, 231, 232 Intoxication, 231, 261, 263 Intracellular, 6, 7, 15, 26, 35, 208, 230, 231, 240, 246, 249, 251, 252, 253 Intracranial Hemorrhages, 227, 231, 258 Intracranial Hypertension, 226, 227, 231

Intrinsic, 15, 17, 21, 32, 200, 205, 231 Invasive, 34, 35, 229, 231, 234 Involuntary, 29, 205, 219, 220, 221, 231, 237, 249, 252, 254 Iodine, 94, 137, 231 Ion Channels, 7, 15, 20, 204, 231, 238, 239, 257 Ionization, 231 Ionizing, 135, 136, 200, 219, 231 Ions, 205, 208, 217, 218, 228, 231, 246 Ischemia, 87, 204, 223, 231 J Joint, 135, 136, 231, 257 K Kainate, 55, 232 Kb, 164, 232 Kidney Disease, 109, 164, 170, 232 Kinetic, 231, 232 L Labile, 213, 232 Laceration, 232, 258 Lactation, 40, 232, 241 Lag, 138, 232 Laminin, 205, 221, 232 Large Intestine, 216, 231, 232, 249, 254 Laryngeal, 25, 42, 44, 71, 232 Larynx, 120, 224, 232, 259, 261 Latent, 232, 246 Lens, 232, 262 Lentivirus, 19, 232 Lesion, 224, 232, 233, 260 Lethal, 58, 71, 72, 232 Lethargy, 227, 232 Leucine, 205, 232 Leukemia, 135, 169, 232 Leukotrienes, 203, 232 Library Services, 194, 232 Life cycle, 206, 223, 233 Ligament, 233, 247 Ligands, 19, 139, 233 Linkage, 20, 210, 233 Linkage Disequilibrium, 20, 233 Lip, 21, 49, 55, 233 Lipid, 72, 103, 211, 225, 233, 236, 260 Lipophilic, 22, 233 Localization, 15, 41, 229, 233 Localized, 38, 121, 216, 225, 230, 232, 233, 244, 258, 260, 261 Locomotion, 33, 233, 244 Locus Coeruleus, 26, 233 Longitudinal study, 18, 233 Loop, 48, 233

272 Sudden Infant Death Syndrome

Lower Esophageal Sphincter, 223, 224, 233 Lycopene, 137, 233 Lymph, 210, 212, 219, 233, 234 Lymph node, 210, 233, 234 Lymphatic, 219, 230, 233, 234, 259 Lymphocyte, 202, 234 Lymphoid, 52, 202, 234 Lymphoma, 169, 234 Lysine, 137, 234 M Magnetic Resonance Imaging, 234 Major Histocompatibility Complex, 226, 234 Malabsorption, 169, 234 Malignant, 17, 74, 169, 207, 234 Malnutrition, 204, 234, 237 Manifest, 144, 234 Mannans, 223, 234 Mastication, 234, 260 Mastitis, 234, 252 Median Nerve, 139, 209, 234 Mediate, 22, 35, 217, 234 Mediator, 42, 211, 234, 252 Medical Records, 20, 234 Medicament, 127, 234 MEDLINE, 165, 168, 170, 234 Medullary, 9, 11, 12, 18, 21, 28, 38, 39, 43, 44, 56, 76, 80, 235 Megaloblastic, 222, 235 Meiosis, 235, 257 Melanin, 233, 235, 244, 260 Melanocytes, 235 Melanoma, 169, 207, 235 Membrane Glycoproteins, 235 Memory, 10, 18, 216, 235 Meninges, 210, 215, 235 Mental deficiency, 221, 235 Mental Disorders, 109, 235, 248 Mental Health, iv, 5, 109, 151, 164, 167, 235, 248 Mentors, 25, 235 Mesencephalic, 38, 233, 235, 249 Metabolic disorder, 19, 121, 235 Metabolite, 123, 235 Methionine, 205, 235, 247, 256 MI, 198, 235 Mice Minute Virus, 235, 242 Microbiology, 54, 56, 58, 60, 63, 68, 70, 84, 87, 199, 235 Microorganism, 213, 235, 263 Microscopy, 26, 29, 205, 227, 236 Microtubules, 12, 236

