ARSENIC A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R EFERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright ©2003 by ICON Group International, Inc. Copyright ©2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Arsenic: 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: 0-597-83743-0 1. Arsenic-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on arsenic. 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 ARSENIC .................................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Arsenic .......................................................................................... 4 E-Journals: PubMed Central ....................................................................................................... 59 The National Library of Medicine: PubMed ................................................................................ 61 CHAPTER 2. NUTRITION AND ARSENIC ........................................................................................ 107 Overview.................................................................................................................................... 107 Finding Nutrition Studies on Arsenic....................................................................................... 107 Federal Resources on Nutrition ................................................................................................. 115 Additional Web Resources ......................................................................................................... 116 CHAPTER 3. ALTERNATIVE MEDICINE AND ARSENIC .................................................................. 119 Overview.................................................................................................................................... 119 National Center for Complementary and Alternative Medicine................................................ 119 Additional Web Resources ......................................................................................................... 133 General References ..................................................................................................................... 137 CHAPTER 4. DISSERTATIONS ON ARSENIC .................................................................................... 139 Overview.................................................................................................................................... 139 Dissertations on Arsenic............................................................................................................ 139 Keeping Current ........................................................................................................................ 144 CHAPTER 5. CLINICAL TRIALS AND ARSENIC .............................................................................. 145 Overview.................................................................................................................................... 145 Recent Trials on Arsenic............................................................................................................ 145 Keeping Current on Clinical Trials ........................................................................................... 152 CHAPTER 6. PATENTS ON ARSENIC............................................................................................... 155 Overview.................................................................................................................................... 155 Patents on Arsenic ..................................................................................................................... 155 Patent Applications on Arsenic ................................................................................................. 192 Keeping Current ........................................................................................................................ 231 CHAPTER 7. BOOKS ON ARSENIC .................................................................................................. 233 Overview.................................................................................................................................... 233 Book Summaries: Online Booksellers......................................................................................... 233 The National Library of Medicine Book Index ........................................................................... 238 Chapters on Arsenic................................................................................................................... 239 CHAPTER 8. MULTIMEDIA ON ARSENIC ....................................................................................... 243 Overview.................................................................................................................................... 243 Bibliography: Multimedia on Arsenic........................................................................................ 243 CHAPTER 9. PERIODICALS AND NEWS ON ARSENIC .................................................................... 245 Overview.................................................................................................................................... 245 News Services and Press Releases.............................................................................................. 245 Academic Periodicals covering Arsenic ..................................................................................... 250 CHAPTER 10. RESEARCHING MEDICATIONS ................................................................................. 251 Overview.................................................................................................................................... 251 U.S. Pharmacopeia..................................................................................................................... 251 Commercial Databases ............................................................................................................... 252 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 255 Overview.................................................................................................................................... 255 NIH Guidelines.......................................................................................................................... 255 NIH Databases........................................................................................................................... 257 Other Commercial Databases..................................................................................................... 259
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APPENDIX B. PATIENT RESOURCES ............................................................................................... 261 Overview.................................................................................................................................... 261 Patient Guideline Sources.......................................................................................................... 261 Finding Associations.................................................................................................................. 265 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 267 Overview.................................................................................................................................... 267 Preparation................................................................................................................................. 267 Finding a Local Medical Library................................................................................................ 267 Medical Libraries in the U.S. and Canada ................................................................................. 267 ONLINE GLOSSARIES................................................................................................................ 273 Online Dictionary Directories ................................................................................................... 273 ARSENIC DICTIONARY............................................................................................................. 275 INDEX .............................................................................................................................................. 357
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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 arsenic is indexed in search engines, such as www.google.com or others, a nonsystematic 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 arsenic, 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 arsenic, 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 arsenic. 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 arsenic, 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 arsenic. The Editors
1 From
the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON ARSENIC Overview In this chapter, we will show you how to locate peer-reviewed references and studies on arsenic.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and arsenic, 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 “arsenic” (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: •
Toxins and Diabetes Mellitus: An Environmental Connection? Source: Diabetes Spectrum. 15(2): 109-112. 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: Several international studies have examined the relationship between environmental influences and diabetes mellitus. This article reports on a study undertaken to comprehensively review those findings from the scientific literature of the past 30 years. Literature relevant to the relationship between diabetes and environmental toxins was reviewed. The findings suggest that two environment toxins, arsenic and dioxin (dibenzo-p-dioxins), may have some relationship to an increased risk for diabetes. The authors note that results only indicate a possible relationship between
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diabetes and environmental toxins. The authors strongly suggest that further studies be conducted to determine the true nature and extent of the relationships reported in the literature. 2 tables. 21 references.
Federally Funded Research on Arsenic The U.S. Government supports a variety of research studies relating to arsenic. 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 arsenic. 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 arsenic. The following is typical of the type of information found when searching the CRISP database for arsenic: •
Project Title: ARSENIC BASED THERAPY OF BCR ABL POSITIVE LEUKEMIAS Principal Investigator & Institution: Bhalla, Kapil N.; Professor of Medicine; Moffitt Cancer Center; University of South Florida 4202 E Fowler Ave Tampa, Fl 33620 Timing: Fiscal Year 2001; Project Start 15-JUN-2001; Project End 31-MAY-2004 Summary: The leukemic clone in virtually all of the patients with chronic myeloid leukemia with blast crisis (CML-BC) and approximately one-third of the adults with acute lymphoblastic leukemia (ALL) expresses the bcr-abl fusion gene encoded p210 and p185 Bcr-Abl tyrosine kinase (TK), respectively. Although the chemotherapeutic regimens or bone marrow stem cell transplantation employed against acute leukemias can also produce complete remissions in Bcr-Abl positive ALL and CML-BC, these remissions are not durable and the overall clinical outcome remains dismal. This creates a strong rationale to test novel strategies in this clinical setting. Arsenic Trioxide (As2O3 or AT) is clinically active against relapsed or refractory acute promyelocytic leukemia (APL), where it downregulates the levels of the fusion protein PML-RARdelta causing partial differentiation and apoptosis of APL cells. Recently, we have demonstrated that clinically achievable levels of AT can also reduce p210 or p185 Bcr-Abl fusion protein levels and induce apoptosis of CML-BC cells. Based on these findings, we propose to conduct a Phase II clinical-pharmacologic trial of AT (NCI/CTEP sponsored) as the induction therapy for relapsed and refractory; Bcr-Abl positive adult ALL and CML-BC. In vitro studies on the patient derived leukemic blasts are proposed to determine the molecular correlates of the clinical response and apoptosis induced by AT. We have also shown that STI571, a relatively specific inhibitor of Bcr-Abl TK activity, induces differentiation and apoptosis of Bcr-Abl positive leukemic cells. Therefore, we also propose to investigate the in vitro apoptotic and differentiation effects of a combination
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).
Studies
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of AT and STI571 in Bcr-Abl positive leukemic blasts. The specific aims of this proposal are: AIM 1: To determine the clinical efficacy, i.e., the rate and duration of clinical and hematologic response and overall survival, secondary to treatment with daily intravenous AT in adult patients with Philadelphia chromosome (bcr-abl fusion gene) positive relapsed or refractory ALL or CML-BC. AIM 2: To determine the pharmacokinetic parameters of AT, i.e., AUC and Css and correlate these with the clinical and cytogenetic response in patients with Bcr-Abl positive ALL or CMLBC. AIM 3: To correlate the clinical response to AT with the decline in the bcr-abl mRNA levels determined by real-time RT-PCR. AIM 4: To correlate the clinical and in vivo molecular response to AT with AT-induced in vitro downregulation of Bcr-Abl and Akt protein levels, histone hyperacetylation as well as differentiation and apoptosis, utilizing the pre-treatment samples of leukemic blasts. AIM 5: To determine the in vitro differentiation and apoptotic effects of STI-571 alone and in combination with AT in the pre-treatment samples of Bcr-Abl positive leukemic blasts. These in vitro and in vivo studies are designed to evaluate AT-based novel strategies against Bcr-Abl positive human leukemias. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: INDUCTION
ARSENIC
CONTAINING
MIXTURES
IN ANGIOSARCOMA
Principal Investigator & Institution: Pott O'brien, Wendy A.; None; Colorado State University Fort Collins, Co 80523 Timing: Fiscal Year 2001; Project Start 15-FEB-1997; Project End 31-JAN-2003 Summary: (Applicant's Description): This project will be executed at the Foothills Campus of Colorado State University by Wendy A. Pott, D.V.M. Dr. Pott's long-term goals involve integrating the disciplines of pathology, toxicology and biomedical engineering in the realm of cancer research. Her immediate goals involve investigating the roles of three common groundwater contaminants, individually and in combination, in the development of hepatic angiosarcoma. The research career development plan Dr. Pott will follow involves an interdisciplinary background of coursework and practical implementation of knowledge and development of skills in the laboratory and in the mathematical modelling arena. The long-term objectives of this project are 1) to evaluate the carcinogenic effects of sub-chronic exposure to three common groundwater contaminants-arsenic, vinyl chloride and 1,2-dichloroethane (1,2-DCE) - implicated as etiologic agents in the development of angiosarcoma; and 2) to use data from these studies with physiologically-based pharmacokinetic/pharmacodynamic (PB-PK/PD) models and statistical and mathematical modelling techniques for the purpose of health risk characterization. The specific aims of this project are 1) to determine the extent to which arsenic alone will act to induce the development of angiosarcoma; 2) to evaluate whether synergistic carcinogenic activity may result when arsenic is combined with vinyl chloride and/or 1,2-DCE; 3) to develop PB-PK/PD models for target tissue dosimetry of single chemicals and combinations of chemicals following exposure to arsenic, vinyl chloride, and/or 1,2-DCE; and 4) to develop cell turnover and carcinogenesis models and integrate them with PB-PK/PD models to characterize cancer risks associated with exposure to arsenic, vinyl chloride and/or 1,2-DCE. These goals will be accomplished using a medium-term angiosarcoma bioassay to investigate the effects of each of the above-mentioned chemicals alone and in combination in inducing hepatic angiosarcoma. Data gathered from these experiments will be used to develop models to determine cancer risks and safe drinking water levels of these chemicals.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARSENIC EFFECTS ON GLUCOCORTICOID RECEPTOR ACTION Principal Investigator & Institution: Bodwell, Jack E.; Physiology; Dartmouth College 11 Rope Ferry Rd. #6210 Hanover, Nh 03755 Timing: Fiscal Year 2002; Project Start 18-SEP-2002; Project End 30-JUN-2006 Summary: (provided by applicant): The overall goal of this research project is to determine the contribution of arsenic (As) exposure to human disease risk. There is growing worldwide concern about the human health effects of chronic, low level arsenic exposure. Arsenic in drinking water has been associated with an increased risk of developing type 2 diabetes, vascular and cardiovascular diseases, reproductive and developmental problems, and several kinds of cancer, notably lung, skin, bladder and liver cancer. We had previously shown that arsenic inhibited glucocorticoid hormonemediated transcriptional gene regulation. We hypothesize that direct biochemical disruption of OR function by arsenic contributes to the pathophysiology of the diseases associated with chronic arsenic exposure. Recent experiments demonstrated that mutant GRs lacking either the N-terminal domain or the C-terminal ligand-binding domain had a similar response to As as wild-type OR. This suggested that the effects of arsenic are primarily mediated through the middle DNA binding domain (DBD). We also have preliminary data suggesting that As binds stoichiometrically to GR at very low intracellular concentrations of As. The specific goal of this project is to determine the biochemical basis for effects of arsenic on GR signaling, focusing principally on As effects on the DBD of OR. In particular, using model mammalian hepatocyte-derived cell lines, wild-type and mutant forms of OR, genetic constructs containing model GRresponsive genes, and various biochemical and genetic techniques, we will examine this question in detail with the following specific aims: 1) Determine the arsenic-OR binding stoichiometry and site(s) of interaction using mass spectrometry and site-directed mutagenesis of OR; 2) Determine the effects of arsenic on the normal functions of the GR DBD, examining in particular whether As alters: a) the formation of cytosolic GR dimers or their transport to the nucleus using mutant and tagged GRs in combination with immunoprecipitation and Western analysis; b) OR monomer-timer interactions with their glucocorticoid response element (GRE) DNA recognition sequences using gel shift and BlAcore analyses; or c) the interaction of OR-GRE complexes with co-activators and other transcription factors using a Chromatin Immuno-Precipitation (ChIP) assay; and 3) mutational analysis of the OR DBD to confirm the key results of specific aims 1 and 2. The goal of these aims is to develop a more detailed understanding of the molecular basis for the effects of arsenic on steroid receptor signaling. This will be important for determining the contribution of these effects to the overall human health effects of arsenic. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ARSENIC EMBRYOTOXOCITY: CELLULAR AND MOLECULAR TARGETS Principal Investigator & Institution: Pisano, M Michele.; Assistant Professor; Mol/Cell/Craniofacial Biology; University of Louisville University of Louisville Louisville, Ky 40292 Timing: Fiscal Year 2002; Project Start 15-MAR-2002; Project End 31-JAN-2004 Summary: (provided by applicant) Arsenic represents a ubiquitous environmental contaminant with adult toxicity in humans and developmental toxicity in laboratory
Studies
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animals. While published reports indicate differential strain sensitivity to induction of NTDs in animal models following prenatal arsenic exposure remain unclear. As such, the need exists to understand the mechanisms underlying interactions between arsenic and maternal/embryonic genotype during development, as well as understand the mechanisms by which suspected human developmental toxicants, such as arsenic, interact with critical aspects of embryonic development. This is particularly true regarding precursor cell populations which populate the early embryo and differentiate during early organogenesis. The proposed research program will investigate the developmental hazards associated with arsenic exposure in a genetically sensitive mouse model in which the folate binding proteins, Folbp1 or Folb2 have been inactivated. Preliminary analysis indicates that animals lacking Flobps demonstrate an increased prenatal risk for arsenic-induced NTDs. The hypothesis to be examined in the present application is that an abnormal folate binding protein genotype increases the risk for arsenic-induced NTDs, the resulting phenotype of which is associated with alterations in cranial neural crest gene expression (i.e. neural crest function). Through breeding of Folbp knockout mice to Wnt1-cre/LoxP mice, a novel "composite" mouse model will be generated which is "genetically sensitive" to arsenic induction of NTDs and in which the neural crest are indelibly (genetically) marked. Such a mouse model will enable analysis of the effects of arsenic on neural crest formation, migration and proliferation under conditions of differing Folbp genotypes (Specific Aim 1). In addition, the application of laser capture microdissection (of neural crest cells) and DNA microarray technologies to this animal model will facilitate generation of isolated neural crest "gene expression profiles" during neural tube morphogenesis and under conditions of arsenic-induced NTDs among embryos of differing Folbp genotypes (Specific Aim 2). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARSENIC EXPOSURE AND BLADDER CANCER IN MICHIGAN Principal Investigator & Institution: Nriagu, Jerome; Professor; Environmental Health Sciences; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): The objective of this proposal is to explore the factors that have contributed to the observed geographic co-clustering in bladder cancer mortality and arsenic concentrations in drinking water in Michigan. The focus will be on the spatial and spatio-temporal patterns of arsenic exposure and how these may relate to the incidence of bladder cancer in those areas of Michigan with elevated levels of arsenic in their drinking water. Reported arsenic concentrations in well waters in the study area range from 1 to 1310 mg/I, with most common levels being 5-50 mg/L. The project being proposed will consist of three components: (1) Construction of exposure scenarios with time dimension that will involve development of the novel space-time information system (STIS) model to be validated using a combination of space-and-timedependent concentrations of arsenic measured in the study, supplementary historical information on arsenic levels in water supplies, hydrogeochemistry of the area, and selfreported residence information and water drinking habits; (2) Biomonitoring of arsenic exposure to be based on analysis of toenails (known to indicate average exposure over a relatively long time) for arsenic and a number of confounding trace elements such as selenium, zinc, copper and antimony; (3) A population-based, case-control bladder cancer study which will be used as an outcome measure for exposure to arsenic in drinking water. Bladder cancer cases (700) and controls (700, matched to cases by sex, race, and +/- 5-year age groups) will be recruited from long-term residents of the 11
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Arsenic
counties (Genesee, Huron, lngham, Jackson, Lapeer, Livingston, Oakland, Sanilac, Shiawassee, Tuscola and Washtenaw) with elevated levels of arsenic in their groundwater. Structured personal interviews will be administered to obtain information on lifetime residential history, current and past water consumption patterns, life-style risk factors (including cigarette smoking and alcohol use), medical history, occupational history, family history of cancer, and dietary habits. The study is designed to shed some light on the dose-response relations for exposure of the U.S. population to arsenic concentrations in the 5-100 mg/L range where no information currently exists. Current efforts by the U.S. Environmental Protection Agency to reduce the maximum contaminant level for arsenic in our drinking water have been bedeviled by contradictory and unvalidated predictions of the risks of chronic exposure to low levels (< 100 mg/L) of arsenic in water. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARSENIC INDUCED MIOTIC ARREST ASSOCIATED APOPTOSIS Principal Investigator & Institution: States, J Christopher.; Associate Professor; Pharmacology and Toxicology; University of Louisville University of Louisville Louisville, Ky 40292 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 30-APR-2008 Summary: (provided by applicant): Arsenic is a natural contaminant of drinking water in many parts of the world, is a known human carcinogen and is #1 on the EPA list of hazardous chemicals. Cancers most often associated with chronic arsenism are squamous and basal cell carcinomas of the skin. How arsenic causes cancer is unknown. However, the National Research Council Report on Arsenic in Drinking Water concluded that the most likely mode of action is induction of numerical and structural chromosomal abnormalities. Arsenite, the carcinogenic form of arsenic found in drinking water, disrupts mitosis causing an anaphase delay and induces aneuploidy in normal diploid human fibroblasts and peripheral blood lymphocytes, and mitotic arrest associated apoptosis (MAAA) in p53 deficient human fibroblasts. The sensitivity of p53 deficient human cells to arsenite induced MAAA suggests that the mechanism of arsenite carcinogenesis is different than sunlight induced skin carcinogenesis in which p53 mutation is an early and common event. The hypothesis to be investigated is that p53 relieves the arsenite-induced anaphase block by activation of the G2 checkpoint response which inactivates cyclin B/cdc2 and derepresses the mitotic exit network and allow the cells to escape arsenite induced MAAA. It is the prevention of apoptosis in arsenic intoxicated cells that allows genetic instability (aneuploidy) after mitotic disruption. Identification of the cellular factors that interact with p53 or the p53 regulated genes to prevent mitotic arrest associated apoptosis and to allow cells to proceed through mitosis with a delay will provide valuable information regarding the mode of action of arsenite. The specific aims proposed are: 1.) Determine activation of the G2 checkpoint pathway in p53(+) and p53(-) cells arrested by arsenite in mitosis; 2.) Test by overexpression and targeted knockdown of G2 checkpoint proteins the role of G2 checkpoint activation in the escape from arsenite induced anaphase block; 3.) Test whether arsenic associated skin tumors are p53 wild type or mutant. The results of these studies will identify players mediating release from arsenite induced mitotic arrest, and will provide valuable information on the mechanism of arsenic induced carcinogenesis, clues to the usefulness of arsenite as a chemotherapeutic agent and valuable information on the mode of action of mitosis disrupting drugs in killing human cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
Studies
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Project Title: ARSENIC INDUCED SIGNALING PATHWAYS IN HUMAN EPIDERMIS Principal Investigator & Institution: Abdel-Malek, Zalfa A.; Research Professor; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2001; Project Start 01-APR-1995; Project End 31-MAR-2005 Summary: (Taken from application) Toxicity due to exposure to high levels of arsenic through dietary, occupational, or medicinal routes has been well documented in different countries. The most obvious and prevalent manifestations of arsenic toxicity are the cutaneous changes that involve hyperkeratosis and increased pigmentation, and latent basal and squamous cell carcinoma. The latter two types of skin cancer differ from the sun induced skin cancer tumors in that they occur mainly on the palms and soles, rather than on sun exposed anatomical sites, and are more invasive and metastatic. Although arsenic induced cutaneous alterations are histologically well characterized, the molecular mechanisms by which they arise are poorly understood. In particular, the mechanisms by which arsenic affects genomic DNA and induces the expression or suppression of specific genes are for the most part unknown. Given that the skin is the first interface between the human body and the environment, and that cutaneous manifestations often reflect internal organ dysfunction, it is important to elucidate the mechanism of action of arsenic on human skin. There is sufficient evidence to support the notion that arsenic induces oxidative stress in mammalian cells. In the cutaneous epidermis, increased keratinocyte proliferation that leads to hyperkeratosis and eventually cancer tumors, as well as hyperpigmentation, may be the outcome of arsenic induced oxidative stress in keratinocytes and melanocytes, respectively. We are proposing to investigate the hypothesis that arsenic induced cutaneous alterations result from oxidative stress that disrupts normal epidermal cell proliferation and differentiation. For this, we will use primary cultures of normal human melanocytes and keratinocytes, as well as a skin substitute model that mimics the skin in situ. The effects of arsenic on genes involved in regulating keratinocyte proliferation and differentiation, and melanocyte pigmentation will be elucidated. The above in vitro models represent an optimal approach to elucidate the mechanism of action of arsenic on human cells and tissues. The results to be obtained should be relevant to other epithelial tissues, such as lung and bladder tissues, that are affected by arsenic. The studies hereby proposed should set the stage for further investigations of the mechanisms by which arsenic might promote the effects of other environmental carcinogens, such as ultraviolet radiation and polycyclic aromatic hydrocarbons. The outcome of this proposal should lead to more effective means for intervening in, and treating the manifestations of arsenic toxicity, and for setting more effective policies regarding safe levels of arsenic exposure. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ARSENIC TRIOXIDE & ASCORBIC ACID FOR MULTIPLE MYELOMA Principal Investigator & Institution: Lee, Kelvin P.; Associate Professor; Microbiology and Immunology; University of Miami Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2007 Summary: (provided by applicant): Despite advances in therapy, greater than 90% of patients with multiple myeloma eventually relapse with chemotherapy-resistant disease. These myeloma cells are typically resistant to a wide range of chemotherapy agents through a number of different mechanisms, including upregulation of efflux
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pumps, mutations in drug targets and resistance to drug-induced apoptosis. It is therefore important to develop new treatment agents that are active against multi-drug resistant myeloma. Arsenic trioxide (As203) has been recently shown to have significant activity against relapsed acute promyelocytic leukemia. We have reported that As203 effectively induces apoptosis in vitro of both drug resistant myeloma cell lines and primary myeloma isolates from relapsed patients. Arsenic-induced apoptosis is triggered through the generation of reactive oxygen species (ROS) and subsequent oxidative cellular damage. We have also found that intracellular glutathione (GSH) protects against the toxicity of As203 (either by reducing ROS or by direct conjugation to arsenic). Addition of ascorbic acid (AA) depletes intracellular GSH and potentiates As203-mediated killing of chemotherapy-resistant myeloma cells. These data led us to open an NCI-sponsored phase I/II clinical trial of arsenic trioxide + ascorbic acid for the treatment of relapsed and refractory multiple myeloma. We have completed the phase I component, and have found that an As203 dose of 0.25 mg/kg/d + AA 1000 mg/d can be safely administered with modest toxicity and promising efficacy. Correlative studies demonstrate a significant association of serum ascorbic acid levels with depletion of intracellular GSH. Our hypothesis is that this combination will have activity against relapsed and refractory multiple myeloma, and propose a phase II clinical trial to determine the efficacy of arsenic trioxide + ascorbic acid in the treatment of relapsed/refractory myeloma. The central components of this proposal are correlative studies will seek to establish biochemical, cellular and genetic correlates of efficacy and toxicity. In addition, we will characterize potential mechanisms by which myeloma cells become arsenic resistance, the effect of this resistance on responses to other drugs, and approaches to overcome this resistance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARSENIC TRIOXIDE AND ACUTE MYELOID LEUKEMIA Principal Investigator & Institution: Jing, Yongkui; Medicine; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2002; Project Start 15-JUL-2002; Project End 30-JUN-2006 Summary: (provided by applicant): Arsenic trioxide (As2O3) induced complete remission in acute promyelocytic leukemia (APL, AML-M3) patients that relapsed after all trans retinoic acid (tRA) and chemotherapy treatment. Clinical results indicated that the therapeutic effect of As2O3 in APL correlated with the expression of PML-RARalpha , the product of the t(15;17) translocation, and was mediated by apoptosis and nonterminal differentiation induction. We have found that As2O3 degraded PMLRARalpha and allowed RARalpha (from the wild-type allele) to drive APL cell partly differentiation. However, the connection between PML-RARalpha expression on one hand, and apoptosis induction by As2O3 on the other hand, is unclear. We have found that 1) APL cells contained low amounts of glutathione-s-transferase pi (GSTpi), glutathione peroxidase (GPx), catalase and high amounts of myeloperoxidase (MPO); 2) APL cells were highly sensitive to As2O3-induced apoptosis in vitro by a hydrogen peroxide (H2O2) mediated pathway; 3) Ascorbic acid selectively increased As2O3induced apoptosis in HL-60 cells (which express high amounts of MPO) not in U937 and normal bone progenitors cells (which do not express MPO). We hypothesize that 1) low levels of GSTpi allow As2O3 to inhibit GPx. GPx inhibition in combination with low catalase expression will result in H2O2 accumulation; 2) accumulated H2O2 is converted into reactive oxygen species by MPO, and then trigger apoptosis; 3) PMLRARalpha sensitizes APL cells to As2O3-induced apoptosis by upregulating MPO and/or downregulating GSTpi, catalase and GPx; 4) Ascorbic acid selectively synergizes
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As2O3-induced apoptosis in MPO positive AML cells by producing H2O2 and depleting reduced form glutathione (GSH), the substrate of both GSTpi and GPx. The initial aim of the project is to confirm that As2O3 induces apoptosis through H2O2mediated pathway. This will be tested by comparing H2O2 amount and apoptosis induction in As2O3 treated AML cells. The second aim will determine the central role of GSTpi to control the sensitivity of cells to As2O3-induced H2O2 accumulation and the third aim will examine the functions of MPO in sensitizing As2O3-induced apoptosis. These will be tested by stably transfecting sense or antisense cDNA and using specific inhibitors. The fourth aim will dissect the connection between PML-RARalpha expression and the levels of GSTpi, GPx, catalase and MPO. PML-RARalpha stably transfected cells will be used for this purpose. Our last aim will evaluate the selective apoptosis-induction and the mechanism of As2O3 in combination with ascorbic acid among AML cells with/without expressing MPO in vitro. SCID models bearing AML cells will be used to test the in vivo effect. Successful completion of the proposed studies will not only contribute to elucidation of the mechanism of As2O3-induced remission in APL, but may also provide innovative usage of As2O3 in other forms of AML. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ARSENIC TRIOXIDE DOWN-REGULATES STAT3 ACTIVITY IN AML Principal Investigator & Institution: Wetzler, Meir; Roswell Park Cancer Institute Corp Buffalo, Ny 14263 Timing: Fiscal Year 2003; Project Start 20-MAY-2003; Project End 30-APR-2005 Summary: (provided by applicant): Acute myeloid leukemia (AML) blasts require hematopoietic growth factors for their survival. Growth factors mediate signal transduction through signal transducer and activator of transcription (STAT) proteins. We have demonstrated that STATs are constitutively activated in approximately 50% of AML cases at diagnosis. Blasts with constitutive STAT3 activity have a unique gene profile and are resistant to apoptosis. We have shown that disease-free survival is significantly shorter in patient with, compared to without, constitutive STAT3 activity. Most of the patients in this study were treated with our in-house clinical trial using high-dose cytarabine and idarubicin. Arsenic trioxide (ATO) has growth suppressing activity in acute promyelocytic leukemia. In other types of AML, ATO induces apoptosis, leading to designation of ATO as an orphan drug for AML. However, the precise mechanisms of action of ATO are unknown. We have discovered that ATO down-regulates constitutive STAT3 activity in AML cell lines. We hypothesize that ATO similarly down-regulates STAT3 in blasts from AML patients and thus enhances their sensitivity to undergo apoptosis. We propose to measure the baseline and changes in STAT3 activity in AML blasts during in vivo therapy with ATO. We will accomplish this goal by performing a phase I study of ATO administered over one hour followed by high-dose cytarabine and idarubicin in patients with newly diagnosed AML < 60 years old. We will determine the maximum tolerated dose of ATO in this study and study the effects of in vivo administration of ATO on STAT3 activity, induction of apoptosis and changes in gene expression profiles in AML cells. In addition, we will attempt to identify the mode by which ATO controls the activity of STAT3 and how this effect alters the gene profile patterns and induces apoptosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ARSENIC TRIOXIDE TREATMENT OF LYMPHOPROLIFERATIVE DISORD Principal Investigator & Institution: Waxman, Samuel; Wiener Professor/ Medical Director; Medicine; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2004 Summary: As2O3, given by an intravenous infusion empirically designed in China, has become a new therapeutic agent of choice in the treatment of refractory acute promyelocytic leukemia (APL). It is an unusual agent since it is effective in APL patients that are chemotherapy-resistant and at the apparent therapeutic concentration of 1-2 M induces clinical remission with minimal myelotoxicity. Similar to all trans retinoic acid, As203 may be uniquely effective in treating APL since it can induce both differentiation and apoptosis in APL cells in vitro and in vivo. Whether As203 can be extended as a cancer treatment remains to be determined. We elected to extend the use of As203 to lymphoproliferative disorders (LPD). Anecdotal, unpublished reports from China and more recent case reports in the United States suggest that As203 may be an effective treatment of LPD. Consistent with this is our observation that As203 (1-2 M) treatment of cell lines and primary cultures of LPD (B-cell lymphoma, CLL, ALL, multiple myeloma but not T-cell lymphoma) causes significant growth inhibition and, in some cells, measurable apoptosis similar to NB4 cells (t(15:17) APL cell line). As303 is also appealing since it effectively inhibits growth and induces apoptosis in malignant cells with mutant p53, in lymphoma cells with t(14:18) that overexpress Bcl-2 and does not demonstrate cross resistance to taxol and doxorubicin in P388 lymphoma cells expressing MDR-1. As203 probably has multiple effects that contribute to the induction of cell death dependent on dose, cell type or cellular environment. In vitro, As203 in some cells increases H202 accumulation which acts on the mitochrondria to induce caspase dependent apoptosis. However, these observations made in vitro should be interpreted with caution since cellular levels of glutathione and H202 may be artifactually altered in tissue culture media and are likely to differ from that of cells in vivo. Little is known about the consequence of in vivo exposure of 1-2 M As203 and its effect on human malignant cells. We will compare and contrast in vitro and in vivo effects of As203 treatment of LPD cell lines and primary cultures of LPD cells obtained from animals and patients. These materials will be used: 1) to evaluate the importance of the intracellular redox profile and accumulation of H202 and arsenic to As203-induced growth inhibition and apoptosis; 2) to characterize the cellular responses to As203 at mRNA level using cDNA microarray in LPD cells obtained from patients treated with As203; 3) to design combination therapies in vitro and in vivo to improve the sensitivity of LPD cells to As203; 4) we have designed a phase II pilot study to evaluate 0.25 mg/kg/day As203 (2-1/2 higher concentration than used in APL) in the treatment of patients with relapsed and refractory indolent LPD. The study is designed to identify potential surrogate markers of As203 activity. Should our laboratory study identify agents or schedules that enhance the response to As203, we will use them to appropriately modify the initial phase II pilot study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ARSENITE ACTIVATION OF SIGNALING PATHWAYS IN HUMAN EPIDERMAL KERATINOCYTES Principal Investigator & Institution: Steinberg, Mark L.; City College of New York 138Th St and Convent Ave New York, Ny 10031 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2007
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Summary: Arsenic is a prevalent environmental pollutant that poses a significant health risk worldwide. There is now compelling evidence that chronic exposure to arsenic is carcinogenic and that such exposure results in cancers of the skin and various internal organs. However, arsenic is not directly mutagenic and the oncogenic mechanism of action remains largely unclear. The overall goal of the experiments described in this proposal is to elucidate growth regulatory pathways effected by arsenic treatment in cultured human keratinocytes with a view towards understanding mechanisms underlying the oncogenic processes induced by long term arsenic exposure in humans. Towards this end we will use cDNA microarray analyses to identify growth regulatory genes in human keratinocytes whose expression is modulated by exposure of the cells to arsenite at low (submicromolar) levels. The microarray data will be subjected to cluster analyses to discern groups of genes that fall into groups based upon the manner in which their expression is modulated by arsenic treatment, in particular genes that show similar up- or down- regulation profiles as functions of time and dose. We will also carry out a series of experiments to examine the role of arsenite-mediated activation of D-type cyclins as effectors of premature exit from the GI: i) We will examine expression levels and phosphorylation status of intermediates in a receptor-mediated pathway that regulates expression of cyclin D1 via beta-catenin in order to determine how arsenic might interact with the beta-catenin pathway to effect changes in the steady-state levels of cyclin D and, 2) We will use a new technique based on transduction of a peptide containing the HIV TAT transduction protein fused to a small segment of the p16 INK4a to specifically block the cyclin D-cdk4/cdk6 kinase. By observing changes in the length of the G1 phase as function of kinase inhibition (Rb phosphorylation) we can determine whether arsenic directly enhances G1 exit via cyclin D-cdk4/cdk 6 kinase activity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AS-GSH CONJUGATION LIMITS AS AVAILABILITY & TOXICITY Principal Investigator & Institution: Lieberman, Michael; Professor and Chairman; Pathology; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 05-JUN-2000; Project End 31-MAY-2005 Summary: The overall goal of this work is to learn more about the detoxification and clearance of arsenic (As) and to examine the role that As-protein conjugates play in toxicity. The major hypothesis to be tested is that clearance of As in vivo is dependent on two separate pathways, a major one involving formation and transport of As-GSH conjugates and a minor one dependent on transport of As ions; further, failure to reduce the reactivity of As b GSH conjugation allows the formation of metal-protein thiols that are toxic to the cell. The project takes advantage of recent advances in mass spectrometry and molecular genetics to address these issues. Although it is widely postulated that GSH conjugates of As are essential for its detoxification, there is no convincing demonstration of their existence in vivo. The investigators have synthesized arsenic triglutathione (ATG) and methyl arsenic diglutathione (MADG) and identified them in the urine of gamma-glutamyl transpeptidase (GGT)-deficient mice and the bile of wild type mice by use of liquid chromatography/mass spec (LCMS) and LC/inductive coupled MS (LC/ICP-MS). Other preliminary data using multidrug resistance-associated protein 2 (MRP2)-deficient rats have shown that As excretion into bile is dependent on this gene. They have also used gamma-glutamyl cysteine synthetase (GGCS)-deficient embryos to develop cells that lack the ability to synthesize GSH and demonstrated that these cells are As-sensitive. They will extend these studies and develop methods to study other As-thiol conjugates in vivo. They will test the
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hypothesis that formation of As-GSH conjugates and their As-cysteine derivatives are quantitatively the most important pathway in As clearance. They will use rodents deficient in MDR proteins and MRPs to test the hypothesis that these proteins function in As-GSH excretion. They have determined that yeast deficient in the ubiquitin/proteasome pathway for protein degradation is sensitive to As. They will use these, GGCS-deficient and GSH-overproducing mammalian cells, and mice deficient in ubiquitin/proteasome function to test the hypothesis that failure to form As-GSH conjugates allows formation of As-protein thiol conjugates that are toxic to the cell. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIOAVAILABILITY OF ARSENIC IN SOILS AS A FUNCTION OF SOIL PROPERTIES Principal Investigator & Institution: Sarkar, Dibyendu; University of Texas San Antonio San Antonio, Tx 78249 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2006 Summary: Years of widespread application of arsenic-based pesticides have reportedly increased the background concentration of this toxic metalloid in agricultural soils. Rapid encroachment of suburban development on lands previously used for agricultural purposes in the last two decades has tremendously increased the potential for human contact with this Group-A carcinogen. The importance of considering soil ingestion from incidental hand-to-mouth activity by children has been repeatedly emphasized in recent studies assessing public health risks associated with long-term exposure to low-level metal-contaminated systems. The long-range objective of the proposed research is to help develop a more accurate risk assessment model for exposure to low doses of arsenic in soils. Studies suggest that bioavailability of arsenic is much less in soils than in water (100% bioavailable), indicating that the current practice of assessing human health risk from ingested soil-arsenic using the water model (due to absence of an appropriate soil model) seriously overestimates potential risk. It also sets much higher limits on soil-cleanup goals, essentially translating to millions of dollars in over-expenditure during the remediation process. In order to avoid overestimation of health risk, and to prescribe more appropriate and cost-effective remedial methods, an accurate assessment of bioavailability based on geochemical fate of arsenic in such soils is required. Realizing the heterogeneity of the soil-plant-water environment and the wide range of interactive bio-physico-chemical parameters, an integrated greenhouse and laboratory study has been proposed by a team of soil scientists, chemists, and plant scientists with the following specific aims: (1) to examine the relationship between geochemical speciation and bioavailability of arsenic as a function of soil properties, (2) to determine the applicability of quantitative models in predicting arsenic retention in complex multi-component systems, such as soils, (3) to evaluate the use of low-cost chemical amendments, such as water treatment residuals in decreasing soil arsenic availability, and (4) to identify the chemical, physiological and genetic mechanisms behind uptake and detoxification of arsenic in plant systems. Collectively, this new knowledge is expected to have a major positive impact on modification of the current human health risk assessment practices by understanding how soil biogeochemical properties influence arsenic uptake and bioavailability. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: BIOLOGICALLY BASED CANCER RISK ASSESSMENT FOR MIXTURES Principal Investigator & Institution: Luebeck, E Georg.; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2001; Project Start 01-SEP-1998; Project End 31-AUG-2003 Summary: In this proposal we address the problems of estimating and predicting carcinogenic risks from exposure to mixtures of carcinogens. Our approach to this problem will be based on the two mutation clonal expansion (TMCE) model of carcinogenesis. This model can explicitly accommodate both initiators and promoters in the risk assessment process. In this proposal, we make a distinction between simple and complex mixtures. Complex mixtures, such as diesel exhaust, emissions from coke oven batteries, and cigarette smoke, contain hundreds of cancer causing chemicals. Often, however, complex mixtures can be treated as single carcinogens when good data on exposure to the entire mixture are available. Thus, the first objective addresses the problem of estimating cancer risk when a small number of component carcinogens is involved. Questions regarding the roles of the carcinogen type (mode of action), exposure pattern, dose-protraction, and dependency on start and stop of exposures are formulated and their impact on cancer risk explored. Specifically, we focus on human exposures to low and high LET radiation and lung cancer (or death from lung cancer) as the endpoint. Three large data sets will serve to illustrate the usefulness and effectiveness of our approach: the Colorado Plateau Uranium Miners cohort, with detailed individual information on joint exposure to cigarette smoking and exposure to radon; the Chinese Tin Miners data set, with detailed individual information on three lung carcinogens: tobacco smoke, radon progeny and arsenic; and the Life Span Study of the atomic bomb survivors. The second objective concerns the development of appropriate methods for analyzing case-control data using biologically-based models. This provides another tool for assessing the carcinogenic potential of mixtures. The third objective concerns the toxicity equivalency factor (TEF) approach for complex mixtures that may contain numerous chemical components like those mentioned above. To evaluate the usefulness of the TEF approach we propose to analyze the Allegheny/nonAllegheny coke oven cohort data, as an example. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CHARACTERIZATION OF A POTENTIAL NUCLEAR PROTEIN DEPOT Principal Investigator & Institution: Maul, Gerd G.; Professor; Wistar Institute Philadelphia, Pa 191044268 Timing: Fiscal Year 2002; Project Start 01-JUL-2002; Project End 30-JUN-2006 Summary: (provided by applicant): Specific nuclear domains named ND10, PML bodies or PODs have reached prominence because proteins contained in these structures are directly or indirectly associated with specific diseases such as acute promyelocytic leukemia, various viral infections, cadmium and arsenic exposure and other environmental toxins. In addition, cellular regulatory loops induced by interferon and thermal stress are correlated with recruitment to or release of regulatory proteins like PML, Daxx and Sp100 from ND10 However, none of the encompassing transcriptional changes appear to occur directly at these nuclear sites. We therefore hypothesize that ND 10 function as nuclear depots, thus separating the functional site of the ND 10associated proteins from that of their highest aggregation at ND 10. To determine what functions are controlled through release or recruitment of ND 10-associated proteins
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and what the benefits are to the cell in combating the induced stress, we plan to identify and characterize the protein composition of ND 10, determine which proteins regulate ND 10 dispersion and analyze the regulatory mechanisms underlying the segregation and dispersion of specific proteins. We will establish the functions of ND10 and their associated proteins by testing for the effects of loss and regulated change of specific ND10-associated proteins on the cells transcriptional profile using knock-out cells and regulatable revertants. We will define the mechanisms used by global effectors such as thermal stress, cadmium and arsenic exposure that activate the regulatory pathways controlled at ND 10. Specifically, we will define the biological significance of the regulated sequestration or release of ND 10-associated proteins in the defense of the cell from toxins and stress. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHEMICAL CHEMOSENSITIVITY
GENETIC
APPROACH
TO
MELANOCYTE
Principal Investigator & Institution: Orlow, Seth J.; Professor; Dermatology; New York University School of Medicine 550 1St Ave New York, Ny 10016 Timing: Fiscal Year 2003; Project Start 25-SEP-2003; Project End 30-JUN-2005 Summary: (provided by applicant): Melanomas are typically resistant to a variety of chemotherapeutic agents. While the basis for chemoresistance of a number of neoplasms is generally understood, the mechanisms leading to melanoma chemoresistance are unclear. Moreover, sensitivity of melanocytes to cytotoxic insult has been implicated in the pathogenesis of vitiligo. Recently, the melanocyte-specific pink-eyed dilution (p) gene product has been implicated in controlling melanocyte sensitivity to cytotoxic compounds including arsenicals and cisplatin. Melanocytes from mice with a deletion of this gene are resistant to these agents and expression of the p gene in yeast leads to increased sensitivity to arsenical compounds and other metalloids. The availability of small molecules to dissect the operative pathways controlling the sensitivity of melanocytic cells to cytotoxic agents would be of value to basic researchers as well as offering potential therapeutic leads. A systems-based "chemical genetics" approach is proposed to further understanding of the pathways controlling these processes. Specific aims of the proposed research are: 1. Screening of a diverse triazine-based tagged library of 10,000 compounds in a simple cytotoxicity assay that will identify those compounds not inherently cytotoxic but capable of overcoming the resistance of melanocytes lacking p gene expression to arsenic and cisplatin. 2. Combinatorial chemistry to maximize the potency of lead compounds and to define structural requirements for activity. 3. Isolation of cellular targets for active compounds by affinity chromatography using immobilized compound. The molecules in this unique library all contain one of several long linkers at one of 3 R positions, allowing the construction of affinity matrices to rapidly isolate the targets of the lead compounds. Microsequencing of affinity-isolated targets will be performed and used to identify targets from protein databases. Findings from the proposed studies will result in a deeper understanding of the cellular pathways underlying melanocyte chemosensitivity, and in new research tools for cell biologists. The data should provide the basis for future therapeutics to treat metastatic melanoma and for purposes of depigmentation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COMMUNITY ASSIST OF SOUTHERN ARIZONA Principal Investigator & Institution: Estrada, Ramon M.; Program Director; Child and Family Resources, Inc. 1040 N Alvernon Way Tucson, Az 85711
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Timing: Fiscal Year 2001; Project Start 15-SEP-2001; Project End 31-AUG-2005 Summary: (provide by applicant) The long term objectives of the community-directed Community Assist of Southern Arizona (CASA) are to reduce the communities' exposures to environmental pollutants, link members of communities who are affected by adverse environmental conditions with healthcare providers, provide relevant and culturally sensitive information about environmental pollutants, promote a communitywide interest in the project, and act as a liaison between researchers and agencies and communities to help disseminate research results in an easy to understand format. The specific aim of this project is to expand the Child Health Champion Campaign (CHCC) in four ways: 1) to include all border regions of southern Arizona where Child & Family Resources, Inc. has an office (Nogales, Douglas, southern metropolitan Tucson, and Yuma; 2) to include additional information on mitigation measures and to assist with families' mitigation; 3) to expand the program to include additional environmental health areas of concern to the communities, in particular childhood lead poisoning; and 4) to further act as liaison between the community and researchers and government agencies. The two measurable goals of CASA are reduction in the number of visits to school nurses caused by respiratory illnesses and reduction in the number of childhood lead and arsenic poisoning cases reported by doctors and laboratories. The objectives which define the design and methods of the project are to finish laboratory analysis of items of concern for heavy metals; to develop survey instruments appropriate for each community; to conduct a minimum of 200 home visits in each community; complete mitigation in at least 75% of those homes requiring and desiring mitigation; to conduct six workshops for parents and children in each community; to develop at least one school program in each community; to present at least one radio broadcast in each community; of those identified with health problems, to assist at least 75% to obtain medical care; to conduct at least one workshop for farmacias and yerberias on the heavy metal content of home remedies; and to complete the evaluation of the project and the input of researchers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE SURVEILLANCE OF OCCUPATIIONAL HEALTH IN NEW YORK Principal Investigator & Institution: Gelberg, Kitty H.; Bureau of Occupational Health 547 River St Troy, Ny 12180 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2005 Summary: New York, with the assistance of the SENSOR and ABLES programs, has established a structure for occupational disease surveillance and follow-up in New York State. Provisions of the New York State (NYS) Public Health Law mandate the reporting of a number of occupational conditions in NYS. Since 1981, the New York State Department of Health, Bureau of Occupational Health (BOH) has operated a Heavy Metals Registry for the reporting of cases of lead, mercury, arsenic, and cadmium poisoning, and an Occupational Lung Disease Registry for the reporting of cases of work related lung disease. Since 1991, BOH has operated a Pesticide Poisoning Registry and receives reports from healthcare providers of suspected pesticide poisonings. While all of these registries are operational, the extent to which there is active surveillance, with aggressive case finding, ascertainment and follow-up, varies. There are a number of reasons for this variability, including differences in how the diseases are diagnosed and the different reporting sources for the various registries. Additional federal resources will permit us to build upon existing reporting laws and infrastructure and expand current surveillance efforts to help us achieve the NIOSH standards for a model