Micturition, 116, 236 Miscarriage, 150, 236 Miscible, 123, 236 Mitochondria, 19, 236 Mitosis, 203, 236 Modulator, 116, 236 Molecular, 6, 7, 8, 16, 19, 21, 26, 33, 39, 54, 75, 165, 168, 201, 206, 214, 236, 249, 260 Monogenic, 20, 236 Monophosphate, 93, 236 Morphine, 30, 236, 237, 241 Morphogenesis, 221, 236 Morphological, 218, 223, 235, 236 Morphology, 11, 17, 236 Motility, 75, 236, 252 Motor Activity, 214, 236 Motor nerve, 39, 236, 240, 244 Motor Neurons, 56, 236 Mucosa, 127, 211, 236 Multiple sclerosis, 94, 236 Muscle Contraction, 15, 236 Muscle Fibers, 237 Muscular Atrophy, 169, 237 Muscular Dystrophies, 218, 237 Mutagenesis, 7, 237 Mutagens, 237 Myasthenia, 137, 139, 237 Mycotoxins, 41, 237 Myelin, 236, 237, 238 Myocarditis, 54, 68, 74, 75, 137, 216, 237 Myocardium, 16, 235, 237 Myofibrils, 208, 237 Myoglobin, 237, 245 Myopathy, 5, 20, 237 Myosin, 237 Myotonic Dystrophy, 169, 237 N Naloxone, 205, 237 Narcosis, 237 Narcotic, 31, 236, 237 NCI, 1, 109, 163, 237 Necrosis, 203, 210, 230, 235, 237 Needs Assessment, 37, 238 Neonatal period, 121, 238 Neoplasia, 169, 238 Neoplastic, 234, 238 Nephropathy, 232, 238 Nerve, 25, 28, 33, 35, 44, 86, 118, 136, 200, 202, 204, 207, 211, 216, 230, 233, 234, 236, 238, 239, 240, 244, 246, 250, 251, 255, 258, 260, 261 Nerve Endings, 35, 238

Index 273

Nerve Growth Factor, 33, 238, 239 Nervous System, 14, 19, 23, 27, 33, 39, 115, 139, 169, 199, 200, 201, 204, 205, 207, 208, 210, 211, 212, 213, 218, 220, 223, 224, 232, 234, 236, 238, 239, 243, 245, 252, 256, 257 Networks, 22, 33, 36, 238 Neural, 8, 12, 22, 27, 35, 36, 200, 238 Neural Pathways, 22, 238 Neuroanatomy, 11, 238 Neuroeffector Junction, 238 Neuroglia, 224, 238 Neurologic, 139, 227, 238 Neuromuscular, 29, 122, 199, 238 Neuromuscular Junction, 29, 199, 238 Neuronal, 7, 12, 15, 23, 24, 26, 32, 33, 38, 51, 63, 76, 208, 237, 238, 239, 243 Neuronal Plasticity, 63, 239 Neuropathy, 139, 239 Neuropeptide, 223, 239 Neurophysiology, 216, 239 Neurosecretory Systems, 219, 239 Neurotoxic, 12, 239 Neurotoxin, 12, 28, 29, 44, 239 Neurotransmitters, 7, 11, 15, 35, 236, 239, 246, 254 Neurotrophins, 33, 239 Neutrons, 200, 207, 239, 249 Niacin, 137, 239, 260 Niacinamide, 137, 239 Nicotine, 9, 16, 19, 21, 33, 45, 51, 63, 73, 77, 92, 93, 239 Nitric Oxide, 93, 239 Nitrogen, 149, 200, 220, 224, 240, 260 Norepinephrine, 200, 217, 240 Nuclear, 22, 59, 205, 218, 238, 240, 258 Nuclei, 12, 43, 51, 75, 93, 200, 218, 234, 236, 239, 240, 248 Nucleic acid, 205, 208, 228, 237, 240 O Obstetrics, 18, 22, 46, 240 Occult, 85, 240 Octreotide, 139, 240 Ocular, 119, 240 Oculomotor, 235, 240 Ointments, 240, 242 Omega-3 fatty acid, 137, 240 Oncogene, 169, 240 Oncogenic, 232, 240 Opacity, 216, 240 Open Reading Frames, 232, 240 Ophthalmologic, 217, 240