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core surveillance system for a range of significant occupational conditions. We propose to conduct general surveillance of existing databases available to the Department of Health such as death certificates and hospital discharge data to assist with documenting the magnitude of occupational injuries and illnesses in New York, and to identify trends and industries occupations at elevated risk. Focus will be primarily upon upgrading our Occupational Lung Disease Registry; however, we will also focus more attention on conducting educational outreach for all of our registries. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE-NEUROTOXICOLOGY/NEURODEGENERATIVE DISEASE RESEARCH Principal Investigator & Institution: Graziano, Joesph H.; Columbia Univ New York Morningside 1210 Amsterdam Ave, Mc 2205 New York, Ny 10027 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: The developing nervous system is vulnerable to adverse effects due to exposures to a variety of substances in the environment, particularly metals and pesticides. At the same time, chronic exposure to low levels of neurotoxicants throughout life can lead to impaired neurologic functioning later in life, particularly in the elderly. As life expectancy increases, and the baby-boom generation approaches retirement age, neurodegenerative diseases such as IPD, Essential Tremor and Alzheimer's Disease will have a significant impact on quality of life, and will represent significant financial costs to the health care system. Collectively, the investigators in this research core are interested in understanding the extent to which, and mechanisms 295 whereby, populations exposed to known quantities of neurotoxicants suffer adverse consequences on the nervous system. The populations under investigation, which include birth cohorts in Yugoslavia and northern Manhattan, populations of adults and children chronically exposed to arsenic in drinking water in Bangladesh, and populations of the elderly in northern Manhattan, represent groups of individuals who have been remarkably well characterized for a variety of chemical exposures and other risk factors for adverse neurologic outcomes. At the same time, laboratory based scientists are exploring the mechanisms whereby the compounds of interest alter normal function. The overall goals of the Neurotoxicology/Neurodegenerative Disease Research Core are: I) to promote and facilitate interdisciplinary neuroscience-related research that will define the magnitude of effect of exposure to substances in the environment that are believed to be involved in the etiology of neurologic disease. These substances include metals (Pb, Mn, Fe and As), pesticides (chlorpyrifos, diazinon, propoxur, and others), 13- carboline alkaloids (harmane and harmine), and other factors; and 2) to unravel the cellular and molecular mechanisms whereby these substances exert their effects. The core is responsible for furthering the development of existing and new investigations of environmental exposures that affect the incidence and/or progression of diseases of the central and peripheral nervous systems. The Specific Aims currently under investigation include: 1) to define the cellular and molecular events involved in chemical models of Parkinsonism and in IPD, with the goal of defining those that are common to each; 2) to elucidate the environmental risk factors associated with the onset of IPD, Essential Tremor, and Alzheimer's Disease; 3) to examine, in both humans and animal models, the relationship between environmental Pb exposure and brain function, with particular interest in the possible mediating effects of Pb on thyroid hormone fate and transport; 4) to determine whether exposure to arsenic in drinking water is associated with adverse neuropsychologic effects in children, and
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polyneuropathy in adults; and 5) to develop biomarkers of prenatal pesticide exposure in humans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENTAL CHEMOTHERAPY Principal Investigator & Institution: Spriggs, David R.; Chief/Associate Attending Physican; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 01-JAN-1978; Project End 30-JUN-2005 Summary: (Applicant's Description) Chemotherapy remains one of the principal means of cancer treatment. Over the past 3 decades, this grant has allowed Memorial Hospital to rapidly test and apply new treatments to a variety of cancers. The overall goal of this project will be to conduct Phase I studies of new single agents and combination therapies developed at Memorial Hospital for application in disease specific Phase II and Phase III trials. Highest priority for new studies will be given to ideas and compounds developed within the Memorial Sloan Kettering Cancer Center for which we hold the IND. The clinical trials to be performed will include both molecular markers of response and pharmacokinetics when appropriate. All trials in this project are Phase I studies. The clinical trials performed in this project will be grouped into 3 specific aims. Specific aim 1 is the development of novel agents including geldanamycin analogs, 10 propargyl-10 deazaaminopterin, arsenic trioxide, PS341, and desoxyepothilone B. Specific Aim Two is a target based therapy program utilizing Pyroxamide and is directed at the development of this putative differentiation agent. Finally, in Specific aim 3 correlative science is described to support these trials. Each of these clinical studies will be linked to pharmacokinetic and molecular laboratory correlative studies. Through this work, we expect to identify new, more active treatments for the successful management of human malignancies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DEVELOPMENTAL TARGETING--PML RARA EXPRESSION IN VIVO Principal Investigator & Institution: Westervelt, Peter; Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 30-JUN-2001 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DISRUPTION OF STEROIDOGENISIS BY ARSENITE Principal Investigator & Institution: Jefcoate, Colin R.; Director, Environmental Toxicology Ctr; Pharmacology; University of Wisconsin Madison 750 University Ave Madison, Wi 53706 Timing: Fiscal Year 2001; Project Start 01-FEB-2000; Project End 31-JAN-2005 Summary: Sodium arsenite, a major form of environmental arsenic, cross-links vicinyl protein sulfhydryl groups, leading to multiple toxic cellular responses, including oxidative stress. We found that arsenite, even at low concentrations, substantially inhibits adrenal steroid production both in rats in vivo and in cultured cells. The key step in the regulation of steroidogenesis by cAMP is the transfer of cholesterol by cAMP is the transfer of cholesterol to the inner mitochondrial cytochrome P450/SCC. The Steroidogenic Acute Regulatory protein (StAR) plays a major role in this process. This
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protein is formed as a 37 kDa precursor that is phosphorylated by protein kinase A (PKA) and is processed to more active 30 kDa in the mitochondria. This processing is coupled to enhanced cholesterol transport from the outer to the inner mitochondrial membrane. This continuous translation and processing is necessary for cholesterol transfer. We will show that arsenite suppresses cholesterol metabolism in adrenal (primary and Y-1) and testis Leydig (MA-10) cells, while also attenuating this essential StAR processing. Arsenite, at very low concentrations, substantially potentiates cAMPinduced StAR transcription prior to suppression at higher concentrations. Another oxidative stress agent, anisomycin, shows a similar biphasic effect on this process and, like arsenite, activates stress-activated protein kinases (SAPK), such as JNK and p38. We propose that SAPK stimulation of StAR transcription provides a protective mechanism to sustain StAR activity as later key steps are inhibited. We will establish, with selective inhibitors that arsenite alters the transcription and the stability of StAR mRNA primarily via the activation of p38. The transcriptional modulation involving arsenite will be analyzed by dissecting the StAR upstream regulatory region, particularly sites recognizing the SF-1 nuclear regulator. Arsenite modulation of the activity of normal and mutated recombinant SF-1 on StAR-luciferase reporters will be used to further define the mechanism. The proposed research will provide mechanistic insight into a novel adrenal response to chemical stress that may be shared by other steroidogenic cells. Effects of arsenite on SF-1 regulation have broader relevance to adrenal/gonadal development regulated by this factor. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DNA REPAIR AND BLADDER CANCER Principal Investigator & Institution: Andrew, Angeline S.; Community and Family Medicine; Dartmouth College 11 Rope Ferry Rd. #6210 Hanover, Nh 03755 Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2005 Summary: (provided by applicant): Each year, 51,200 people in the United States are diagnosed with bladder cancer and 10,600 die of the disease. Exposure to environmental chemicals as well as genetic factors play a significant role in initiation of bladder cancer. Epidemiologic investigations have clearly shown an increased risk of bladder and other cancers associated with arsenic exposure, but the level at which it poses a measurable health risk has been the topic of considerable debate, and its precise mechanism of action remains unknown. Furthermore, a number of studies have reported an interaction between smoking, genetic polymorphisms and cancer risk. We will test the hypothesis that polymorphisms in the nucleotide excision repair pathway are associated with increased bladder cancer risk. We will address this hypothesis using exposure data and blood samples collected in a large population-based study of bladder cancer in the New Hampshire (850 cases, 1,365 controls). The specific aims of the project will be to 1) test the hypothesis that genetic variants in the nucleotide excision repair pathway genes (XPD, XPC, XPA, and ERCC1), are associated with increased risk of bladder cancer, and 2) determine whether environmental exposures (arsenic, smoking) and nucleotide excision repair polymorphisms interact to increase bladder cancer risk. This study presents a unique opportunity to clarify how genetic and environmental factors affect DNA repair and contribute to bladder cancer susceptibility. Through our study, we hope to contribute to both our mechanistic understanding of bladder cancer and to identify subgroups of the population that may be at greater risk of environmentallyinduced cancers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EASTERN COOPERATIVE ONCOLOGY GROUP Principal Investigator & Institution: Sparano, Joseph A.; Medicine; Yeshiva University 500 W 185Th St New York, Ny 10033 Timing: Fiscal Year 2002; Project Start 01-JUN-1978; Project End 30-APR-2004 Summary: The general aims of the proposal are to expand our knowledge of the biology of cancer, to utilize this knowledge to design new treatments for patients with cancer, to test such new treatments in multi-institutional prospective, randomized clinical trials, and to disseminate the results of such trials through peer review publication in scientific and medical journals, and by presentation at scientific and medical meetings. These aims will be accomplished by 1) accrual of patients to ECOG therapeutic and other trials and by collecting and reporting accurate data from those trials to ECOG in a timely fashion, 2) playing scientific and administrative leadership roles in the Group, 3) conducting local clinical and laboratory pilot studies the results of which may serve as bases for larger ECOG studies, and 4) by utilizing our ECOG participation in the training of oncology fellows and junior faculty in clinical methodology. Our specific aims in the next funding period are to increase accrual to ECOG therapeutic and other trials, and to serve as study chairs of several ECOG trials based entirely or in part on pilot data from this institution, including a study of thrombo-poietin in elderly adults with acute myeloid leukemia, a study of theophylline in chronic lymphocytic leukemia, and a study of arsenic trioxide in relapsed acute pro-myelocytic leukemia. In addition, laboratory investigations in colon cancer, cervical cancer and leukemia utilizing fresh and banked samples from patients enrolled on ECOG studies group wide are proposed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EFFECT OF METAL MIXTURES ON GENE EXPRESSION AND CARCINOGENESIS Principal Investigator & Institution: Perhouse, Mark A.; University of Montana University Hall 202 Missoula, Mt 598124104 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: Arsenic poses a serious environmental threat to human health. It contaminates numerous water supplies nationwide, from natural or industrial sources, and can be found in our food supply. Complicating this picture is the occurrence in many contaminated sources of additional metals such as copper, manganese, lead, zinc, and cadmium, each with a link to human health problems. Specific progress has been made recently in the development of transgenic animal models of arsenic carcinogenesis. These models function to recapitulate tumor formation when challenged with arsenic or other carcinogens in a controlled laboratory setting. This study aims to address the molecular and cellular changes taking place in a transgenic murine model of arsenic carcinogenicity, the Tg.AC mouse. This model will allow us to determine if there is toxic synergy, anergy, or additive effects following chronic administration of arsenic and other metals. We will study molecular and cellular responses to individual metal(loids) or mixtures using high-density cDNA microarrays, as well as any morphological changes, Our hypothesis is that the relative risk to human health from complex mixtures of metal(Ioid)s can be predicted based on an improved understanding of the molecular and cellular events taking place in a mammalian model of tumor formation. For the proposed grant period we propose the following specific aims.(1) to assess the reproducible gene expression changes during chronic metal(Ioid) mixture administration in five tissues of the Tg.AC mouse model that have particular human disease relevance: lung, bladder, blood, liver, and skin. Our hypothesis is that there exist
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tissue-specific and metal-specific expression signatures, and that novel signatures will be attainable for mixtures, suggesting mechanisms by which these mixtures interact to increase or decrease tumorigenicity. (2) to assess the carcinogenic potential of complex mixtures of metal(Ioid)s in the Tg.AC transgenic mouse model. Our hypothesis is that mixed metal(Ioid)s will affect the number and severity of tumors induced through synergistic, antagonistic, or additive mechanisms. Our understanding of these mechanisms will be generated from gene expression results in specific aim 1. Tissue at the site of tumors, as well as from other organs, will also be examined for pathological changes reflective of carcinogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ELIMINATION OF CHEMOTHERAPY IN NEWLY-DIAGNOSED APL Principal Investigator & Institution: Estey, Elihu; Leukemia; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2005 Summary: (provided by applicant): Administration of all-transretinoic acid (ATRA) + myelotoxic chemotherapy results in long-term remission in 70% of patients with newly diagnosed acute promyelocytic leukemia (APL). It is becoming clear however that this approach is associated with development, several years later, of myelodysplastic syndromes and AML. The demonstration of the effectiveness of arsenic trioxide (ATO) in APL makes it feasible to assess, in newly diagnosed APL, whether the combination of ATO + ATRA will enable elimination of myelotoxic therapy. To test this hypothesis (SA#1) we will conduct a trial of ATO + ATRA, with myelotoxic therapy added only if minimal residual disease (MRD), as judged by the standard manual PCR assay, persists or recurs. For safety monitoring we will use a published Bayesian "multiple outcome" design that allows early termination if the rates of either CR, or PCR negativity at 6 months from CR date, are too low. More effective means of measuring MRD would obviously make similar trials more feasible in the future, and SA#2 tests the hypothesis that use of high sensitivity quantitative real-time PCR, rather than the standard assay, and blood rather than marrow will increase the accuracy of current methods. Similarly, understanding of mechanisms underlying resistance to ATRA would increase the possibility of eliminating myelotoxic therapy, and SA#3 tests the hypothesis that addition of ATO to ATRA, while decreasing the overall relapse rate, increases the frequency of missense mutations in the PML-RAR( gene among patients who do relapse. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ENVIRONMENTAL EPIDEMIOLOGY OF LUNG CANCER IN NEW HAMPSHI Principal Investigator & Institution: Duell, Eric J.; Dartmouth College 11 Rope Ferry Rd. #6210 Hanover, Nh 03755 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 30-JUN-2008 Summary: This project integrates spatial analytic techniques and traditional case-control methods in epidemiology to study environmental risk factors for lung cancer in New Hampshire. We will adopt a three-phase approach. First, a geographic information system (GIS), which is the technical environment in which spatial analyses are performed, will be used to reveal spatial patterns and relationships between environmental factors (such as fine particulate air pollution) and lung cancer in New Hampshire. Second, traditional population-based, case-control methods of
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epidemiology will be used to study individual-level risk factor information (collected from questionnaires, drinking water samples, toenails clippings, sera, and germ-line DNA). This will permit us to model causal relations between environmental factors and risk of incident lung cancer in New Hampshire. As part of this approach, we will explore potential modifications in relative risk due to synergy between exposures (arsenic and smoking), host genetic susceptibility, dietary factors, and gender. We also will employ multilevel modeling (hierarchical regression) of individual lung cancer risk using group-level (ecologic/geographic) exposure information (e.g., fine particulate air pollution) and individual-level exposure information (e.g., smoking status, age, gender, education, occupation, use of wood burning stoves, water arsenic concentration, toenail arsenic concentration, DNA repair genotype, and other variables). Multilevel modeling will allow us to improve estimates of individual lung cancer risk by including grouplevel data that have no individual-level analogue (e.g., exposure to fine particulate air pollution). Third, using spatial environmental data and risk models built in phase 2, we will create a risk map of lung cancer in New Hampshire. We will test the validity of our environmental models and our risk map of lung cancer using newly collected lung cancer incidence data from New Hampshire. Through this three-phase approach, we expect that new etiologic factors for lung cancer will be uncovered and that this information will aid scientists and policy makers regarding risk assessment and disease prevention. This project will also set the stage for a comprehensive regional environmental health information system that will serve as a database and knowledgebase for future environmental health studies of lung diseases and other health outcomes in New Hampshire. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENVIRONMENTAL POLLUTANTS & OXIDATIVE STRESS Principal Investigator & Institution: Karin, Michael; Professor; University of California San Diego 9500 Gilman Dr, Dept. 0934 La Jolla, Ca 92093 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2002 Summary: Many Superfund site toxicants exert their chronic toxicity by causing damage to cellular macromolecules via oxidative stress. Exposure to such pro-oxidants also results in induction of a gene expression program whose primary function is to protect cells from oxidative stress. Little is known about the components of the mammalian oxidative stress response and its regulatory logic. To rectify these deficiencies, Project 1 will use a variety of genetic, cell biological and biochemical approaches to investigate the role of already identified stress activated protein kinases in the mammalian response to oxidative stress, identify new components of this induction responses and determine the mechanism of gene induction by a few model toxicants found at Superfund sites, such as arsenite and carbon tetrachloride. We will also search for new regulatory molecules, including protein kinases and transcription factors, involved in the oxidative stress response. Once identified, the pathophysiological function of these molecules will be analyzed through generation of constitutive and conditional knockout mouse mutants. We will investigate how such genetic alterations affect the ability of these animals or cells derived from them to withstand exposure to Superfund site toxicants that are believed to act via induction of oxidative stress. In addition to elucidating the basic regulatory logic underlying the mammalian response to oxidative stress, this project will have two practical outcomes relevant to the mission of the Superfund Research Program; it will create: 1) gene arrays, cell lines and transgenic mice that can be used as biosensors for monitoring exposure to toxicants that cause oxidative stress; 2) strains of mice that are deficient in activation of the protective response to oxidative
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stress. Such mice should be supersensitive to pro-oxidants and thus will facilitate the detection and evaluation of new suspected toxicants and mixtures of chemicals from Superfund Sites for their ability to cause oxidative stress mediated toxicity. To accomplish these goals this project will collaborate and interact with Projects 2, 3, 4 and 5 and will rely on all research support cores. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EXPRESSION OF ANTIBODY DIVERSITY DURING IMMUNE RESPONSES Principal Investigator & Institution: Manser, Timothy L.; Professor; Microbiology and Immunology; Thomas Jefferson University Office of Research Administration Philadelphia, Pa 191075587 Timing: Fiscal Year 2001; Project Start 01-APR-1986; Project End 31-MAR-2003 Summary: The investigator will study the process of antigen selection and hypermatutation, and how they contribute to B cell memory, in the mouse response to phenylarsonate (Ars). This project involves the identification of clones in the Ars response at different stages of their differentiation, and the development of a correlation between this maturation stage and position in the spleen relative to the putative sites of antigen selection and somatic mutation. The Ars response is a well-characterized system by many laboratories. Two broad aims are proposed that are subdivided into several subaims. First, the investigator will characterize the anti-Ars response of A/J mice via the determination of spatial organization of anti-Ars-specific clones with the location of antibody forming cells (AFC) and germinal centers (GC). The first subaim will address the appearance and timing of Ars-specific clones by the use of an anti-Ars V gene antibody and PCR analysis. The investigator will distinguish between two principle models for antigen-driven B cell maturation. A second subaim will employ the same methodologies to evaluate the spatial organization of memory anti-Ars clones. The second broad aim will utilize the investigator s transgene system for study. In the previous period, the investigator has developed a transgene model where an anti-Ars specific rearranged IgVh gene is able to be recruited into the anti-Ars response (and undergo somatic mutation). Using these transgenic mice, they will study the organization of the transgene-encoded anti-Ars clones and B cell maturation. In the first subaim of this section, the investigator will compare the transgene-encoded clonotype (high affinity to Ars) with endogenously emerging clones (low affinity to Ars) for their population of spatial sites of B cell maturation, AFC and GC. For this study an additional antibody reagent will be employed that is more specific for the transgene clonotype. In the second subaim of this section, using the same general methodologies, they will characterize the relationship between affinity for Ars by these two antibody types and the somatic mutation levels of these genes. In a third subaim they will determine whether there is a positive relationship between sites of apoptosis in a GC and the relative incidence of affinity maturation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GALLIUM ARSENIDE SUPPRESSION OF ANTIGEN PROCESSING Principal Investigator & Institution: Mccoy, Kathleen L.; Associate Professor; Microbiology and Immunology; Virginia Commonwealth University Richmond, Va 232980568 Timing: Fiscal Year 2001; Project Start 30-SEP-1994; Project End 31-JUL-2004
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Summary: (Adapted from the Investigator's Abstract) Gallium arsenide (GaAs) is a semiconductor used in the electronics industry. GaAs exposure of animals induces profound immunosuppression. The major objective of this research proposal is to define the mechanism by which GaAs modulates antigen processing by macrophages for activation of antigen-specific helper CD4+ T cells. Previous toxicological studies with GaAs-exposed mice showed that splenic macrophages at a distant site exhibit defective antigen processing, whereas macrophages at the exposure site have an augmented processing ability. Both consequences of GaAs exposure correlate with altered cathepsin proteolysis and will be studied. The impact of intratracheal GaAs exposure will be defined by examining several aspects of antigen processing. The relationship between the structure of a particulate antigen and the processing defect of GaAs-exposed splenic macrophages will be determined by modifying sheep erythrocytes. One form will maintain the particulate nature of sheep cells, and another will disrupt cellular integrity. Sheep cells will be coated with antibody for Fc receptor-mediated entry and delivery to secondary lysosomes. Third, the contribution of GaAs components to the antigen processing defect will be determined. Splenic macrophages will be incubated in vitro with metal chelators to reverse the defect. Fourth, inhibition of cathepsins, the proteases mediating antigen processing, by GaAs components will be determined by kinetic analyses. Proteolytic reactivation by metal chelators will be assessed. GaAs' interference with the transport sorting signal of cathepsins will be examined. Fifth, a correlation between cytokine production and altered macrophage antigen processing will be investigated. A panel of cytokines with varying functions will be measured by ELISA. Mutant nude mice that lack functional T cells, an important cytokine source, will be exposed to GaAs, and antigen processing by alveolar and splenic macrophages will be determined. Finally, co-stimulation is another critical function of presenting cells for T cell activation. GaAs' effect on macrophage co-stimulation will be studied. Expression of co-stimulatory molecules on alveolar and splenic macrophages will be measured by two-color immunofluorescence staining and flow cytometry. The function of macrophage co-stimulatory molecules will be determined by cell titration and antibody blocking experiments. Knowledge concerning the mechanism by which GaAs influences macrophage functions may provide insights into preventing the chemical's impact on the immune system. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CHEMICALS
GENETIC/EPIGENETIC
SUSCEPTIBILITY
TO
SUPERFUND
Principal Investigator & Institution: Costa, Max; Professor and Chairman; Environmental Medicine; New York University School of Medicine 550 1St Ave New York, Ny 10016 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAR-2005 Summary: This application entitled Genetic/Epigenetic Susceptibility to Superfund Chemicals utilizes the disciplines of biomedicine, molecular biology, ecology, and engineering to assess the potential hazardous impact of toxic metals on humans and upon aquatic ecosystems. An underlying theme involves factors responsible for differences in genetic susceptibility of human responses to carcinogenic and toxic metals. The ecology and engineering projects will study how to reduce human exposure to these same Superfund toxic metals. The focus of the research for most project is on arsenic, chromium, and nickel and their interactions with toxic organics, such as PAH's. There are 4 biomedical projects: 1) Epigenetic Effects on Individual Susceptibility to Heavy Metal and Polycyclic Aromatic Hydrocarbon-induced DNA damage (E. Tang); 2)