Opioid Peptides, 31, 92, 217, 241 Opium, 236, 241 Optic Chiasm, 228, 241 Organ Culture, 16, 241 Oropharynx, 115, 241 Orthostatic, 240, 241 Ossification, 86, 241, 251 Ovaries, 221, 241, 250 Overdose, 47, 241 Overweight, 95, 115, 241 Ovum, 224, 233, 241, 263 Oxidation, 6, 19, 199, 203, 225, 241, 258 Oxygen Consumption, 241, 250 Oxygenase, 24, 241 Oxygenation, 228, 241 Oxytocin, 46, 241 P Pacemaker, 22, 23, 28, 32, 39, 241 Palate, 115, 241, 254, 261 Palliative, 37, 242, 258 Pancreas, 199, 206, 216, 242, 254 Pancreatic, 169, 209, 211, 223, 242 Pancreatic cancer, 169, 242 Pancreatic Juice, 223, 242 Paraffin, 58, 79, 242 Paraganglia, Chromaffin, 212, 242 Paralysis, 29, 148, 235, 242 Parathyroid, 242, 251 Parathyroid Glands, 242, 251 Paroxysmal, 169, 242, 243, 263 Particle, 242, 254, 260 Parturition, 240, 242 Parvovirus, 79, 235, 242 Patch, 7, 8, 9, 15, 22, 24, 26, 242 Pathogenesis, 6, 21, 42, 44, 45, 67, 120, 166, 242 Pathologic, 14, 42, 54, 199, 203, 214, 228, 242, 250 Pathologic Processes, 203, 242 Pathologies, 19, 39, 242 Pathophysiology, 15, 42, 242 Patient Education, 177, 192, 194, 198, 242 Pelvic, 242, 247 Penicillin, 202, 243 Penis, 243, 250 Peptide, 16, 93, 205, 211, 221, 223, 241, 243, 245, 247, 259 Perfusion, 228, 243 Perinatal, 19, 22, 34, 41, 60, 64, 79, 81, 82, 84, 92, 150, 230, 243 Peripheral Nerves, 139, 243, 255

274 Sudden Infant Death Syndrome

Peripheral Nervous System, 243, 247, 254, 256 Pertussis, 56, 87, 243, 263 Petechiae, 70, 226, 243 Petroleum, 242, 243 PH, 26, 159, 243 Pharmaceutical Preparations, 135, 210, 224, 243 Pharmacologic, 202, 243, 259 Pharynx, 223, 241, 243, 261 Phenotype, 8, 243 Phenylalanine, 137, 244, 260 Phospholipids, 100, 221, 230, 244 Phosphorus, 208, 242, 244 Phosphorylase, 208, 244 Photoperiod, 122, 244 Phrenic Nerve, 25, 244 Physical Examination, 224, 244 Physiologic, 11, 12, 19, 34, 107, 200, 206, 226, 244, 249, 250, 252, 260 Physiology, 8, 11, 12, 13, 15, 19, 26, 27, 30, 41, 42, 44, 63, 70, 99, 218, 239, 244 Pigment, 233, 235, 237, 244 Pilot study, 34, 244 Pineal Body, 244 Pineal gland, 122, 244 Pitch, 101, 244 Pituitary Gland, 221, 244, 247 Plants, 200, 208, 211, 212, 213, 224, 236, 240, 244, 255, 259, 260 Plasma, 10, 52, 122, 123, 202, 210, 222, 224, 226, 227, 244, 245, 252 Plasma cells, 202, 245 Plasticity, 17, 33, 245 Platelet Aggregation, 201, 239, 245, 258 Platelets, 58, 92, 208, 239, 245, 258 Platinum, 233, 245 Plethysmograph, 29, 245 Plethysmography, 10, 245 Poisoning, 113, 118, 131, 231, 245 Policy Making, 225, 245 Polycystic, 170, 245 Polymers, 132, 245, 247 Polymorphic, 16, 20, 245 Polymorphism, 83, 245 Polypeptide, 201, 213, 237, 245, 254, 263 Polysaccharide, 202, 210, 225, 245, 247 Pons, 207, 222, 245, 250 Pontine, 38, 245 Porphyrins, 93, 245 Posterior, 201, 204, 217, 241, 242, 244, 246, 261

Postnatal, 6, 14, 15, 23, 30, 33, 34, 36, 92, 221, 246, 255 Postsynaptic, 14, 238, 246, 253, 257 Postural, 25, 246 Potassium, 7, 15, 137, 246 Potassium Channels, 7, 15, 246 Potentiating, 61, 246 Potentiation, 17, 246, 253 Practice Guidelines, 167, 185, 246 Precipitating Factors, 30, 246 Precursor, 21, 22, 116, 203, 211, 217, 218, 219, 223, 240, 244, 246, 247, 260 Predisposition, 9, 20, 61, 118, 142, 246 Pregnancy Outcome, 40, 246 Pregnancy Tests, 224, 246 Prenatal, 18, 19, 21, 33, 40, 73, 79, 93, 127, 178, 183, 218, 221, 246 Prenatal Care, 127, 178, 183, 246 Pressoreceptors, 205, 246 Presumptive, 178, 246 Presynaptic, 27, 204, 238, 246, 257 Presynaptic Terminals, 204, 238, 246, 257 Prevalence, 10, 16, 26, 37, 57, 67, 247 Probe, 17, 247 Progression, 202, 247 Progressive, 133, 212, 216, 217, 225, 237, 247 Projection, 29, 240, 247, 249 Promoter, 83, 247 Prone, 35, 42, 48, 53, 61, 67, 84, 89, 126, 129, 131, 154, 183, 247 Prone Position, 42, 61, 89, 131, 247 Pro-Opiomelanocortin, 223, 241, 247 Prophase, 247, 257 Prophylaxis, 32, 132, 133, 247 Prospective study, 233, 247 Prostaglandins, 203, 247 Prostate, 169, 247, 250 Protein C, 137, 201, 205, 221, 247, 261 Protein S, 149, 170, 206, 247 Proteoglycans, 205, 221, 247 Proteolytic, 213, 247 Protocol, 10, 40, 248 Protons, 200, 228, 231, 248, 249 Protozoa, 235, 248, 255 Proximal, 217, 246, 248 Proxy, 54, 248 Psychiatric, 34, 82, 235, 248, 254 Psychiatry, 18, 64, 72, 82, 248, 256, 262 Public Health, 12, 42, 54, 145, 148, 149, 151, 154, 159, 167, 187, 248 Public Policy, 165, 248