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Detection of Cr-DNA Adducts in Human Cells (M. Costa); 3) Metal-induced Inflammatory Factors, Oxidative Stress, and Suppression of Their Effects (K. Frenkel); 4) Identification and Genetic Analysis of the Human Arsenic Efflux Pump (T. Rossman). There are 3 non-biomedical projects: 1) Mechanisms of Resistance of Aquatic Vertebrate Populations to Mixtures of Aromatic Hydrocarbon and Metal Contaminants (I. Wirgin); 2) Microbial Biogeochemical Cycling of Arsenic and of Chromium Coupled to the Biodegradation of Aromatic Contaminant Compounds (L. Young); 3) Water-Sediment Model and Criteria for Arsenic and Chrome (D.Di Toro). There is one Molecular Biology Research Support Core which supports the biomedical projects by providing expertise in utilizing the UvrABC excision method in combination with ligation-medicated PCR to map sites of metal and polycyclic aromatic hydrocarbon-induced DNA adducts. The Molecular Biology Core also supports the Affymetrix GeneChip technology and other molecular biology instruments. This program project is directed by an Administrative Core which will be responsible for planning and coordination. The Administrative Core supports a unique Government Liaison unit which reaches out to local EPA Region 2 scientific personnel. With the involvement of the EPA, Outreach specialist, molecular biologists, biomedical scientists, and engineers, we have created a truly multidisciplinary program. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENOMICS OF AML-M3: RELAPSE AND RESISTANCE FACTORS Principal Investigator & Institution: Dipersio, John F.; Cheif, Division of Oncology; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 19-SEP-2003; Project End 31-AUG-2007 Summary: The long-term goal of this project is to identify the genetic events that contribute to the development of relapsed and resistant acute promyelocytic leukemia (APL). We hypothesize that relapsed/resistant AML is associated with specific genetic events that can be defined with high throughput genome-wide scans for mutations. By mining the genetic information from humans and mice with relapsed and resistant APL, specific genes relevant for relapse and resistance will be discovered and validated. The identification of these target genes may lead to improved therapies for these patients. We propose the following Specific Aims: Specific Aim 1. We will generate and "bank" murine APL samples selected in vivo for resistance to ATRA, liposomal ATRA, or arsenic trioxide. We will demonstrate in vivo resistance by showing that survival of treated secondary recipients is not statistically different than the survival of recipients treated with diluent controls. We will also assess banked APL samples for resistance to ATRA or arsenic trioxide in vitro. We will incubate APL cells with these compounds for 24 hours and measure the expression of gelatinase B (which is expressed at its highest levels in terminally differentiated myeloid cells) using quantitative PCR. We will correlate in vitro and in vivo resistance. Specific Aim 2. We will identify candidate loci associated with APL resistance using RNA profiling and comparative genomic hybridization (CGH) techniques. The samples generated in Aim 1 will be subjected to genome wide scans for alterations in gene expression, and for regions of chromosomal amplifications or losses using high resolution CGH. We will also compare paired RNA profiles from human APL patients with de novo vs relapsed and/or resistant disease. Specific Aim 3. We will resequence the exons of candidate genes that have been associated with the development of resistance. Candidate murine and human loci identified in Aim 2 will be resequenced in de novo and resistant APL samples. The approximately 450 leukemia-associated genes in Projects 1 and 4 will also be
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resequenced in a limited number of paired samples from patients with de novo vs. resistant disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HEALIH EFFECTS AND GEOCHEMISTRY OF ARSENIC AND LEAD Principal Investigator & Institution: Graziano, Joseph H.; Professor Public Health And; Div/Environmental Hlth Scis; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAR-2005 Summary: This proposal is submitted in response to RFA ES-99-001, entitled with Superfund Hazardous Substances Basic Research Program. The contamination of soils and drinking water with As and Pb are associated with major public health, remedial, and environmental policy problems. As is found in soil or water at the majority of Superfund sites while Pb is a soil-borne contaminant of concern at approximately 300. This proposal seeks to obtain new knowledge, and train multi-disciplinary pre- and post-doctoral students, concerning the bioavailability of soil Pb in humans, and the bioavailability and/or geochemistry at four Superfund sites in the U.S., two contaminated with Pb and two with As. It also encompasses epidemiologic and geochemistry studies of As in drinking water in Bangladesh which focus on carcinogenic, reproductive and childhood effects of As exposure. We also devote resources to the development of practical remediation strategies for As in wastewater in drinking water. The proposal includes four biomedical research projects: 1) Bioavailability of Soil Pb and As in Humans; 2) Genotoxic Mechanisms of As in Mammalian Cells; 3) A Cohort Study of Aresnicosis in Bangladesh; 4) Environmental As, Pregnancy, and Children's Health. The biomedical research is directly related to that which occurs in three non- biomedical projects: 5) As Mobilization and Bangladesh Groundwater; 6) Redistribution of As at Sites in NF and Maine; and 7) Assessment and Remediation for as Enrichments in Groundwater. The research projects are supported by three Research Support Core Labs: 8) Trace Metals; 9) Geochemistry; and 10) Hydrology An Administrative Core includes an Information Dissemination Program and a Government Liaison & Outreach Program. Finally, a Training Core coordinates multi- disciplinary education and interaction among pre- and post-doctoral trainees support by this proposal as well as other training grant. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HEALTH RISK REDUCTION--METAL ACCUMULATING DESERT PLANTS Principal Investigator & Institution: Gardea-Torresdey, Jorge L.; Dudley Professor of Chemistry And; University of Texas El Paso El Paso, Tx 79968 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2007 Summary: (provided by applicant): Widespread soil contamination in the El Paso/Juarez region poses serious public health risk, mostly due to windblown particulate matter originating at numerous industrial sites polluted with heavy metals. To reduce the detrimental public health effects caused by heavy metals, it is imperative to remediate these areas. Cost effective and environmentally sound approaches are necessary to clean up these sites. The use of plants to up take heavy metals is an innovative technology proven to be successful in both soil and aqueous heavy metal clean up operations. However, most of the plants that have been identified as potential metal hyperaccumulators only grow in areas that are more fertile and cannot survive in
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desert regions. Investigation into the potential for desert species to uptake heavy metals will contribute significantly to the growing body of knowledge of the mechanisms of plants that allow them to uptake heavy metals (phytoremediation). This technology is especially appropriate in desert regions where the soils are light textured and can become air-born at very low wind velocities. Because there are numerous industries in the El Paso/Juarez area that generate heavy metals as by-products of their industrial processes, inhalation of air-borne contaminants has become a major health concern. In order to develop a method to ameliorate this situation, the specific aims of our study include: 1) The growth of desert plant seedlings in climate-controlled agar, hydroponic, and soil media using the following plants: Guayule (Parthenium argentatum); Fourwing saltbush (Atriplex canescens); Desert willow (Chilopsis linearis); Palo verde (Cercidium spp.); and Tar bush (Flourensia cernua); 2) To perform multi-metal solution experiments in the three media types mentioned in (1); 3) The determination of the specific metalchelating agents (phytochelatins) in desert plants that allow them to uptake heavy metals. Microscopic and spectroscopic techniques will be used to establish specific uptake pathways. The long term goal of this research is to identify suitable species for phytoremediation and define a protocol for screening desert plants to assess their metal uptake capability. Inhalation of wind-born heavy metal contaminated particulates has been documented in this region as a significant health problem. The continuing research is directly related to the reduction of the public health risks for the local population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HEAVY BIOMARKERS
METALS
IMPACT
USING
GENETIC
VARIATION
Principal Investigator & Institution: Walsh, Elizabeth J.; University of Texas El Paso El Paso, Tx 79968 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2007 Summary: (provided by applicant): It is well known that heavy metals can be detrimental to human health even at low concentrations. Traditionally, effects of heavy metals have been assayed singly, monitoring the effects of a particular metal or a suite of individual metals on model organisms. Rotifers have been used as model organisms for toxicity testing of water supplies because of their short life spans, high reproductive outputs, and ease of manipulation. These features make them ideal for rapid toxicological assessment. During the last 10 years, there has been a great deal of interest in the use of sublethal indicators of exposure and effects of environmental contaminants on health. One of the newest biomarkers being explored by environmental scientists is the use of genetic diversity to assess ecological health. Genetic diversity within a species normally is quite varied. This diversity is the basis for a large gene pool that allows populations of organisms to persist in the face of environmental change. The genetic integrity of populations is critical to their long-term survival. Recent studies have shown that genetic diversity is compromised in contaminated environments. The lack of species diversity in degraded environments has been documented for many years, but genetic diversity within a species also appears to be reduced. The goals of the proposed research are to determine whether exposure to heavy metals (Arsenic, copper and lead) can impact the genetic structure of a population over 20 generations, and how exposure impacts organisms' responses to secondary exposures. A model organism, the rotifer Plationus patulus, will be subjected to metal exposures over 20 generations. Genetic variation will be monitored in the initial population, at generations 5, 10 and 20. Amplified fragment length polymorphism will be used as the biomarker of genetic variation. This is a DNA fingerprinting technique that allows the calculation of genetic
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variation and a number of other population genetic statistics. Concentrations of all metals will be at environmentally relevant levels. Following metal exposure, animals will be monitored for response to low pH, low food levels and a pesticide. Results obtained using organisms with rapid generational turnover times, such as rotifers, may give us some idea of what to expect when longer- lived species, including humans, are exposed to toxicants over generations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HEMATOLOGIC ONCOLOGY Principal Investigator & Institution: Nimer, Stephen D.; Professor and Head; SloanKettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 01-JAN-1978; Project End 30-JUN-2005 Summary: (Applicant's Description) The overall aims of the Hematologic Oncology Project are to develop and test new and effective strategies for treating hematologic neoplasms using targeted therapies and biologic agents. The SPECIFIC AIMS for this revised proposal are to: Develop novel therapeutic strategies in hematologic malignancies, including a) histone deacetylase inhibitors, such as depsipeptide b) geldanamycin in the treatment of CML c) desoxyepothiline B in the treatment of nonHodgkin's Iymphoma. Evaluate the use of targeted therapies using: a)monoclonal antibodies in dose-intense strategies, with autologous stem cell support for myeloid leukemias and myelodysplastic syndromes, using a radio labeled humanized monoclonal antibody (HuMl95; anti-CD33) to deliver targeted radiotherapy b)monoclonal antibodies for treatment of minimal residual disease in acute promyelocytic leukemia using all-trans retinoic acid for induction, followed by unlabeled HuM195, arsenic trioxide, and then idarubicin for consolidation c) ''tumorspecific'' vaccine approaches in patients with peptide vaccine in patients with myelodysplastic syndromes or AML. Evaluate tumor specific endpoints using a)Correlative in vitro assays of HDAC inhibition b) Serial quantitative levels of BCRABL protein (or rnRNA) c) MR Spectroscopy to assess response (for d) RT-PCR based assays to detect residual APL cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HIGH CAPACITY SNP GENOTYPING IN ARSENIC INDUCED DISEASE Principal Investigator & Institution: Jensen, Ronald H.; Professor in Residence; Cancer Center; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2002; Project Start 06-JUN-2002; Project End 31-MAR-2005 Summary: (provided by applicant): It is well known that the causes of common multifactorial diseases are both genetic and environmental in origin. Epidemiological studies (including the investigators? own international investigations) have shown that consuming drinking water with high levels of inorganic arsenic results in high health risk. A current challenge is to identify genetic polymorphisms in a set of environmentally-associated genes that may independently confer modest risk, but collectively comprise high risk profiles that predispose an individual to poor health consequences from arsenic exposure. The primary objective of this planning grant is to form a consortium with the capability to meet this current challenge. To accomplish this objective, this project has 3 specific aims. The first specific aim is to organize a cohesive group of multidisciplinary researchers with a shared mutual understanding of the
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methodologies, issues and problems involved in carrying out molecular epidemiology studies. The proposed consortium has researchers from 4 institutions: University of California San Francisco, University of California Berkeley (UC Berkeley), Children?s Hospital Oakland Research Institute and National Cancer Institute (NCI), NIH. The second specific aim is to create and perform a series of pilot studies designed to investigate concepts, hypotheses and technologies relevant to molecular epidemiology of arsenic-exposed populations. Three such studies are included in this application: (1) to determine the most feasible high output DNA SNP technology for investigating genotypic differences between individuals, (2) to identify the most appropriate set of specific genes and SNPs for investigations of arsenic-exposed populations, and (3) to develop appropriate methodologies for discriminating and prioritizing the results of the multiple statistical testing involved in epidemiology studies using SNP genotyping. After completion of these pilot projects, the third specific aim is to prepare and submit to NIH a detailed proposal to perform a molecular epidemiology study to systematically investigate genetic factors that influence susceptibility to arsenic-induced skin lesions in a population in India. About 400 blood samples for this population have already been collected and are held in frozen storage. As a result of this systematic study, individuals at particular risk for arsenic-induced effects will be identified and subject to intensified surveillance screening. In addition, mechanistic information will provide potential targets for preventive and curative interventions in exposed populations (e.g., nutrients or drugs). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: HIGH RESOLUTION GOLD LABELS FOR EM Principal Investigator & Institution: Hainfeld, James F.; Biophysicist; Brookhaven Science Assoc-Brookhaven Lab Brookhaven National Lab Upton, Ny 11973 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): Heavy atom labels can augment electron microscopy of biological structures by: a) revealing the site on a specific structure within a complex, and b) facilitating location and alignment of an overall complex. A useful EM label has two components: 1) a dense object which gives a high signal-to-noise ratio under the circumstances of observation, and 2) a linker which confers specificity, rigidity, and high occupancy without affecting biological function. Previously we have optimized labels for STEM. In this proposal we will better adapt the technology to cryoEM and modern molecular biology. New technology developed for protein engineering provides a variety of tags which can be inserted into the structure genetically and used for purification. These include: His-tags, Flag-tags, GST-tags, and strept-tags. Some of these same tags appear ideally suited as linkers for rigid, highaffinity attachment of density labels. Therefore, we propose to develop a labeling toolkit for cryoEM based on these new capabilities. In particular we will primarily evaluate five tags that bind to specialized gold clusters: 1) Ni-NTA-gold binding to 6x-His tags, 2) negatively charged gold to 6x Arg tags, 3) monomaleimido gold linked to cysteine, 4) arsenic-gold to tetra-Cys tags, and 5) gold targeted to a gold-binding sequence. These labels will then be used to determine subunit positions in several important protein complexes: The DNA repair complexes consisting of subcomplexes: human Ku70/Ku80/DNA-PK complex, human ligase IV/Xrcc4 complex, human RAD50/Mre11/Nbs1 complex, and the human chromatin remodeling complex ACF. The gold labels will additionally be used to better align the complexes to improve reconstructions from conical tilt pairs using cryoEM. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HOUSEHOLD ENVIRONMENTAL RISK REDUCTION IN RURAL CHILDREN Principal Investigator & Institution: Butterfield, Patricia G.; Associate Professor; University of Montana University Hall 202 Missoula, Mt 598124104 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: More than seven million families participate in Women, Infants, and Children (WIC) and other pediatric public health programs. Providing environmental health information to these families is a common-sense way of integrating risk reduction efforts into existing public health programs. However, the success of such efforts will be predicated on testing interventions that can be easily delivered in home and clinic settings. The proposed study will yield evidence addressing: 1) baseline estimates of rural children's exposure to multiple agents in the home setting, and 2) the effectiveness of a risk reduction intervention delivered by public health nurses. Subjects will include child-parent dyads residing in rural Montana; there is preliminary evidence that exposures to children living in the rural West may differ significantly from those living in other parts of the country. The research involves four phases. In Phase 1, biomonitoring (i.e., children's blood lead, urinary cotinine), household (i.e., analysis of water for total coliforms, E-coli, lead, nitrate/nitrite, arsenic, mercury, and a pesticide and petroleum screen; air monitoring for radon and carbon monoxide), and parents' knowledge / attitude / behavior data will be collected from 50 families. In Phase 2, these data will be reviewed by an expert panel to identify priority agents--there is preliminary evidence that these will include radon, lead, arsenic, and nitrate/nitrite. Phase 3 will focus on finalizing agent-specific and general risk reduction interventions. General risk reduction actions will be based on national pediatric health recommendations. During Phase 4, the intervention will be tested with a sample of 150 families using private wells; 75 treatment families will receive the home visit intervention and 75 control families will receive an alternate (addressing a nonenvironmental health topic) intervention. The intervention will be delivered by local public health nurses who are already making home visits to families participating in child health programs for lower-income families. Outcome measures of interest include: 1) estimates of exposure (biomarkers and household monitoring), and 2) parents' knowledge and attitudes toward reduction actions on behalf of their children. The proposed research is consistent with recommendations that communitybased environmental health programs be framed and delivered in a manner that is meaningful to families and high-risk subgroups. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: INNOVATIVE CONCEPT FOR A 3-MICRON LASER SCALPEL Principal Investigator & Institution: Prasad, Coorg R.; Science and Engineering Services, Inc. 4032 Blackburn Ln Burtonsville, Md 20866 Timing: Fiscal Year 2001; Project Start 10-SEP-2001; Project End 30-SEP-2002 Summary: (Verbatim from the Applicant's Abstract): Due to the strong water absorption bands in the about 3micro spectral region, 3-micro laser radiation is extremely appropriate for surgical intervention, especially where only shallow cutting beam penetration (incision depth of the order of 20-30 micro) is needed. The aim of the proposal is to develop a novel 3-micro laser scalpel technology for stereotactic surgery using a technical approach that would go around the well-known problem of the 3micro radiation delivery to internal organs. Out innovative approach is based on replacing the presently technically complicated fiber delivering of the operative3-micro
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radiation to the undergoing surgery organ by a well developed fiber delivering of the laser diode source radiation in the 0.9-1-micro region of spectrum with its subsequent down-conversion into a 3-micro laser radiation directly in a small surgical instrument tip. We will develop a miniature 30 hz repetition rate, 3mJ/pulse source of the 3-micro laser radiation, which is based on an activated dielectric single crystal pumped through a commercially available low-loss silica glass optical fiber by a commercial InGaAs diode bar stack. Based on mature laser diode pump source/fiber optics technologies, the proposed system in truly easily commercializable and will be then incorporated into a phase II fiber-tip laser scalpel for stereotactic surgery. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MAP KINASE REGULATION OF B-LYMPHOCYTE APOPTOSIS Principal Investigator & Institution: Muscarella, Donna E.; Microbiology and Immunology; Cornell University Ithaca Office of Sponsored Programs Ithaca, Ny 14853 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2004 Summary: Immunosuppressive disorders constitute a significant human health problem associated with increased individual susceptibility to infectious and neoplastic diseases. Human populations may be at risk for clinically significant immunosuppression following exposure to environmental metals, pesticides, or immunotoxic drugs. It is now known that induction of apoptosis in lymphoid cells is an important mediator of immunotoxicity following chemical exposure. However, lymphoid cell populations among and within individuals can vary extensively with respect to their sensitivity to undergo chemically induced apoptosis. Thus, differences in the mechanisms underlying the execution of pro- and anti-apoptotic pathways in resistant and susceptible cell populations need to be understood before the consequences of exposure to environmental contaminants can be fully appreciated. This study utilizes a unique panel of human B-lineage lymphocyte (BLL) cell lines that show large differences in their sensitivity to apoptosis induction by various chemicals to test the hypothesis that the differential activation of specific mitogen-activated protein (MAP) kinases is a critical factor in determining chemical sensitivity in BLLs. The activation of the three major MAP- kinase pathways, ERK1/2, JNK1/2, and -38 following exposure of the BLL-cell lines to the environmental pollutants arsenic and cadmium, and selected drugs that share with these metals the ability to perturb mitochondrial function will be examined. Specific chemical inhibitors and dominant negative strategies will be used to establish causality between activation of these kinases and induction of apoptosis in susceptible cell lines. In addition, the roles that these kinase pathways play in acquired sensitivity to apoptosis induction in resistant cell lines following low-level chemical exposure will also be studies. Experiments will also be performed to determine whether low-level chemical exposure can sensitize BLLs to the induction of apoptosis by engagement of the IgM receptor. IgM-induced apoptosis is an important mediator of negative selection of B- lymphocytes during development which, similar to chemically induced apoptosis, involves the activation of specific MAP kinase pathways. This research is expected to identify important mechanisms regulating differential lymphoid cell sensitivity to apoptosis induction and to contribute a novel model system for examining thresholds for adverse effects of environmental chemicals on B-lineage lymphoid cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MEASUREMENT ERRORS IN CANCER EPIDEMIOLOGY Principal Investigator & Institution: Rosner, Bernard A.; Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 17-JUL-1989; Project End 31-JAN-2003 Summary: (Adapted from the Applicant's Abstract): The types of exposures studied in cancer epidemiology pose special challenges from a data analytic standpoint. For example, nutritional exposures form the basis for many etiologic hypotheses concerning cancer. However, nutrient intake is difficult to measure precisely. The degree of measurement error may mask true underlying relationships due to the regression dilution problem. It is the role of measurement error correction methods to estimate the relationship between cancer incidence and "true" nutrient intake. To accomplish this requires data from both a main study where disease and the surrogate exposure are measured, and a validation study where both the surrogate measure and the gold standard for nutrient intake are assessed. In this proposal, we seek to extend the previous work on measurement error correction which is based on intake reported at a single survey to the situation where diet is reported at multiple surveys over time. Another focus of this proposal is to extend previous measurement error models which were specified at the nutrient level to models specified at the food level, which is the level at which people actually report their intake. The issue is that different foods have different degrees of measurement error, which should be taken into account when considering measurement error both at the food and nutrient level. Another issue is that many nutrients have contributions from both foods and supplements which are likely to have differing degrees of measurement error. We also consider measurement error issues for non-nutritional exposures in cancer epidemiology. For example, proband studies using family registers for a specific type of cancer collect data from a cancer case and other nonaffected people in the same family. Special analytic methods are required to take account of the familial nature of the data. We propose to extend measurement error correction to be applicable to this type of data structure. Second, some exposuredisease relationships are inherently non-linear, and are best captured using splines (e.g., the relationship of skin cancer to low levels of arsenic in drinking water). We propose to extend measurement error correction methods to curves fitted with splines. Also, ROC curves are used in imaging studies for breast cancer detection but are based in imperfect continuous measures. We propose to assess the impact of measurement error on the estimation of the ROC curve. Finally, there is inevitably misclassification in the pathological classification of disease stage in some types of cancer (e.g., pancreatic cancer). We propose to investigate the impact of this misclassification on estimated racial differences in survival for persons with pancreatic cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISM OF AN ATP-COUPLED ARSENICAL PUMP Principal Investigator & Institution: Rosen, Barry P.; Professor and Chairman; Biochem and Molecular Biology; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2001; Project Start 01-MAY-1997; Project End 31-AUG-2005 Summary: Resistance to arsenic and antimony is widely spread in both gram-positive and gram-negative bacteria. The best- characterized system encoded by the clinically isolated resistance factor plasmid R773 in E. coli confers resistance against oxyanions of arsenic (arsenite and arsenate) and antimony (antimonite). The ars operon codes for two regulatory (ArsR and ArsD) and three structural (ArsA, ArsB and ArsC) proteins. Resistance correlates with active extrusion of arsenite from the cell by a primary pump.