Index 275

Publishing, 45, 94, 150, 248 Puerperium, 240, 248 Pulmonary, 6, 17, 41, 69, 74, 136, 200, 206, 208, 214, 228, 232, 248, 250, 256, 262 Pulmonary Alveoli, 228, 248 Pulmonary Artery, 206, 248, 262 Pulmonary Ventilation, 228, 248, 250 Pulse, 117, 121, 236, 248 Purpura, 226, 248 Pyridoxal, 224, 248 Pyrogenic, 56, 248 R Race, 126, 248 Radar, 41, 249 Radiation, 135, 136, 219, 222, 228, 231, 249, 263 Radioactive, 228, 231, 240, 249 Radiography, 224, 249 Radioisotope, 249, 259 Randomized, 218, 249 Raphe Nuclei, 12, 249 Reagent, 249, 254 Receptors, Serotonin, 249, 252 Recombinant, 5, 19, 249, 262 Rectum, 203, 207, 216, 222, 223, 229, 232, 247, 249 Recurrence, 184, 212, 249 Red blood cells, 220, 241, 249 Red Nucleus, 204, 249 Refer, 1, 213, 223, 233, 239, 249 Reflective, 126, 249 Reflex, 7, 18, 27, 30, 42, 43, 148, 249 Reflux, 64, 139, 223, 224, 249 Refraction, 249, 255 Regeneration, 222, 249 Regimen, 218, 249 Regurgitation, 223, 249 Remission, 249, 250 Reproduction Techniques, 246, 250 Reproductive system, 136, 250 Research Design, 30, 250 Research Support, 179, 250 Resorption, 227, 250 Respiration, 22, 23, 25, 26, 118, 119, 120, 121, 124, 125, 126, 132, 203, 208, 211, 236, 250 Respiratory distress syndrome, 118, 208, 250 Respiratory failure, 133, 250 Respiratory Muscles, 31, 250 Respiratory Physiology, 250, 262 Respiratory syncytial virus, 59, 250

Respiratory System, 27, 43, 250 Restoration, 27, 250, 263 Reticular, 76, 250 Reticular Formation, 76, 250 Retina, 232, 238, 241, 250, 251, 262 Retinal, 217, 241, 250 Retinoblastoma, 169, 251 Retrograde, 22, 32, 251 Rhinitis, 208, 251, 252 Riboflavin, 100, 137, 251 Ribose, 199, 251 Rickets, 121, 251 Rigidity, 130, 244, 251 Rigor Mortis, 4, 251 Rod, 205, 212, 251 S Saliva, 251 Salivary, 86, 216, 242, 251 Salivary glands, 86, 216, 251 Schizoid, 251, 263 Schizophrenia, 251, 263 Schizotypal Personality Disorder, 251, 263 Sclerosis, 137, 139, 169, 236, 251 Screening, 54, 113, 114, 122, 151, 212, 251 Second Messenger Systems, 239, 251 Secretion, 63, 212, 223, 232, 240, 251, 252 Secretory, 86, 212, 238, 252, 257 Secretory Vesicles, 212, 252 Sedative, 211, 252 Seizures, 242, 252 Selenium, 94, 95, 137, 252 Semen, 247, 252 Sensor, 116, 126, 132, 133, 252 Sensory Deprivation, 98, 252 Septicaemia, 252 Serologic, 229, 252 Serotonin, 9, 11, 12, 14, 28, 47, 77, 83, 249, 252, 260 Serotypes, 20, 29, 252 Serum, 58, 113, 201, 203, 213, 229, 252 Sex Determination, 170, 252 Shivering, 29, 252, 258 Shock, 55, 67, 94, 102, 184, 201, 252, 260 Side effect, 200, 206, 253, 259 Signal Transduction, 230, 253 Silicon, 137, 253 Silicon Dioxide, 253 Single Parent, 184, 253 Skeletal, 5, 20, 212, 228, 237, 253, 254 Skeleton, 199, 231, 253 Skull, 13, 121, 215, 253, 257 Skull Base, 121, 253