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The arsA gene product is an ATPase that serves as the catalytic subunit of the pump. ArsA is a 63-kDa peripheral membrane protein that catalyzes As(III)/Sb(III)- stimulated ATP hydrolysis. ArsA has two homologous halves, A1 and A2, connected by a short linker. Each has a consensus nucleotide binding site (NBS), and both NBS are required for activity. ArsA binds to ArsB, which s the ion-conducting subunit of the pump. ArsB is a 45-kDa integral membrane protein that spans the inner membrane 12 times. ArsB has a novel dual mode of energy coupling depending on its association with ArsA. Arsenic efflux bacteria can be catalyzed by either ArsB alone functioning as a secondary transporter or by the ArsAB complex, functioning as a transport ATPase. Our overall goal is elucidation of the molecular mechanism of the ArsAB pump. Analysis includes the following specific aims: 1. Structure and function of the ArsA ATPase: The function and properties of the metal binding site, nucleotide binding sites and signal transduction sites of ArsA will be examined. The composition and function of residues that form the interface between A1 and A2 will be determined. 2. Catalytic mechanism of the ArsA ATPase will be examined using single tryptophan ArsA mutants as spectroscopic probes, by isotope trapping and by vanadate trapping and cleavage experiments. 3. Structure of the ArsAB pump: Residues that form the sites of interaction of the ArsA and ArsB subunits will be identified. The stoichiometry of the ArsA and ArsB subunits in the pump will be determined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISM OF ARSENIC INDUCED VASCULAR DISEASE Principal Investigator & Institution: Barchowsky, Aaron; Associate Professor; Dartmouth College 11 Rope Ferry Rd. #6210 Hanover, Nh 03755 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2002 Summary: The primary objective of the proposed studies is to define the cellular and molecular mechanisms responsible for changes in vascular cell phenotype and proliferation, which promote occlusive cardiovascular disease following exposure to low levels of arsenite. The hypothesis for these studies is that arsenite causes vascular disease by stimulating oxidant- mediated signaling in endothelial and smooth muscle cells. In addition the oxidants caused by arsenite exposure may deprive the vasculature of nitric oxide required for vasodilation and suppression of smooth muscle cell proliferation. Studies in the first funding period made the distinction between oxidantsensitive cell regulation and oxidant stress in response to increasing amounts of arsenite. Low, environmentally relevant levels of arsenite and oxidants were shown to be regulatory and proliferative, while high levels activate stress pathways and cell death. The proposed studies will continue to use primary endothelial and smooth muscle cells to define the source of arsenite-stimulated reactive oxygen and the downstream signals that promote phenotypic change and proliferation. Focus will be on the signal cascades that initiate superoxide production by NAD(P)H oxidase. Dominant negative strategies, with highly expressed adenoviral vectors, will demonstrate the role of the monomeric GTPase, Rac1, in initiating this activity and in promoting the activation NF-B, an oxidant-sensitive transcription factor that promotes expression of cytoprotective genes and cell proliferation. Finally, mice will be chronically exposed to low levels of arsenite to test the hypothesis that arsenite decreases vasodilator-induced nitric oxide release and promotes NF-B dependent thickening of brain blood vessels. These studies will be facilitated by in vivo electron paramagnetic resonance spectroscopy and an adenoviral construct that suppresses NF-B activation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISM OF ARSENIC-INDUCED DIABETES Principal Investigator & Institution: Styblo, Miroslav; Pediatrics; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2003 Summary: (provided by applicant) This project examines the role of arsenicals in the induction of diabetes mellitus. Inorganic forms of arsenic (iAs) are highly toxic and are classified as human carcinogens. Drinking water contaminated with iAs, along with industrial emissions, are major sources of exposure to iAs for populations worldwide. Numerous epidemiological studies have linked environmental exposures to iAs to increased incidences of various types of cancer and noncancerous diseases. Among diseases associated with chronic exposure to iAs, diabetes mellitus remains a significant problem especially in arsenic-endemic areas with large populations exposed to this metalloid from drinking water (e.g., Taiwan and Bangladesh). The adverse health effects associated with chronic exposure to iAs are also being intensively studied in the U.S. where hundreds of thousands of residents drink water with iAs levels that exceed the current maximum contaminant level (MCL) of 50 milligrams of arsenic per liter of water. Mechanisms by which iAs induces cancer, diabetes mellitus or other noncancerous disease are unknown. iAs species that contain trivalent arsenic (iAs-III) are potent oxidants that induce oxidative stress in laboratory animals and cultured cells. iAs-III species are also inhibitors of numerous enzymes and receptors involved in key metabolic and cell signaling pathways. Interactions of iAs-III with catalytically-active thiols have been shown to underlie these effects. In humans, iAs is metabolized to yield methylarsenic (MAs) and dimethylarsenic (DMAs) metabolites. Because of the redox nature of the metabolic reactions, both trivalent and pentavalent arsenicals (iAs-III, iAsV, Mas-V, DMAs-III, DMAs-V) are intermediates of final metabolites in this pathway. Recent reports from this and other laboratories have shown that trivalent methylated metabolites (Mas-III and DMAs-III) are more potent cytotoxins and enzyme inhibitors than iAs-III. The thioredoxin reductase/thioredoxin (TR/Trx) system that plays a key role in numerous regulatory mechanisms in the cell (e.g., antioxidant defense, activation of transcriptional factors and cellular receptors, cytokine expression or insulin excretion by B cells) has been shown to be a primary target for MAs-III in intact cells. In addition, unlike iAs-III, Mas-III and DMAs-III can damage DNA in intact cells. The investigators have shown that both Mas-III and DMAs-III are produced by human hepatic cells exposed to iAs and are present in the urine of individuals chronically exposed to iAs from drinking water. Thus, Mas-III and DMA-III, toxic products of iAs metabolism in humans, can significantly contribute to adverse affects associated with exposure to iAs. This pilot project is designed to examine effects of trivalent arsenicals, especially Mas-III and DMAs-III, on basic mechanisms that regulate utilization of glucose: (1) production of insulin in the pancreas and (2) metabolism of glucose in peripheral tissues. Effects of arsenicals will be examined in cultured cells (pancreatic B cell lines, adipocytes and skeletal muscle cells) and in mice. Induction of oxidative stress and inhibition of TR/Trx activities will be examined as possible mechanisms underlying the induction of diabetic symptoms. Arsenic metabolites responsible for these effects will be identified. In addition, the role of cellular and nutritional antioxidants in protection against arsenicinduced diabetes will be examined, providing information that may be critical for prevention and/or treatment of diabetes in arsenic-exposed individuals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS AND BIOMARKERS OF OXIDATIVE STRESS FOLLOWING ARSENIC EXPOSURE Principal Investigator & Institution: Martin, Brooke; University of Montana University Hall 202 Missoula, Mt 598124104 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: Arsenic is a toxic and carcinogenic element with widespread environmental contamination and human exposure. Currently, elemental arsenic levels are used as a monitor of arsenic exposure. There is, however, increasing evidence that arsenic speciation both within the environment and enzymatic speciation upon consumption may profoundly affect the toxic and genotoxic parameters of arsenicals. The hypothesis to be tested is that the reaction between arsenite and the energy generating enzymes of the mitochondria is a significant cause of the oxidative stress and mitochondrial damage observed upon arsenic exposure. These interactions as well as the ensuing oxidant stress will be examined to identify potential biomarkers of arsenic-induced damage as distinct from exposure. Aim 1 of this proposal is to characterize the nature of the mitochondrial oxidative stress induced by sulfhydryl reactive arsenite using enzyme kinetic measurements of the Kreb's cycle and electron transport enzymes. We will quantify this disruption of mitochondrial oxidative metabolism in order to characterize the role of the mitochondria in arsenic-induced oxidative stress. Classical enzyme kinetics and arsenic binding studies in vitro and in a cell based system will be used to establish the site(s) of inhibition. Aim 2 of this proposal is to identify biomarkers of arsenite toxicity and oxidative stress. A family of arsenylated enzyme conjugates, including the mono- and dimtheylarsenic analogs of arsenite, will be synthesized as standards for analysis of biological samples and as antigens for polyclonal antibody generation. Classical markers of oxidative stress in the mitochondria and genomic extracts will also be monitored. Aim 3 of this proposal will establish a proteomics profile of arsenicals in yeast. The emphasis will be on identifying sentinel proteins as biomarkers of arsenic-specific toxicity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF ARSENIC CARCINOGENESIS Principal Investigator & Institution: Hei, Tom K.; Professor; Radiation Oncology; Columbia University Health Sciences New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 12-JUL-2002; Project End 30-APR-2006 Summary: (provided by applicant): Although arsenic is a known human carcinogen and induces cancers of the skin, lung, liver and bladder, the underlying carcinogenic mechanism(s) is not known. The US Environmental Protection Agency has placed arsenic at the top of its superfund contamination list. One of the main difficulties in studying mechanisms of arsenic carcinogenesis is the lack of a suitable human cell model whereby the various tumorigenic stages can be dissected and the molecular changes associated with each stage examined. While preliminary data obtained by the applicant has shown that arsenic can induce malignant transformation of papillomavirus-immortalized human bronchial epithelial (BEP2D) cells, this model is not ideal due to the presence of viral oncoproteins. The newly established telomerase (hTERT) -immortalized human bronchial epithelial (IMNHBE) cell transformation model that has normal p53 and p16 functions represents an attractive alternative to further ascertain the mechanism involved in arsenic-induced bronchial carcinogenesis. A series of cellular and molecular assays will be conducted using isolated clonal cell lines at each stage of the carcinogenic process to identify the necessary changes essential
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for arsenic carcinogenesis. The proposal has 2 main objectives: The first is to establish an in vitro human epithelial cell transformation model for arsenic carcinogenesis using two independent, telomerase-immortalized bronchial epithelial cell lines; and the second goal is to examine the mechanism(s) involved, particularly loss of tumor suppressor functions, associated with each stage of the carcinogenic process. A series of 7 specific aims are proposed to address 4 testable hypotheses. The IM NHBE cells are anchorage dependent and do not form tumors in immunosuppressed host animals. CDNA arrays coupled with functional analysis at the gene level will be conducted using tumors and cells from intermediate transformation stages to provide a mechanistic basis for arsenicinduced bronchial carcinogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MECHANISMS DEVELOPMENT
OF
ARSENIC
TOXICITY
IN
VASCULAR
Principal Investigator & Institution: Coffin, J Douglas.; Associate Professor; Pharmaceutical Sciences; University of Montana University Hall 202 Missoula, Mt 598124104 Timing: Fiscal Year 2002; Project Start 15-MAR-2002; Project End 31-JAN-2004 Summary: (provided by applicant) Arsenic is a prevalent toxin in ground water and soil around areas with extractive industries. Exposure to arsenic is linked to several developmental defects in the nervous system and limbs, pregnancy complications and miscarriage. Vascular defects are often the underlying basis for limb deformations and developmental anomalies in other systems and vascular abnormalities often form the basis for placentation defects linked to miscarriage. The overall goal of this project is to define the developmental mechanisms for how arsenic toxicity causes developmental defects and miscarriage, and to characterize the molecular mechanisms for arsenic mediated alteration of endothelial cell physiology. Our preliminary data suggest that arsenic and arsenic-metal mixtures dramatically alter endothelial cell physiology. We hypothesize that arsenite toxicity causes defects in vascular development, predisposing the embryo to other developmental anomalies and miscarriage. The following aims have been designed to test this hypothesis: (1) Characterize the molecular mechanisms for arsenic-mediated alteration of endothelial cell physiology. Cultured endotheiial cells will be exposed to arsenic and analyzed for alterations in the molecular regulatory pathways for vascular development. (2) Define the developmental mechanisms for how arsenic toxicity causes developmental defects. The effects of arsenic toxicity on angiogenesis and vasculogenesis will be assessed using quail-chick chimeras with arsenic-treated tissue transplants. The resulting growth and development of the quail angioblasts through vasculogenesis and angiogenesis will be analyzed by immunocytochemistry with QH-1. (3) Determine how arsenic exposure affects fecundity, placentation and vascular morphogenesis in vivo. Timed- pregnant mice will be exposed to arsenic and arsenic-metal mixtures in their drinking water. The rate of live births from treated mice will be compared to controls to assess fecundity. Embryos harvested at E4.5, E 7.5, E9.5, E10.5 and E15.5 from arsenic-treated tie2-LacZ transgenic (TgLacz) mice will be examined for vascular abnormalities. The key molecular regulatory elements for vascular development will be assayed in each group for comparison to the in vitro data collected in Specific Aim l. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF CARDIOVASCULAR DISEASE FROM ARSENIC EXPOSURE Principal Investigator & Institution: Beall, Howard D.; University of Montana University Hall 202 Missoula, Mt 598124104 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2007 Summary: Arsenic is widely dispersed in the earth's crust and is released into the air, soil and water by human activities such as mining, smelting, manufacturing and pesticide application. Epidemiological studies suggest that exposure to arsenic in drinking water increases the risk of mortality from cardiovascular disease (CVD). Ingestion of arsenic produces reactive oxygen species (ROS) and reactive nitrogen species (RNS) in tissues. ROS/RNS may exacerbate CVD by altering vessel wall physiology through regulatory pathways that include eicosanoids, growth factors and nitric oxide. We propose an investigation of the potential for arsenic to increase morbidity and mortality from CVD with a focus on atherosclerosis, or coronary artery disease (CAD). The overall objective of this application is to identify the mechanisms and regulatory pathways involved in arsenic-induced CAD. The central hypothesis is that arsenic facilitates development of CAD. The specific aims for testing this hypothesis are 1. characterize arsenic-mediated formation of reactive species in endothelial cells, 2. define changes in expression of key atherogenic regulatory molecules in endothelial cells upon treatment with arsenic, and 3. determine the effects of arsenic on expression of key CAD regulatory molecules in the ApoE(-/-) atherosclerotic mouse model. An important ROS/RNS is peroxynitrite, a powerful oxidant that is capable of nitrating tyrosine residues. Peroxynitrite and nitrotyrosine formation will be the primary focus of the endothelial cell studies in Specific Aim 1. In Specific Aim 2 (endothelial cells) and Specific Aim 3 (mouse), expression of inflammatory regulators including cyclooxygenase-2 (COX-2), 5-lipoxygenase (5-LOX) and inducible nitric oxide synthase (iNOS) will be assayed. The eicosaniod products of COX-2 and 5-LOX will also be measured along with pertinent growth factors and cytokines. Antioxidants and enzyme inhibitors will be used throughout these studies to elucidate the most important pathways in arsenic-induced atherogenesis. These studies will provide important data for determination of health risks associated with arsenic exposure and potential CAD prevention strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MECHANISMS OF MUTAGENESIS OF METALS & PAH/METAL MIXTURES Principal Investigator & Institution: Dixon, Kathleen C.; Professor; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2001; Project Start 01-APR-1995; Project End 31-MAR-2005 Summary: (Taken from application) The long-range goal of this research is to understand the mechanisms of action of the carcinogenic metals/metalloids chromium and arsenic, and to determine the impact of these metals on the mutagenic activity of polycyclic aromatic hydrocarbons (PAH). Both metals are important contaminants at Superfund sites, and in many cases they exist in complex mixtures with PAHs. Exposure by inhalation to chromate compounds has been associated with the development of lung cancer, particularly in cigarette smokers. Exposure to arsenite in drinking water has been associated with the development of skin cancer, as well as internal cancers of the lung, liver, and bladder. Chromate has been shown to be mutagenic in a variety of test systems; in contrast, arsenite and arsenate have generally tested negative for
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mutagenesis. However, there is evidence that arsenic is clastogenic and it appears to enhance the mutagenic activity of other agents in co-exposures. During the previous grant period, we demonstrated that chromate induces oxidative damage to DNA in a process that involves intracellular glutathione(GSH)-mediated reduction of chromate (CrVI). Furthermore, the mutagenic specificity of chromate is consistent with oxidative DNA damage in yeast, mammalian cells and the lungs of transgenic mice. In this renewal application, we propose to characterize further the mutagenic potential and mutagenic specificity of chromate, particularly with respect to the induction of deletion mutations. In addition, we propose to expand our investigation of mechanisms of metalinduced mutagenesis to include the analysis of the mutagenic potential of arsenic. We are particularly interested in determining the activity of these metals as co-mutagens in combination with PAHs, because environmental exposures often involve complex mixtures of the two classes of carcinogenic compounds. We propose to test the following two hypotheses: 1) Arsenic and chromium function as mutagens by mechanisms involving interaction with intracellular GSH and generation of reactive oxygen species. 2) Arsenic and chromium act as co-mutagens by potentiating the mutagenic activity of PAHs We propose to address these hypotheses by investigating the mutagenic, and co-mutagenic potential with PAHs, of arsenic and chromium in yeast, mammalian cells, and transgenic mice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MENTORED TRAINING IN RESEARCH ON ARSENIC Principal Investigator & Institution: Steinmaus, Craig M.; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122 Timing: Fiscal Year 2001; Project Start 15-SEP-2001; Project End 31-AUG-2006 Summary: (provide by applicant) The goal of this application is to support the candidate's development in patient-orientated research. This will be done through a program combining didactic teaching, mentoring, and scientific research focusing on the pharmacokinetics of ingested arsenic. Millions of people worldwide are exposed to arsenic in their drinking water, and recent evidence suggests that these exposures may lead to substantial risks of lung cancer. Currently, little is known about the human toxicokinetics or pulmonary toxicity of ingested arsenic. The candidate proposes three studies in arsenic exposed populations to increase our knowledge of these topics. The first will assess the role of 13 dietary and metabolic factors in arsenic methylation, the primary detoxification pathway of inorganic arsenic. Serum levels of these factors will be compared to arsenic methylation patterns based on the urinary excretion of arsenic metabolites. Previous studies have shown that individuals vary greatly in the degree they methylate arsenic, thus investigating factors that regulate methylation may allow susceptible sub- populations to be identified, and therefore may provide information useful in drinking water regulation. The second study is a cross-sectional cadaver study on the intracellular distribution of arsenic and its metabolites in human tissues. Tissue samples from the six organs will be collected from 20 subjects during routine autopsies performed by the coroners offices of arsenic exposed and unexposed population. The levels of arsenic and its metabolites will be determined in the subcellular components of each organ. Identifying specific patterns of arsenic accumulation may further support the hypothesis that ingested arsenic is a potent lung carcinogen, and may explain why the lung appears more susceptible to arsenic than other tissues. In addition, providing information on the distribution patterns of specific metabolites, particularly monomethylarsonous acid, may add new insight into the role of methylation in arsenic carcinogenesis. The final project is the design of an epidemiological study of lung cancer
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and low exposures of drinking water arsenic. Currently, little information is available on the cancer effects of arsenic at doses below 100 ug/L. This project will involve the development of all major aspects of study design and implementation with the ultimate goal of preparing an investigation that will provide dose-response data useful in drinking water regulation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: METAL TOXICANT EFFECTS ON SMALL HEAT-SHOCK PROTEINS IN HSP22 Principal Investigator & Institution: Benndorf, Rainer; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2006 Summary: The mental cadmium and the metalloid arsenic (collectively referred to as toxic metals, TM) are important environmental pollutants causing known human health problems. Among the affected organs and tissues are muscles. E.g. one of the critical target of the cadmium toxicity is the vascular smooth musculature resulting in sustained contraction with systemic consequences like hypertension. At molecular levels, the impact of TMs on muscles is only poorly understood. Identified cellular changes involve stimulated signal transduction cascades including the MAP kinases, Erk and p38, and profound rearrangements (fragmentation) of the actin filaments. In recent years, the socalled small heat shock proteins (sHSPs) of mammals were reported to be involved in the cellular response to TMs, including both elevated abundance and degree of phosphorylation. At the same time, sHSPs were identified to play an important role in function and protection of striated and smooth muscles. The long-term objective of this project is to investigate and understand the involvement if sHSPs in mediating the detrimental effects of TMs in muscles. It is hypothesized that the muscle toxicity of TMs is mediated in part by the action of sHSPs resulting in complex changes in interactions. Of sHSPs with each other and with other sHSPs in muscle. It will be investigated how the interaction of sHSPs with themselves and with the actin filaments is regulated in muscles, and how TMs interfere. According to the specific aims, the goals of this project are: 1) To determine in muscle i) the effect of TMs on the amount, phosphorylation and complkex-forming properties of sHSPs, and ii) the specific serines and/or threonines of each sHsp phosphorylated in response to TM treatment; 2. To analyze using genetic and in vitro biochemical assays the interaction between these sHSPs and the effect of TMcaused phosphorylation on these interactions; 3) To analyze in vitro and in vivo i) the regulation of muscle microfilament assembly and organization by sHSPs; and ii) the effects of TM-caused phosphorylation of sHSPs on actin filament assembly and organization; and 4) To identify and study other muscle proteins interacting specifically with HSP22, and the impact of TMs on this interaction. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: METAL TOXICANT EFFECTS ON SMALL HEAT-SHOCK PROTEINS IN KIDNEY PODOCYTES Principal Investigator & Institution: Smoyer, William E.; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2006 Summary: The most abundant toxic metals in our environment include arsenic, cadmium, lead and mercury, and each of these metals is known to produce cellular injury to the kidney. Their toxicities are almost certainly related at least in part to the
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fact that urinary elimination is major route of elimination of these toxins from the body. Although the most common manifestation of this toxicity is development of tubular proteinuria associated with interstitial nephritis, significant glomerular disease can also result from toxic metal exposure. This has been most clearly demonstrated by the development of nephrotic syndrome (NS) after the use of mercury-containing compounds or occupational or environmental exposure or environmental exposure to inorganic mercury salts. However cadmium has also been reported to induce glomerular disease in addition to its well-known toxicity to kidney tubules. Exposure to toxic metals is known to induce a cellular stress response, including increased expression and phosphorylation of the small heat shock protein, hsp27, a known regulator of actin polymerization. We thus hypothesize that this regulation of actin filament by hsp27 in podocytes is mediated through a novel mechanism involving hsp27-binding proteins. To test these hypotheses we will: 1) Determine if exposure to mercury, cadmium, or combinations of these alters hsp27 expression and phosphorylation in podocytes in vitro and in vivo, and whether these metals induce podocyte structural changes characteristic of NS, 2) Determine whether induced alterations in hsp27 in vitro and in vivo result in protection from toxic metal exposure and/or podocyte structural changes characteristic of podocyte dysfunction in NS, and 3) Determine the molecular basis for the interaction between hsp27 and the recently identified hsp27-binding protein, hic-5, and analyze the role of hic-5 in regulating the podocyte cytoskeletal after toxic metal exposure. The in vitro studies will include short and long term exposure of cultured "differentiated" podocytes before and after specific hsp27 and hic-5 transfections to mercuric chloride, cadmium chloride and mixtures of these metals, with subsequent analyses of hsp27 transgenic mice treated with these metals. Identification of an important role of hsp27 and hic-5 transfections to mercuric chloride, cadmium chloride and mixtures of these metals, with subsequent analyses of hsp27 expression and phosphorylation and specific podocyte structural alterations. Correlative in vivo studies will involve similar analyses of normal rats and hsp27 transgenic mice with treated with these metals. Identification of an important role of hsp27 in regulating podocyte structure after toxic metal exposure would improve our understanding of the mechanism(s) by which toxic metals induce human disease and permit the development of more highly targeted therapies for toxic metal-induced for toxic metal-induced glomerular disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MITOCHONDRIAL RESPONSE TO OXIDATIVE STRESS Principal Investigator & Institution: Bogenhagen, Daniel F.; Professor; Pharmacology; State University New York Stony Brook Stony Brook, Ny 11794 Timing: Fiscal Year 2002; Project Start 10-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant) Mitochondria play a vital role in cell physiology and the response to environmental stress. A number of cellular toxins, including rotenone, 1methyl-4-phenylpyridine (MPP+) and paraquat act to impair mitochondrial electron transport, generating ROS. Reactive oxygen species are also important in the toxicity of arsenic, amyloid, and ceramide. Mitochondria have been viewed as a potential source of ROS that may contribute to Parkinson's disease, aging and other pathological conditions. Since mitochondria contain only a small 16.5 kb mtDNA genome, encoding only 13 proteins, the organelle depends on the nucleus for most gene products, including all of the factors required for DNA replication, expression and repair. Recent studies from our laboratory and others have revealed an increasing collection of proteins that function in both mitochondria and other cellular compartments. A number
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of these proteins function in repair of oxidative damage to mtDNA. One significant consequence of mitochondrial pathology is the generation of mutations in mtDNA, many of which have a tissue-specific incidence, occurring most commonly in postreplicative tissues such as nerve and muscle. The investigators propose to test the hypothesis that mitochondria in differentiated cells may contain a different complement of proteins than actively dividing cells which may predispose post-replicative cells to a higher rate of mtDNA mutations or may alter the ability of cells to enter apoptosis. To accomplish this, they will study the effect of oxidative stress on the mitochondrial proteome in both embryonal carcinoma cells that are actively dividing and in cells that have been induced to differentiate along a neuronal pathway. Both 2-D gel methods and quantitative isotope-coded affinity tag (ICAT) methods will be used to compare the abundance of mitochondrial proteins in control cells and cells exposed to oxidative stress. The broad proteomic screen will permit the discovery of novel gene products not previously known to function in mitochondria. Data will be analyzed to provide new insights into networks of proteins acting to repair oxidative damage to mtDNA or to detoxify ROS. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MODULATION OF PROSTAGLANDINS BY ARSENIC Principal Investigator & Institution: Vaillancourt, Richard R.; Associate Professor; Pharmacology and Toxicology; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2002; Project Start 10-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant) Arsenic (As) is an inorganic environmental contaminant of major concern due to its ubiquitous presence. Chronic exposure to arsenic frequently results in peripheral vascular disease, as well as skin, lung, bladder, and kidney cancer. Recent evidence demonstrates that arsenite stimulates cyclooxygenase (COX-II) expression suggesting that arsenite affects prostaglandin synthesis. The investigator's published studies with arsenic have demonstrated that the serine/threonine kinase, MEKK4, is involved in arsenic signal transduction. To further understand the molecular mechanism by which arsenic causes its deleterious effects and how the activity of MEKK4 contributes to arsenic toxicity, efforts by the investigators have focused on characterizing the activity of MEKK4 in vascular smooth muscle cells since it appears to function upstream of COX-II. The hvpothesis of this proposal is that the prostaglandin biosynthetic pathway is regulated by MEKK4 and that arsenic affects the vascular system by modulating prostaglandin homeostasis through MEKK4. The Specific Aims are to: 1. To identify and characterize tyrosine phosphorylation of MEKK4. Our data indicate that Pyk2 phosphorylates MEKK4. This site is not known and will be identified by LC-MS. Then, the site will be mutated and MEKK4 catalytic activity will be characterized to assess the significance of the phosphorylation site. 2. To characterize the mechanism by which SHP-2 interacts with MEKK4 and how arsenite inhibits SHP-2 activity. SHP-2 associates with MEKK4 in a stimulus-dependent manner. Intracellular calcium promotes dephosphorylation of MEKK4, while arsenite inhibits the tyrosine dephosphorylation of MEKK4. 3. To identify and characterize the MEKK4 substrate. Candidate proteins include members of the MAP kinase family or novel proteins that will be identified using a modification of the "tethered" MEKK4 approach and LC-MS. It is possible that MEKK4 phosphorylates and regulates cytosolic phospholipase A2 (cPLA2), a key enzyme involved in prostaglandin biosynthesis that is regulated by phosphorylation. 4. To characterize the mechanism by which MEKK4 regulates prostaglandin synthesis. The kinase-inactive mutant of MEKK4 functions as a
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dominant-negative protein, and the investigators have shown that expression of this protein inhibits transcription of a Cox-II promoter/luciferase chimeric plasmid. This result suggests that endogenous MEKK4 functions upstream of pathways that regulate prostaglandin synthesis. The proposed research will provide a further understanding of the importance of the arsenic-induced signaling processes and how it adversely affects the peripheral vascular system and promotes tissue injury. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR EPIDEMIOLOGY OF NON-MELANOMA SKIN CANCER Principal Investigator & Institution: Nelson, Heather H.; Cancer Cell Biology; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-JUL-2003 Summary: Non-melanoma skin cancer is the most prevalent malignancy in the US, resulting in significant morbidity and health-care expense. Epidemiologic investigations have identified exposure to ultraviolet radiation as the primary risk factor for this disease; other environmental exposures that contribute to risk include ionizing radiation, arsenic, polycyclic aromatic hydrocarbons, and chronic immunosuppression. Host factors associated with increased risk for non-melanoma skin cancer include increasing age, male gender, and sun sensitive skin type. Basal cell and squamous cell carcinomas have been shown to contain alterations in the p53 gene, and recent work has identified a gene on chromosome 9q22, ptch, that is hypothesized to be critical in basal cell carcinoma tumorigenesis. These findings, while informative, are derived from relatively small, selected groups of patients and reflects the paucity of population-based molecular epidemiology for this disease. We propose to expand a large, well-established case-control study of non-melanoma skin cancer in New Hampshire to include investigation of genetic susceptibility. The project will focus on genes that potentially modify ultraviolet radiation exposure, including polymorphisms in the glutathione Stransferases (GSTM1, GSTT1, and GSTP1) and the newly identified variants in DNA excision repair genes (ERCC2/XPD, and XPF). In addition, we will collect tumor specimens from cases for characterization of mutations at p53 and 9q22/ptch. We will determine mutation spectra examine associations of mutation with carcinogenic exposures and patient traits, and refine a novel model of skin tumorigenesis. These studies will increase our understanding of host susceptibility to non-melanoma skin cancer and advance current models of skin carcinogenesis through identification of patterns of gene inactivation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MOLECULAR MECHANISMS OF COMPLEX MIXTURE TOXICITY Principal Investigator & Institution: Puga, Alvaro; Professor; Environmental Health; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2001; Project Start 16-JAN-2001; Project End 31-DEC-2005 Summary: The long-range goal of this research is to develop an understanding of the mechanisms underlying the adverse health effects and toxicity resulting from exposure to complex mixtures of polycyclic aromatic hydrocarbons (PAH) and the carcinogenic metals arsenic and chromium, often found as co-contaminants in the environment. The objectives of this research project are, (1) to elucidate the mechanisms by which arsenic and chromium affect inducible gene expression, and (2), to evaluate the effect of mixtures of benzo[alpha]pyrene (B[alpha]P), a prototypical PAK and chromium and
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arsenic on the expression of phase I and phase II detoxification genies. Development of environmental policy relies on risk information about the chemicals to which individuals are exposed. Although mechanisms are in place to test the health effects of individual chemicals, there is little data on the toxicity of complex environmental mixtures. In the absence of specific data, default assumptions must be used when conducting risk assessment for mixtures. For example, in the absence of evidence. to the contrary, two chemicals having similar toxic effects are assumed to act in an additive manner. This approach is not satisfactory for many complex mixtures in which a wide spectrum of interactions, from repression of effects to synergy, exist. Since most humane are exposed to complex mixtures of environmental contaminants, methods for assessing the risk of these exposures need to be developed. Most if not all the toxic effects of PAH exposure are mediated by the aromatic hydrocarbon (Ah) receptor, a ligand-activated transcription factor that, in combination with the Ah receptor nuclear translocator (ARNT) causes the transcriptional activation of phase I detoxification genes, such as those coding for the cytochromes P450 monooxygenases CYP1Al, CYP1B1 and CYPIA2, and of phase II detoxification genes, such as those coding for quinone oxidoreductase (NQO1), glutathione-S-transferase (GSTP) and UDP-glucuronosyl transferase (UGTIA6). Phase II genes can also be induced by antioxidants and electrophiles through Ah receptor-independent mechanisms. Preliminary work from our laboratory has shown that exposure of cultured mammalian cells to chromate or arsenite disrupts the coordinate induction of phase I and phase II genes by dioxin, the protype halogenated aromatic hydrocarbon Ah receptor ligand. Chromate inhibits induction of phase II genes to a greater extent than induction of phase I genes, whereas arsenite inhibits phase I gene induction and elicits a dose-dependent oxidative stress response that superinduces electrophile response element (EpRE)- mediated transcription of phase II genes. These observations lead us to me hypothesis that combined exposure to a mixture B[alpha]P and chromate or arsenite, (1) Will disrupt the regulatory mechanisms that control transcription from B[alpha]P- inducible gene promoters, and (2) will cause an uncoupling of phase I and phase II gene expression and concomitant imbalance in B[alpha]P metabolism. Results from this work will help develop a means to predict the health risks arising from exposure to chemical mixtures. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MUTATION & RECOMBINATION IN MICE EXPOSED TO TOXIC METALS Principal Investigator & Institution: Stringer, James R.; Associate Professor; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2001; Project Start 01-APR-1995; Project End 31-MAR-2005 Summary: (Taken from application) The goal of this project is to better understand the genotoxic effects of chromium and arsenic in mammals, when these metals are introduced either alone, or combined with benzo[a]pyrene. The research design employs a battery of novel mouse strains designed to detect frameshift and recombination events. One set of such mice uses a human PLAP (Placental Alkaline Phosphatase) gene. The PLAP gene was rendered inactive by insertion of 7 G:C basepairs. The frameshifted PLAP transgene is transcribed ubiquitously in all mouse tissues. Consequently, when the frameshift mutation in the PLAP transgene reverts, active PLAP enzyme is produced and deposited on the surface of the cell, where it is detected by a histochemical stain. This approach provides information about where mutant cells arise in different tissues. Mice that use PLAP expression to detect deletional recombination between direct repeats (PLAP-del mice) are under construction. While
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the PLAP-del mice are being developed, interstitial deletion after exposure to metals will be studied in a mouse strain called pink-eyed unstable. These mice have been used to show that sodium arsenate can induce recombination in mice. However, pink-eyed unstable mice can detect recombination in embryonic premelanocytes only. By contrast, the PLAP-del system reports recombination in all tissues. We will also study mitotic recombination by using another mouse strain we have developed. These mice are heterozygous for the aprt gene. Lymphocytes derived from cells that have undergone mitotic recombination at any point between aprt and the centromere on chromosome 8 can be selected because such cells lack APRT function and survive in 2, 6 diaminopurine. We propose to test the following hypotheses: 1) Chromium and arsenic induce frameshift mutations and homologous recombination in the cells of diverse tissues of mice. 2) Combining one or another of these metals with benzo[a]pyrene has a synergistic effect on mutation. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NEURONAL FUNCTION OF JNK Principal Investigator & Institution: Xia, Zhengui; Associate Professor; Environmental Health; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): The c-Jun NH2-terminal protein kinases (JNK) are a family of MAP kinases that are preferentially activated by cell stress-inducing signals, such as trophic-withdrawal, heat shock and UV. JNKs have been implicated in several physiological functions including regulation of apoptosis, inflammatory responses, cell proliferation, differentiation and tissue morphogenesis. For example, JNK may play a role in the induction of apoptosis in neurons during development. However, the mechanism for JNK-mediated neuronal apoptosis is undefined. Using arsenite as a model for toxicant-induced neuronal apoptosis during development, we have begun to elucidate the molecular and cellular mechanisms underlying JNK-induced neuronal cell death. Sodium arsenite is an environmental toxicant that causes developmental defects in the CNS. Our data indicate that JNK isoforms may be differentially regulated during neuronal apoptosis. There are three JNK genes; JNK1, JNK2, and JNK3, cortical neurons express kinase activities for all JNKs. We showed that JNK contributes to arseniteinduced apoptosis in cultured neurons. Furthermore, JNK3 but not JNK1/2 is activated by arsenite. Since JNK3 is the only neural specific JNK isoform, it may provide a neurospecific target for blocking neuronal apoptosis. We propose to test the hypothesis that JNK3 but not JNK1 or 2, may be important for stress-induced neuronal apoptosis both in vivo and in vitro. We propose to address this issue using primary cultured cortical neurons, hippocampal slice cultures and high precision stereotactic delivery of apoptotic agents to the hippocampus and cortex. Moreover, we propose to use JNK3-/mice as well as transgenic mice over-expressing JBD specifically in neurons in the hippocampus and cortex to elucidate the function of JNK in neuronal apoptosis in vivo. We also propose a novel mechanism for JNK induction of apoptosis in which JNK activation induces post-translational modification that leads to caspase activation, and transcriptional regulation of cell death genes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NORTHERN NEW JERSEY COMMUNITY CLINICAL ONCOLOGY PROGRAM Principal Investigator & Institution: Rosenbluth, Richard J.; Hackensack University Medical Center 30 Prospect Ave Hackensack, Nj 07601
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Timing: Fiscal Year 2002; Project Start 01-SEP-1983; Project End 31-MAY-2007 Summary: (provided by applicant): The Northern New Jersey CCOP (NNJCCOP) provides access to clinical trials for cancer treatment and cancer control to almost half of the 8.4 million population of New Jersey, as well as adjacent New York and Pennsylvania. Forty-three physicians have access to trials, including pediatric and adult hematology/oncologists, surgeons, urologists, radiation oncologists, gynecologic oncologists and urologists. 37 Additional physicians are actively involved in the work of the CCOP. Extensive outreach ensures broad physician referral for cancer control. They are supported by a well-trained cadre of research nurses, pharmacists and data managers. The CCOP has created an effective and experienced infrastructure to ensure compliance with the highest standards of clinical research. The physicians build on a long tradition of closely-knit integration at the three clinical sites at two component hospitals. Hackensack University Medical Center (HUMC) includes a pediatric program, Tomorrows Children?s Institute (TCI) and an adult program, the Northern New Jersey Cancer Center (NNJCC). Trinitas Hospital, a component hospital resides in Union County, serving a high minority population. The two hospitals are primary sources of oncology care in their catchment areas and together accrue more than 2400 new cancer patients each year. The specific aims of the program are to: reduce cancer incidence, morbidity and mortality through expansion of clinical trials; develop creative and innovative means of communication, collaboration and education among physicians, health providers and citizens to accelerate cancer prevention, detection and treatment; ensure broader participation in trials among minority and female participants; and assure high standards of excellence and quality in cancer trials. Strong leadership, an effective organizational structure and proven track record support the goals of accelerated outreach, broad recruitment, expanded accrual, effective followup, accurate data management, compliance with quality assurance standards and active participation in the design, and implementation of new clinical trials. For the grant period, 2002-2007, the NNJCCOP projects accrual of 1482 adult credits (420 treatment and 1062 cancer control and follow-up) and 318.2 pediatric credits with 298 treatments and 20.2 cancer control credits. This represents a combined 5-year projected accrual of 1800.2 credits. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PHI-381: A NOVEL ANTI-LEUKEMIC AGENT Principal Investigator & Institution: Waurzyniak, Barbara; Paradigm Pharmaceuticals, Llc 2685 Patton Rd St. Paul, Mn 55113 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2004 Summary: (provided by applicant): Microtubules, which are formed by the selfassociation of the alpha/beta-tubulin heterodimers, provide structural support for a cell and play key roles in cell motility, mitosis, and meiosis. They are also the targets of several anticancer agents, indicating their importance in maintaining cell viability. Currently available tubulin binding anticancer drugs, including new taxol derivatives and epothilones, interact with beta-tubulin subunit of the alpha/beta-tubulin heterodimers and have no effect on microtubule minus ends. Furthermore, cancer cells with an altered beta-tubulin expression profile may be resistant to these agents. We used a three-dimensional computer model of tubulin constructed based upon its recently resolved electron crystallographic structure for rational design of a novel monotetrahydrofuran (THF)-containing synthetic anticancer drug targeting a unique narrow binding cavity on the surface of alpha-tubulin. We discovered a previously unidentified region with a remarkable abundance of leucine residues, which is located between the