276 Sudden Infant Death Syndrome

Skull Fracture, Depressed, 253 Skull Fractures, 121, 253 Sleep apnea, 8, 12, 14, 32, 39, 61, 76, 77, 99, 115, 132, 133, 139, 186, 253, 254 Sleep Apnea Syndromes, 99, 253 Sleep Deprivation, 14, 69, 254 Sleep Stages, 101, 254 Small intestine, 217, 227, 231, 254, 262 Smooth muscle, 74, 201, 208, 236, 254, 256 Sneezing, 130, 243, 254 Snoring, 115, 132, 133, 254 Social Support, 37, 72, 254 Sodium, 38, 52, 254 Sodium Cyanide, 38, 254 Solitary Nucleus, 204, 254 Solvent, 123, 225, 254 Somatostatin, 11, 93, 139, 240, 254 Sound wave, 249, 254 Spasm, 235, 254, 255 Spasmodic, 243, 255 Specialist, 189, 216, 255 Species, 9, 11, 12, 138, 210, 219, 227, 232, 235, 236, 242, 248, 255, 256, 260, 262, 263 Specificity, 200, 208, 255 Spectrum, 125, 126, 255 Sphincter, 232, 255 Spike, 15, 255 Spinal cord, 15, 32, 100, 101, 204, 207, 210, 211, 219, 234, 235, 238, 239, 243, 249, 255, 256 Spinal Nerves, 243, 255, 258 Spontaneous Abortion, 137, 246, 255 Sporadic, 251, 255 Spores, 41, 255 Steel, 212, 255, 261 Stem cell transplantation, 6, 255 Stem Cells, 255 Stillbirth, 33, 40, 100, 147, 150, 246, 255 Stimulant, 208, 255 Stimulus, 26, 43, 128, 217, 218, 220, 230, 231, 232, 249, 255, 258 Stomach, 108, 113, 135, 157, 176, 183, 199, 216, 220, 223, 224, 227, 233, 243, 249, 254, 255 Stool, 134, 229, 232, 256 Stress, 6, 19, 28, 33, 42, 69, 78, 101, 135, 136, 154, 204, 209, 212, 246, 256, 261 Stroke, 22, 109, 164, 209, 256 Stupor, 232, 237, 256 Subacute, 230, 256 Subclinical, 230, 252, 256 Subcutaneous, 100, 223, 256

Subspecies, 255, 256 Substance P, 235, 252, 256 Substrate, 16, 22, 256 Sudden cardiac death, 7, 8, 20, 30, 98, 256 Sudden death, 7, 9, 16, 29, 30, 36, 37, 115, 118, 126, 127, 128, 137, 188, 256 Sulfur, 220, 235, 256 Supine, 115, 121, 183, 185, 256 Supine Position, 115, 121, 183, 256 Supplementation, 98, 100, 256 Support group, 143, 145, 151, 179, 180, 188, 198, 256 Surfactant, 73, 256 Sympathetic Nervous System, 204, 212, 256 Sympathomimetic, 217, 219, 240, 256 Symphysis, 247, 257 Synapses, 27, 238, 239, 255, 257 Synapsis, 257 Synaptic, 14, 17, 22, 23, 29, 32, 39, 239, 253, 257 Synaptic Transmission, 14, 239, 257 Synaptic Vesicles, 257 Synergistic, 72, 257 Synostosis, 121, 257 Systemic, 28, 201, 206, 216, 219, 230, 231, 257, 260, 261 Systolic, 228, 257 T Tachycardia, 20, 124, 257 Talc, 124, 257 Taurine, 137, 257 Telangiectasia, 170, 257 Temporal, 21, 122, 257 Tetani, 257 Tetanic, 257, 258 Tetanus, 87, 257 Thalamic, 204, 258 Thalamic Diseases, 204, 258 Thalamus, 22, 207, 216, 258 Therapeutics, 7, 102, 103, 258 Thermal, 28, 207, 217, 239, 258 Thermogenesis, 29, 258 Thermoregulation, 93, 122, 244, 258 Thiamine, 137, 258 Third Ventricle, 203, 228, 244, 258 Thoracic, 207, 216, 231, 234, 258 Thoracic Nerves, 231, 258 Thorax, 52, 132, 199, 231, 258, 261 Threshold, 220, 228, 258 Thrombin, 245, 247, 258 Thrombocytes, 245, 258