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GDP/GTP binding site and the taxol binding site. This unique region contains a narrow cavity with elongated dimensions, which could accommodate a fully stretched aliphatic chain with a length of up to twelve carbon atoms. Using this model, a comprehensive structure search of the organic compound files in the Parker Hughes Institute Drug Discovery Program led to the identification of the recently reported chiral THF-epoxides as potential molecular templates for the rational synthesis of novel anti-cancer drugs containing structural elements capable of hydrophobic binding interactions with this leucine-rich binding cavity of tubulin. Our lead compound designated as COBRA-1, inhibited GTP-induced tubulin polymerization in cell free turbidity assays. Treatment of human breast cancer and brain tumor (glioblastoma) cells with COBRA-1 caused destruction of microtubule organization and apoptosis. Like other microtubuleinterfering agents, COBRA-1 activated the pro-apoptotic c-Jun N-terminal kinase (JNK) signal transduction pathway, as evidenced by rapid induction of c-jun expression. The further development of COBRA-1 as an anticancer agent will depend on in vivo efficacy, and toxicity studies in relevant animal models. We are now proposing to use the severe combined immunodeficiency (SCID) mouse model for detailed in vivo anticancer activity in SCID mice challenged with human breast cancer or glioblastoma cells. Our specific aims are: (i) To study the in vivo toxicity profile of COBRA-1 in BALB/c mice and (ii) To study the in vivo anti-cancer activity of COBRA-1 in a SCID mouse model of metastatic human breast cancer and glioblastoma. The knowledge gained from these studies described under Specific Aims 1-2 is expected to facilitate the design of innovative treatment regimens employing COBRA-1 for the treatment of metastatic solid tumors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PHYTOFILTRATION OF ARSENIC-CONTAMINATED DRINKING WATER Principal Investigator & Institution: Elless, Mark P.; Edenspace Systems Corporation 15100 Enterprise Ct, Ste 100 Dulles, Va 20151 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 30-JUN-2002 Summary: (Applicant's Abstract): Arsenic contamination of drinking water poses significant health risks to millions of people worldwide. Current cleanup technologies have substantial drawbacks, including high cost and high-volume toxic byproducts. Edenspace Systems Corporation proposes to propose to study the ability of a recently identified arsenic-hyperaccumulating fern to remove arsenic from drinking water. The investigator's preliminary research demonstrates that this fern is able to concentrate arsenic to levels more than 16,000 fold higher than the concentration in the soil solution and to rapidly remove arsenic from water containing 200 ug/L of arsenic, 4-fold higher than the current drinking water standard. In the proposed research, the investigators will study the ability of this fern to reduce arsenic levels below the proposed EPA drinking water limit of 5 ug/L by varying factors (plant density, water pH, chlorination/fluoridation, and arsenic species) that are likely to affect arsenic removal rates from drinking water and will also test both a batch and a flow-through technique for phytofiltration of arsenic-contaminated drinking water. This research will provide the foundation for development of a solar-powered (photosynthetic) hydroponics technique, enabling cost-effective, small-scale cleanup of arsenic-contaminated drinking water. PROPOSED COMMERCIAL APPLICATION: NOT AVAILABLE Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PHYTOREMEDIATION OF CONTAMINATED SOILS Principal Investigator & Institution: Shann, Jodi R.; University of Cincinnati 2624 Clifton Ave Cincinnati, Oh 45221 Timing: Fiscal Year 2001; Project Start 01-APR-1995; Project End 31-MAR-2005 Summary: (Taken from application) The goal of the proposed research is to develop a mechanistic understanding of the processes contributing to phytoremediation of soils contaminated with complex mixtures of polycyclic aromatic hydrocarbons (PAHs) and metals. Specific focus will be on pyrene and benzo[a]pyrene co-occurring with chromium, arsenic, nickel, cadmium, and lead. The approach takes into consideration both the ability of the plant to remove contaminants from the soil, as well as the ability of the plant to change degradative soil biofilms through the release of root exudates. The effect of metal and PAH availability in the soil will be monitored by soil extraction and bioindicators, throughout these investigations. The specific aims are: (1) to investigate potential mechanisms controlling phytoremediation, including uptake, rhizosphere degradation, and bioavailability, (2) to characterize root exudates and identify the specific components that enhance PAH degradation, and (3) to examine variation in root exudate production across plant species and under differing environmental conditions. The results of the experiments conducted under the above specific aims will allow the discernment of the extent to which either uptake or input (to the rhizosphere) is responsible for soil remediation in the presence of plants. It will also be possible to determine if concurrent phytoremedial processes operate in an additive, synergistic or antagonistic manner in soils contaminated with metals, PAHs, or mixtures of these. By identifying the specific exudate components that enhance PAH degradation, we will have a basis for screening plants for use in phytoremediation. This information will be directly applicable to the management of actual Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) (Superfund) sites and will further the development of phytoremediation as an in situ technology. In addition, the role of bioavailability will be examined here after we validate that our methods are providing an accurate estimate. Validated soil extraction methods for determination of bioavailable soil metals and PAHs will be a significant contribution to the tools needed for effective soil remediation and site assessment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PILOT: ARSENIC FROM CCCA-TREATED WOOD Principal Investigator & Institution: Cai, Young; Florida International University Division of Sponsored Research and Training Miami, Fl 33199 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 30-JUN-2006 Summary: (provided by applicant): Limited information is available about the ultimate fate of the arsenic found in chromated copper arsenate (CCA) during the service life and disposal of the treated wood product. This lack of information coupled with the large quantity of arsenic currently in service associated with treated wood (130,000 tons estimated), results in a potential risk of human and ecological exposure. The toxicity of arsenic is strongly a function of the speciation of the metalloid, with the inorganic species being more toxic than the methylated forms. Within the inorganic forms, species that are characterized by a lower valence are the most toxic. The objectives of the current study are to evaluate the toxicity of arsenic in leachates from CCA-treated wood by measuring the species of arsenic that are leached from different environmental samples. A considerable effort will be placed on method development, which will expand the applicability of cartridges designed to preserve samples in the field. Leaching will be
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evaluated in both laboratory and field settings. Laboratory studies will focus on standardized leaching tests aimed at simulating the impacts of rainfall, seawater, and landfill conditions. Laboratory samples evaluated will include CCA-treated wood at various retention levels. Field work will focus on evaluating the impacts of decks and marine docks constructed of CCA-treated wood on the surrounding environment. Samples will be routinely analyzed for arsenite (As(III)), arsenate (As(V)), monomethylarsonic acid (MMAA), and dimethylarsinic acid (DMAA). Other arsenic species, if any, will be detected and quantified on a periodic basis. Metals species will be routinely measured in the dissolved phase, and methods will be developed for measuring arsenic speciation within the particulate phase. Results will be used to estimate the total U.S. arsenic releases from CCA-treated wood structures. These data will be useful as inputs into environmental risk models that evaluate the probability of human disease or other environmental outcomes associated with the use or disposal of CCA-treated wood. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROGRESSION OF HEPATIC NEOPLASIA BY PCB/ARSENIC MIXTURES Principal Investigator & Institution: Painter, Jon T.; Colorado State University Fort Collins, Co 80523 Timing: Fiscal Year 2001; Project Start 21-AUG-2000; Project End 31-JUL-2005 Summary: (Taken from the Investigator's Abstract) Exposure to environmental chemicals may pose hazards to human health, including carcinogenesis. Exposures are more likely to chemical mixtures, especially near hazardous waste sites. Polychlorinated biphenyis (PCBS) and arsenic are two common contaminants which can be found together in mixtures. PCBs are divided into two classes. Coplanar congeners, such as PCB 126, have dioxin(TCDD)-like activity, and nonplanar congeners such as PCB 153 have phenobarbital-like activity. Both have been shown to promote hepatic neoplasia. Coplanar and nonplanar PCBs are likely to be found together in complex mixtures and the combination can act antagonistically on hepatic preneoplastic focus formation in promotion assays. Arsenic, a clastogen thought to influence carcinogenesis at the level of progression, also inhibits pre-neoplastic focus formation. The interaction between PCBs 126 and 153 will be evaluated using a 26-week in vivo initiation/promotion/progression (IPP) assay in the rat using dimethylnitrosamine (DEN) initiation, partial hepatectomy, and subchronic PCB mixture treatment. Promotion and progression will be quantified using glutathione-S-transferase (GST-P) and TGF-alpha positive hepatic foci, respectively. Later studies will incorporate arsenic into the mixture. The role of TGF-beta in cell proliferation and apoptosis will also be evaluated. An in vivo/in vitro IPP assay will be developed using hepatocytes harvested from DEN-initiated rats. Cultured cells will be exposed to mixtures of both PCB congeners as well as arsenic to evaluate interactions between the compounds using assays similar to the in vivo experiments. Results will be compared to the in vivo model in order to validate the cell culture technique as an inexpensive and efficient alternative for evaluating carcinogenesis. Data will be used in a quantitative risk assessment model for PCB and arsenic mixtures. The candidate on this project is Jon Todd Painter, DVM. Dr. Painter's goals are to prepare for a research career combining his training in toxicologic pathology and molecular carcinogenesis. Dr. Painter will have completed his residency training in anatomic pathology and will spend at least 90% of his time on this research at the Center for Environmental Toxicology and Technology at Colorado State
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University. He will be mentored by a Faculty Committee with research expertise in toxicology, pathology, molecular biology, cell culture, and carcinogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROSPECTIVE STUDIES OF DIET AND CANCER IN MEN AND WONEN Principal Investigator & Institution: Willett, Walter C.; Professor and Chairman; Nutrition; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2001; Project Start 23-AUG-1991; Project End 31-MAR-2006 Summary: (provided by Applicant) This proposed Program will use prospectively collected dietary data and frozen plasma and DNA specimens to address a series of hypotheses regarding major cancers in men and women. In addition, these nutritional and genetic exposures will be examined in relation to specific molecular characteristics of tumors. The cancers to be studied are those of the prostate, colon and rectum, bladder, lung, kidney, and ovary. This Program Project supports, and depends on, the continued follow-up of 51,529 men who completed an extensive dietary questionnaire first in 1986 and again in 1990, 1994, and 1998 (the Health Professional?s Follow-up Study, HPFS), and is also closely linked to the Nurses? Health Study (NHS) of 121,700 women. The Program Project has already contributed substantially to information on diet and cancers of the breast, prostate, colon, and bladder. The proposed continuation will extend and refine observations from the first twelve years of follow-up and will also address new hypotheses related to both cancer incidence and survival. Project 1 will examine dietary (lycopene, calcium, and N-3 fatty acid intakes) and other predictors of prostate cancer incidence in relation to risk of PSA relapse among men with apparently successful treatment for localized prostate cancer. In addition, a series of dietary and hormonal factors will be related to specific characteristics of incident cancers, including expression of PTEN and COX-2 and markers of angiogenesis. Project 2 will address hypotheses relating intakes of folic acid, calcium and red meat and plasma levels of IGF1 and its binding proteins to risks of both colorectal cancer and adenomas. Interactions with germline polymorphisms and relationships with specific molecular tumor characteristics will be examined. Project 5 will examine dietary and related risk factors for bladder cancer in both men and women. Exposures will include intakes of cruciferous vegetables and total fluids, and biochemical indicators of selenium and arsenic exposure. Interactions with polymorphisms in carcinogen metabolizing genes and specific association with p53 expression in tumors will also be examined. Project 4 pools data from all eleven major published prospective studies of diet and cancer. Precise and unique information has already been obtained for breast, lung and colon cancers, and the proposed work will extend analyses to cancers of the pancreas and ovary. These highly interrelated studies that integrate dietary factors, established nondietary risk factors, endogenous hormone levels, genetic susceptibility, and molecular characteristics of tumors, will contribute importantly to the understanding and prevention of the major cancers of men and women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROSPECTIVE STUDY OF DIET AND BLADDER CANCER Principal Investigator & Institution: Stampfer, Meir J.; Professor and Chair; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2001; Project Start 23-AUG-1991; Project End 31-MAR-2006
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Summary: (provided by Applicant) This project aims to identify dietary, reproductive and genetic factors related to bladder cancer in two large ongoing prospective cohorts of men and women. Risk factors of bladder cancer are largely unknown but this important disease is likely to be largely preventable, given the large regional variations in incidence rates. Compared to some other cancers, bladder has received little attention and support. There are exciting opportunities to improve the understanding and ultimately prevention of this disease. We propose to study bladder cancer in the Nurses? Health Study and the Health Professionals Follow-up Study. By 2004, we project that 562 men and 391 women will be diagnosed with bladder cancer in these two cohorts. We will conduct prospective analyses using both cohorts, and nested casecontrol analyses among members who have provided blood, cheek cells, or toenails. We propose to obtain tumor specimens from participants with bladder cancer to examine specific tumor alterations (specifically p53 overexpression). We propose to examine dietary factors in detail among women who completed the initial dietary questionnaire in 1980; the ?diet? cohort we will have 312 women with bladder cancer. Selenium and arsenic levels will be assessed from toenails of over 500 men and women with bladder cancer and will be compared to 500 controls selected from the same cohorts. We will also examine specific dietary interactions with three polymorphic genes that have been previously related to bladder cancer risk (NAT1, NAT2 and GSTM1). We will use p53 overexpression as an alternative endpoint to determine if specific dietary factors can predict p53 mutations in bladder cancer. Stratified analyses and multiple logistic regression will be used to control for potential confounding by age, smoking, and other relevant nutrients or foods. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROTEOTOXICITY NEPHROTOXICITY
BIOMARKERS
FOR
CISPLATIN
Principal Investigator & Institution: Flaws, Jodi A.; Associate Professor; Epidemiology and Prev Medicine; University of Maryland Balt Prof School Baltimore, Md 21201 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2005 Summary: (provided by applicant):There is a pressing need to better understand the mechanisms of platinum-based anti-cancer drug toxicity to the kidney and to utilize this basic scientific information for the development of biomarkers to detect early manifestations of renal damage in patients treated with these and other nephrotoxic anti-cancer agents. It is our hypothesis that treatment of renal proximal tubule cells to platinum-based drugs will produce specific oxidative cellular effects that will be intrinsically linked to increased excretion of specific oxidized proteins of renal derivation into the urine via chaperoning by specific stress protein families. In vitro studies which will compare the responses of primary cultures of both human and rat kidney cells to cisplatin using a short term dose-response design. These studies will provide a mechanistic basis for testing the hypothesis that stress proteins play a central role in the excretion of specific oxidized proteins from this target cell population. Data from these studies should will also determine whether this proposed mechanism of platinum-induced toxicity is similar in rat and human proximal tubule cells. This hypothesis will be further tested via studies involving acute in vivo exposure of rats to platinum- based drugs using a dose-response, time course design. Examination of urine samples from these animals will be focused on those proteins found to be preferentially excreted by the proximal tubule cells in culture. Data from these studies will be essential for understanding the extent to which urinary biomakers derived in rats may be used for predicting platinum-induced human nephrotoxicity. The utility of these new
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biomarkers for earlier detection of platinum-induced nephrotoxicity in humans will hopefully be evaluated under a future R33 grant application that will apply knowledge derived from these studies to other nephrotoxic anti-cancer agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF CYTOKINES IN MYELOMA PATHOGENESIS Principal Investigator & Institution: Anderson, Kenneth C.; Professor of Medicine; DanaFarber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 01-DEC-1990; Project End 31-MAY-2008 Summary: (provided by applicant): Multiple myeloma (MM) affected 14,400 new patients with in the United States in 2001, with 50,000 total patients, and unfortunately remains incurable despite conventional and high dose chemotherapy. In past studies sponsored by this grant in our Jerome Lipper Multiple Myeloma Center, we have characterized the role of growth factors in MM pathogenesis and derived novel therapies to improve patient outcome based upon targeting cytokines and their signaling cascades both in the MM cell as well as its bone marrow (BM) microenvironment. To achieve this goal, we have developed systems for studying the growth, survival, and drug resistance mechanisms intrinsic to MM cells. Importantly, we have also developed both in vitro systems and in vivo animal models to characterize mechanisms of MM cell homing to BM, as well as cytokines promoting MM cell growth and drug resistance in the BM milieu. These model systems have allowed for the development of several promising biologically-based therapies, including thalidomide (Thal) and its immunomodulatory analogs (IMiDs), proteasome inhibitor PS 341, and arsenic trioxide (As2O3). Once preclinical promise has been demonstrated, we have rapidly translated these laboratory studies to phase I and II clinical trials to evaluate their clinical utility and toxicity. Importantly, ongoing gene array studies of samples obtained from patients treated on these protocols is directed to identify in vivo targets and mechanisms of drug action on the one hand, versus mechanisms of drug resistance on the other. These studies have suggested the critical role of cytokines in growth, survival, drug resistance, and migration of MM cells, providing the framework for validating their role in MM pathogenesis and as targets for novel therapies, as proposed in this competitive renewal application with the following three specific aims: Specific Aim 1 To characterize the role of growth factors in mediating growth, survival, drug resistance, and migration of MM cells in vitro; Specific Aim 2 To validate the signaling events mediating cytokine-induced growth, survival, drug resistance, and migration of MM cells as therapeutic targets; and Specific Aim 3 To validate novel therapeutics targeting in vivo cytokine-induced signaling cascades in animal models for evaluation in phase I/II clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SORBENTS FOR REMOVAL OF ARSENIC AND HEAVY METALS Principal Investigator & Institution: Lovell, John S.; Ada Technologies, Inc. 8100 Shaffer Pky, Ste 130 Littleton, Co 801274124 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2004 Summary: (provided by applicant): In response to the recent Environmental Protection Agency (EPA) announcement that affirmed a national standard for maximum arsenic content in drinking water of 10 parts per billion (ppb), ADA Technologies, Inc. is proposing to develop and commercialize a novel, low-cost sorbent for the removal of arsenic and other heavy metals from drinking water. ADA has assembled a project team
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with a complementary mix of experience and skills to develop the sorbent and to package it for use in small and large-scale water treatment systems. The sorbent will combine novel technology from ADA to chemically amend a substrate clay material to increase its capacity for arsenic with emerging technology from Texas A&M to bind the clay to sand or other materials that increase the porosity of the sorbent and allow its use in water treatment. The Texas A&M technology has been developed with funding from the NIEHS under the Superfund Basic Research Program (SBRP), addressing one of the recommendations in the solicitation to which this proposal responds. The expertise of CH2M-Hill, an internationally known architect/engineering firm, will be tapped to package the novel sorbent in configurations that are amenable to use in commercialscale water treatment systems. The overall goal of the project is to demonstrate the costeffective removal of arsenic from groundwater using the amended clay sorbent technology. Specific activities include the preparation of several variants of the new sorbent, completion of laboratory tests to optimize the formulation, design and fabrication of prototype hardware in two sizes, and ten-month field trials of both pilots on arsenic-contaminated waters in Colorado's San Luis Valley, an area with arsenic content in excess of the new EPA standard. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SOUTHERN NEVADA CANCER RESEARCH FOUNDATION--CCOP Principal Investigator & Institution: Ellerton, John A.; Ccop Investigator; Southern Nevada Cancer Research Fdn Research Foundation Las Vegas, Nv 89106 Timing: Fiscal Year 2002; Project Start 30-SEP-1983; Project End 31-MAY-2007 Summary: (provided by applicant): The Southern Nevada Cancer Research Foundation (SNCRF) was established to conduct cancer research under the Community Clinical Oncology Program (CCOP) structure. It is a free standing non-hospital based CCOP. The long-term objectives have been: 1) to accrue a minimum of 50 credits annually to CCOP approved cooperative group treatment clinical trials; 2) to accrue a minimum of 50 credits annually to CCOP approved cooperative group cancer control studies; 3)to provide to the cooperative groups in the NCI timely data of high quality; 4)to promote quality and state-of-the-art treatment in the community through the participation in protocol studies by: (a) involving all CCOP physicians and staff in scientific and educational activities of the research bases; (b) expanding the knowledge, awareness and involvement of the primary health care providers and other specialists for the development and use of cancer control research; 5) to actively support other professional education programs and cancer control outreach services to under-served rural areas, and to identify women and minority groups that may be under-served and make a special effort to involve them in clinical trials; and 6) to actively work with the NCI to develop a community cancer network in order to facilitate the growth and development of important new cancer initiatives. In order to better accomplish all of these goals, the CCOP has expanded to include 45 investigators from varied medical specialties. The addition of Washoe Medical Center in 1999 as an affiliate in Reno expanded the CCOP statewide as the only CCOP in Nevada covering the entire state of Nevada. The CCOP continues to add new physicians every year to meet the growing population of the state. This will provide increased access to patients and increase public and medical awareness of the CCOP. The methods for accomplishing these goals will be through the application of CCOP grant money. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STRUCTURAL INVESTIGATIONS OF METALLOPROTEIN METAL SITES Principal Investigator & Institution: Penner-Hahn, James E.; Professor; Chemistry; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 01-APR-1987; Project End 30-NOV-2004 Summary: (Adapted from applicant's abstract) The long term objective of this proposal is to characterize in detail the structural and functional properties of Zn(II) in biological systems. Zinc is the most common metal found in metalloproteins and is the only metal that is known to be required for every major class of enzyme catalysis. Hundreds of zinc proteins have been isolated and thousands of potential zinc binding sites have been identified in protein sequences. Imbalances in the levels of Zn, or errors in its transport or regulation can have profound health consequence. Despite its importance, there is relatively little information available about biological Zn(II) sites due to the difficulty of studying this spectroscopically "silent" metal. X-ray absorption spectroscopy, one of the few methods able to provide structural information for non-crystalline materials, will be used to determine their structures. Three major, inter-related objectives are proposed: X-ray absorption spectroscopy will be used to characterize the Zn binding sites in a series of important proteins, with particular emphasis on a novel class of Zn-alkyl transfer enzymes. -Detailed comparisons will be made of the metal binding sites in a series of structurally defined peptides. The objective of this second set of experiments is to determine the relative importance of metal stereochemical preference and protein structure in defining the structure of a metal binding site. For this work, structures will be compared for a series of spectroscopically silent d10 metal ions (Cu(I), (Ag(I), Cd(II), Hg(II)) and metalloids As(III). -X-ray absorption spectroscopy, x-ray microprobe imaging, microprobe spectroscopy, and x-ray microtomography will be used to characterize the role(s) of Zn in embryo development in zebra fish and Xenopus laevis. Spatially and temporally-resolved spectroscopy will be used to determine the Zn speciation in developing embryos. Coupled capillary-electrophoresis/x-ray fluorescence will be used to resolve and characterize Zn containing proteins. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: STRUCTURE/FUNCTION OF AN ION MOTIVE ATPASE Principal Investigator & Institution: Gatti, Domenico L.; Biochem and Molecular Biology; Wayne State University 656 W. Kirby Detroit, Mi 48202 Timing: Fiscal Year 2001; Project Start 01-JUN-1998; Project End 31-MAY-2004 Summary: (Adapted from applicant's Abstract) The arsenical resistance (ars operon of the Escherichia coli plasmid R773 encodes a system for the active extrusion from cells of the toxic oxyanions arsenite (As(III)O21-) and antimonite (Sb(III)O21-) via an ATPdriven pump. The arsA and the arsB genes o the operon encode, respectively, the catalytic subunit (ATPase) and the membrane subunit of the pump. The arsC gene codes for a reductase that convert arsenate (As(V)O43) to arsenite and appears to channel it into the ArsA-ArsB pump, thus extending bacterial resistance also to the pentavalent state of arsenic. Crystals diffracting at high resolution (2.0 Angstrom) were obtained for both the catalytic subunit of the pump (ArsA) and for the reductase (ArsC) and native data sets have been collected. Structural studies are proposed to identify ArsA and ArsC binding sites for substrates and/or for allosteric effectors, and the regions of interaction with other proteins (e.g., ArsA with ArsB, ArsC and ArsA). Since expression of the arsB gene is highly toxic in E. coli, production of the protein in other hosts (Archaebacteria,