Index 277

Thrombomodulin, 247, 258 Thrombosis, 247, 256, 258 Thromboxanes, 203, 258 Thymus, 229, 234, 259 Thyroid, 231, 242, 259, 260 Thyroid Gland, 242, 259 Thyroid Hormones, 259, 260 Thyrotropin, 11, 25, 44, 259 Thyroxine, 244, 259 Tidal Volume, 120, 228, 259 Tin, 209, 245, 259 Tolerance, 31, 73, 93, 259 Tonic, 38, 259 Tooth Preparation, 199, 259 Topical, 228, 242, 259 Toxic, iv, 6, 29, 41, 135, 136, 203, 205, 216, 219, 225, 229, 239, 252, 259 Toxicity, 217, 259 Toxicology, 20, 50, 166, 259 Toxins, 29, 42, 56, 72, 202, 208, 230, 237, 259 Trace element, 94, 207, 212, 222, 253, 259 Tracer, 32, 259 Trachea, 66, 120, 207, 232, 243, 259 Traction, 212, 260 Tractus, 26, 31, 43, 260 Transduction, 5, 20, 24, 253, 260 Transfection, 7, 206, 260 Transfer Factor, 229, 260 Transmitter, 117, 130, 133, 199, 204, 217, 231, 234, 238, 240, 257, 260 Transplantation, 212, 218, 229, 234, 260 Trauma, 4, 18, 101, 121, 220, 237, 260 Tremor, 235, 260 Trigeminal, 25, 43, 44, 260 Triglyceride, 100, 260 Trophic, 33, 260 Tropism, 19, 260 Tryptophan, 213, 252, 260 Tuberculosis, 214, 260 Tuberous Sclerosis, 170, 260 Tubulin, 236, 260 Tyrosine, 11, 33, 137, 217, 260 U Ulcer, 260 Ulceration, 135, 260 Ultrasonography, 224, 260 Unconscious, 131, 228, 261 Urban Population, 82, 261 Urea, 127, 149, 261 Ureters, 261 Urethra, 243, 247, 261

Urinary, 127, 219, 227, 229, 261 Urinary tract, 127, 261 Urinary tract infection, 127, 261 Urinate, 261, 263 Urine, 116, 123, 206, 217, 219, 226, 229, 236, 251, 261 Urticaria, 201, 261 Uterine Contraction, 241, 261 Uterus, 211, 221, 222, 223, 241, 250, 261 Uvula, 254, 261 V Vaccine, 29, 98, 248, 261 Vagal, 10, 27, 75, 86, 261 Vagina, 211, 250, 261 Vagus Nerve, 254, 261 Vanadium, 137, 261 Vascular, 87, 139, 201, 205, 219, 230, 239, 246, 259, 261 Vascular Resistance, 205, 261 Vasoconstriction, 43, 219, 262 Vasodilatation, 209, 262 Vasodilator, 207, 217, 262 Vector, 6, 19, 138, 260, 262 Vein, 240, 262 Venom, 28, 262 Venous, 210, 247, 262 Ventilation, 22, 33, 38, 129, 138, 208, 209, 228, 262 Ventral, 9, 11, 12, 24, 25, 28, 38, 42, 43, 44, 115, 203, 228, 231, 240, 245, 255, 262 Ventricle, 248, 257, 262 Ventricular, 10, 16, 20, 30, 98, 227, 262 Vertebrae, 17, 255, 262 Veterinary Medicine, 165, 262 Villi, 227, 262 Viral, 19, 60, 135, 137, 208, 222, 240, 260, 262 Viral vector, 19, 262 Virulence, 87, 204, 259, 262 Virus, 5, 27, 100, 205, 208, 210, 250, 260, 262 Visceral, 204, 261, 262 Visceral Afferents, 204, 261, 262 Vitamin A, 87, 103, 230, 262 Vitreous Humor, 66, 68, 262 Vitro, 27, 32, 39, 262 Vivo, 32, 39, 263 Void, 21, 263 Volition, 231, 263 Voltage-gated, 8, 263 W Wakefulness, 25, 38, 44, 45, 263

278 Sudden Infant Death Syndrome

Weight Gain, 127, 263 White blood cell, 202, 234, 245, 263 Whooping Cough, 243, 263 Withdrawal, 6, 31, 263 Womb, 250, 261, 263 Wound Healing, 222, 263

X Xenograft, 202, 263 X-ray, 29, 222, 240, 263 Y Yeasts, 223, 244, 263 Z Zymogen, 247, 263

Index 279

280 Sudden Infant Death Syndrome