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yeast) will be pursued to obtain a large amount of pure protein for crystallization. Arsenical resistance is a useful model for the study of multiple drug resistance in both eukaryotic and prokaryotic cells. The ArsA-ArsB pump exhibits structural and functional similarity to the P-glycoprotein: both are efflux pumps for toxic compounds, have two nucleotide binding sites, are substrate-dependent ATPases, have 12 membrane spanning alpha-helices, and are each able to detoxify structurally distinct drugs. The latter point is illustrated for the ArsA-ArsB pump by the fact that while arsenate and arsenit are both oxyanions of arsenic, they are chemically dissimilar. The ArsA protein is also the only other ion-motive ATPase, besides the mitochondrial F1 ATPase, for which three-dimensional crystals have been obtained. Analysis of the similarities and differences between these two enzymes will further our understanding of how ions are transported across biological membranes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SUPERFUND TOXIC SUBSTANCES--EXPOSURE AND DISEASE Principal Investigator & Institution: Monson, Richard R.; Professor of Epidemiology; Environmental Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, Ma 02460 Timing: Fiscal Year 2001; Project Start 01-APR-1992; Project End 31-MAR-2005 Summary: Our theme is the understanding and assessment of risk to human health from exposure to hazardous substances. We approach this theme from the perspective of an interdisciplinary team that integrates exposure assessment, biologic pathogenesis, and epidemiologic studies. Our biomedical studies revolve around three classes of illness: reproductive health, cardio-respiratory health, and cancer. Our non-biomedical studies relate to health of the ecosystem and to factors that affect aquatic organisms. These studies encompass specific exposures to metals and to organo-chlorine compounds. Reproductive health is being evaluated in relation to environmental exposure to lead, mercury, polychlorinated biphenyls (PCBs) and related compounds; cardio-respiratory health is being evaluated in relation to occupational exposure to fuel oil ash, which contains a high level of vanadium and other metals; the occurrence of cancer and its precursors are being evaluated in relation to arsenic in drinking water supplies; the health of the ecosystem, specifically of aquatic organisms, is being evaluated in relation to the presence of metals, PCBs, and polyaromatic hydrocarbons (PAHs). Our general goal is to evaluate the relation between chemicals in the environment and their relation to human ill health. Our objectives include the following: - to assess the use of calcium supplements to minimize the adverse effects of lead on the fetus - to assess uncertainties in development effects in children related to multiple environmental exposure to metals and organic compounds - to evaluate the effects of in utero exposure to ambient levels of PCBs on growth and development of the child and on female reproductive health. - to evaluate the cardiac and respiratory effects of fuel-ash oil on the human lung and to determine the mechanism through which vanadium and other metallic components of fuel-ash adversely effect the heart and the lung - to evaluate the nature of the association between arsenic and skin and skin bladder cancers and their precursors and to assess the epigenetic mechanisms through which arsenic may affect human health - to evaluate the effects of these and related chemicals on the aquatic ecosystem so that a comprehensive approach can be developed to assess the health of the ecosystem - to develop an approach for exposure assessment and health evaluation in the community that will enable enlightened interaction between scientists and the community. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TOXIC METAL COMPLEXATION BY DE NOVO DESIGNED PEPTIDES Principal Investigator & Institution: Pecoraro, Vincent L.; Professor; Chemistry; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2003; Project Start 09-JUN-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Heavy metal poisoning by elements such as mercury, lead, cadmium, and arsenic is a significant human health problem. Understanding the interaction of heavy metals with proteins is essential for defining the mechanism of toxicity, developing ways to minimize human exposure and to provide therapeutic regimens for removal of toxic ions. Our goals are (1) to develop peptide systems that provide a groundwork for the understanding of metalloregulatory proteins and metallochaperones, (2) to develop peptidic systems that can efficiently and selectively sequester heavy metal ions from aqueous solutions, and (3) to understand the thermodynamics and kinetics of metal binding to these designed peptides. To achieve these goals we will use a de novo peptide system based on the three-stranded coiled coil peptide aggregate motif that encapsulates with high affinity single heavy metal ions and provides spectroscopic models of mercury, cadmium and arsenic binding sites in biological systems. We will generate high resolution structures of this peptide system in the presence and absence of these heavy metals, elucidate the kinetic and thermodynamic mechanisms of heavy metal encapsulation, and expand the array of characterized systems to transition metal ions Fe(II), Cu(I), Ni(II), Co(II) and Zn(II). We will also extend the original design to include single chain peptides that encapsulate heavy metals and coiled coils that provide different coordination environments than the original design and those that encapsulate more than one heavy metal ion. These studies will expand the foundation of knowledge that has been laid by the scientific community investigating metallopeptide design, metalloregulatory proteins and heavy metal detoxification. These objectives will develop insight into the interplay between metal coordination and apopeptide structure in defining the overall metallopeptide fold, an important aspect of metallopeptide design. Also, development of highly efficient and specific heavy metal sequestering peptides could, ultimately, provide a viable and biodegradable means of removing heavy metals from contaminated water. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TRACE ELEMENTS AMONG IOWA PESTICIDE APPLICATORS Principal Investigator & Institution: Dennis, Leslie Epidemiology; University of Iowa Iowa City, Ia 52242
K.;
Assistant
Professor;
Timing: Fiscal Year 2003; Project Start 01-JUL-2003; Project End 30-JUN-2005 Summary: (provided by applicant): The Agricultural Health Study (AHS) is an established, on-going prospective cohort study examining the relationship between agricultural exposures, such as pesticide use, and disease among applicators in Iowa and North Carolina. The AHS in Iowa involves 36,793 licensed pesticide applicators, plus 21,773 spouses who are exposed either directly or indirectly to pesticides and other agricultural exposures. Prostate cancer incidence and mortality are higher among farmers, making this a high-risk cohort. The mechanism of potential exposure among farmers is unclear, so research into this subgroup of Americans is important. Current literature suggests associations with prostate cancer and arsenic, cadmium and low selenium levels but studies have not been consistent. We propose a nested case-control pilot study of incident prostate cancer within the existing AHS, identified through semi-
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rapid reporting of prostate cancers by the Iowa Cancer Registry (ICR), to examine trace elements found in toenails including arsenic, cadmium and selenium, all long-lived indicators, along with other trace elements that fit into this classification. We will compare these elements in 86 incident prostate cancer cases to 172 controls (frequency matched on age, completion of the diet survey, and a recent PSA test) from within the AHS cohort. We will use neutron activation analysis (NAA) to analyze for the targeted trace elements. We justify examining the other trace elements as a cost efficient, hypothesis generating sub-study. A secondary aim of this pilot study is to examine the validity of arsenic and selenium measured in toenails compared with standard questionnaire measurements of dietary selenium and arsenic pesticides collected prior to diagnosis in this cohort. In residentially stable populations, biomarkers of trace elements may be a good measure of exposure reducing the need for questionnaires with long detailed lists of pesticides and complex food frequency questionnaires (FFQs). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: USE OF GIS IN ANALYZING ENVIRONMENTAL CANCER RISKS Principal Investigator & Institution: Harris, Robin B.; Assistant Professor of Public Health; None; University of Arizona P O Box 3308 Tucson, Az 857223308 Timing: Fiscal Year 2001; Project Start 27-SEP-2001; Project End 31-AUG-2004 Summary: The overall goals of this proposal are to examine geographical variation in the association between cancer risk and potential environmental exposures, in particular arsenic exposure, and to then determine the homogeneity of the associations as the geographical scale changes. Uses of Geographic Information Systems (GIS) have made it more feasible to link multiple sources of descriptive attribute information for various geographic levels with health outcome data. The use of GIS allows the spatial relationships between the data elements to maintained and analyzed. Arsenic exposure may be a causal agent in the development of bladder, lung, kidney, and skin cancers. Furthermore, arsenic is known to vary across geographical locations. Several geographically delineated data sets exist in the State of Arizona that allow for epidemiological exploration of the relationship between arsenic exposure and cancer occurrence. Geocoded cancer incidence and mortality data are available from the Arizona Cancer Registry for bladder, kidney, and lung cancer. Skin cancer data are available from a completed population-based case control study. Arsenic concentrations are available from a multimedia, multipathway survey conducted in Arizona. The specific aims for this proposed research are 1) to evaluate spatial scales and determine relationships between the scale used by the Atlas of Cancer Mortality and scales potentially more useful within the state and 2) to evaluate the relationships between the various cancers and arsenic exposure for the various geographical scales. This proposal presents a cohesive research team that encompasses faculty and staff from various colleges within the University of Arizona and state health agencies and will utilize archival data collected by various state agencies and completed epidemiological studies of skin cancer and environmental exposures. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: USE EPIDEMIOLOGIC*
OF
WATER
QUALITY
SURVEILLANCE
DATA
IN
Principal Investigator & Institution: Mueller, Beth A.; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2004
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Summary: (provided by applicant): Drinking water is of importance for cancer studies attempting to measure both environmental and dietary exposures. Potentially useful data exist in water quality databases that have been created as part of routine, federally mandated surveillance activities. In many states these databases have existed for several decades, containing information about levels of contaminants such as nitrates, arsenic, or pesticides in drinking water supplies. Given the suspected long latent period between exposure and tumor diagnosis, or the potential importance of cumulative effects, these data may provide an opportunity to obtain measurements of exposures relevant to time periods prior to diagnosis for subjects in research studies. Our general purpose is to evaluate whether water contaminant levels obtained from an historic water surveillance database in Washington State can be used to estimate past and current individual exposure. We propose to focus on selected contaminants (nitrates and arsenic) that have been potentially associated with cancer occurrence. In Phase I of this project, geographic information systems methods (GIS) will be used to measure the correlation of tap water nitrate levels measured at residences of subjects enrolled in a previous cancer study, with nitrate levels measured in public water supplies from the same geographic coordinate. This will allow us to evaluate the extent to which it may be possible to measure prior exposure to drinking water contaminants using existing water quality surveillance data. In Phase 2, we will identify a new sample of residences located in regions where newly diagnosed cancer cases reside and measure tap water nitrate and arsenic levels, and conduct a similar evaluation to learn whether recent exposures may be estimated using the surveillance database. Phase 2 will also include an interview in which the level of tap water use (vs. bottled water or other source) for drinking, food preparation, and other modes of exposure are determined. If these data are correlated with tap water levels of contaminants, this method may be used to estimate previous and current exposures using methods that are less expensive and easier to employ in the context of epidemiologic studies. These methods may also be applicable to environmental databases with other types of exposures, or for examining other exposures (like pesticides) within drinking water surveillance databases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: X RAY ABSORPTION SPECTROSCOPY OF METALLOENZYMES Principal Investigator & Institution: Scott, Robert A.; Professor and Head; Chemistry; University of Georgia 617 Boyd, Gsrc Athens, Ga 306027411 Timing: Fiscal Year 2001; Project Start 01-APR-1989; Project End 30-NOV-2002 Summary: X-ray absorption spectroscopy (XAS) will be used, as a component of multidisciplinary biochemical and biophysical structure/function studies, to provide high-resolution local structural information about metal sites in a number of metallobiochemical systems. Proposed studies focus on the unique contribution to be made by XAS in studying "spectroscopically difficult" metals, including Zn, Cd, Hg, As, Sb. Many of the proposed experiments involve the role of metals in the important biological processes of transcription and its metalloregulation, heavy metal toxicity and resistance, and metal homeostasis. In particular, presumptive metal-binding motifs in basal eucaryal and archaeal transcription factors will be examined for metal binding, specificity, and requirement. The initial target for this effort is TFIIB. Other experiments will characterize the metal-binding residues and coordination environments of the metalloregulatory proteins MerR, ArsR, ArsD, and CadC. The correlation of metal coordination changes and allosteric regulation associated with protein conformational changes will be studied. Site-directed mutagenesis designed to alter the specificity for metal inducers, creating a Cd(II)-sensitive ArsR, for example, will require XAS for metal
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site characterization. Biophysical characterization of metal-binding affinity and specificity of MerP, a prototypical example of a widely distributed ca. 40-residue sequence motif containing a GmtCxxC sequence (Met2 and Thr3 are nearly conserved) will be carried out. The occurrence of variants of this "heavy metal associated" (HMA) motif in a family of CPx-type ATPases, all of which are involved in heavy metal efflux or homeostasis for mercury, cadmium, and copper (at least), makes a characterization of their specificity particularly attractive. Six copies of these HMA motifs occur near the Ntermini of the products of the MNK and WND genes, which have been associated with the copper-based Menkes and Wilson's diseases, respectively. The use of directed evolution to develop the MerP HMA motif into a specific recognition domain for any given metal ion will require XAS to characterize the metal coordination. 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 “arsenic” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for arsenic in the PubMed Central database: •
An Escherichia coli chromosomal ars operon homolog is functional in arsenic detoxification and is conserved in gram-negative bacteria. by Diorio C, Cai J, Marmor J, Shinder R, DuBow MS.; 1995 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=176848
•
Arsenic and drinking water. by Weir E.; 2002 Jan 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=99233
•
Arsenic and pressure-treated wood: the argument moves to the playground. by Sibbald B.; 2002 Jan 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=99243
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Arsenic poisoning rampant in Bangladesh. by Sibbald B.; 2002 Jun 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=113817
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Arsenic Trioxide Is a Potent Inhibitor of the Interaction of SMRT Corepressor with Its Transcription Factor Partners, Including the PML-Retinoic Acid Receptor [alpha] Oncoprotein Found in Human Acute Promyelocytic Leukemia. by Hong SH, Yang Z, Privalsky ML.; 2001 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=99892
3 Adapted 4
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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Arsenic-induced PML targeting onto nuclear bodies: Implications for the treatment of acute promyelocytic leukemia. by Zhu J, Koken MH, Quignon F, Chelbi-Alix MK, Degos L, Wang ZY, Chen Z, de The H.; 1997 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20553
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Association of arsenic-induced malignant transformation with DNA hypomethylation and aberrant gene expression. by Zhao CQ, Young MR, Diwan BA, Coogan TP, Waalkes MP.; 1997 Sep 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23527
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Detoxification of Arsenic by Phytochelatins in Plants. by Schmoger ME, Oven M, Grill E.; 2000 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=58915
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Expression and Regulation of the Arsenic Resistance Operon of Acidiphilium multivorum AIU 301 Plasmid pKW301 in Escherichia coli. by Suzuki K, Wakao N, Kimura T, Sakka K, Ohmiya K.; 1998 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=106059
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Homology of Escherichia coli R773 arsA, arsB, and arsC Genes in Arsenic-Resistant Bacteria Isolated from Raw Sewage and Arsenic-Enriched Creek Waters. by Saltikov CW, Olson BH.; 2002 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=126541
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Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity. by Liu SX, Athar M, Lippai I, Waldren C, Hei TK.; 2001 Feb 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=29310
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Isolation and Characterization of a Novel As(V)-Reducing Bacterium: Implications for Arsenic Mobilization and the Genus Desulfitobacterium. by Niggemyer A, Spring S, Stackebrandt E, Rosenzweig RF.; 2001 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=93345
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Mechanisms of Arsenic Hyperaccumulation in Pteris vittata. Uptake Kinetics, Interactions with Phosphate, and Arsenic Speciation. by Wang J, Zhao FJ, Meharg AA, Raab A, Feldmann J, McGrath SP.; 2002 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=166674
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Microbial Methylation of Metalloids: Arsenic, Antimony, and Bismuth. by Bentley R, Chasteen TG.; 2002 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=120786
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Mutagenicity of arsenic in mammalian cells: Role of reactive oxygen species. by Hei TK, Liu SX, Waldren C.; 1998 Jul 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20936
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PIC-1/SUMO-1-Modified PML-Retinoic Acid Receptor [alpha] Mediates Arsenic Trioxide-Induced Apoptosis in Acute Promyelocytic Leukemia. by Sternsdorf T, Puccetti E, Jensen K, Hoelzer D, Will H, Ottmann OG, Ruthardt M.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=84360
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Pink-eyed Dilution Protein Modulates Arsenic Sensitivity and Intracellular Glutathione Metabolism. by Staleva L, Manga P, Orlow SJ.; 2002 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=138627
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Rapid and Simple Method for the Most-Probable-Number Estimation of ArsenicReducing Bacteria. by Kuai L, Nair AA, Polz MF.; 2001 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=92996
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Reduction and Coordination of Arsenic in Indian Mustard. by Pickering IJ, Prince RC, George MJ, Smith RD, George GN, Salt DE.; 2000 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=58951
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Reduction of Arsenate to Arsenite by the ArsC Protein of the Arsenic Resistance Operon of Staphylococcus aureus Plasmid pI258. by Ji G, Silver S.; 1992 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50154
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Short-term solution suggested for Bangladesh's arsenic crisis. by [No authors listed]; 2002 Oct 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=134199
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The Chromosomal Arsenic Resistance Genes of Thiobacillus ferrooxidans Have an Unusual Arrangement and Confer Increased Arsenic and Antimony Resistance to Escherichia coli. by Butcher BG, Deane SM, Rawlings DE.; 2000 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=101419
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Transformation of Escherichia coli with a large plasmid of Acidiphilium multivorum AIU 301 encoding arsenic resistance. by Suzuki K, Wakao N, Sakurai Y, Kimura T, Sakka K, Ohmiya K.; 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168498
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Trypanothione Overproduction and Resistance to Antimonials and Arsenicals in Leishmania. by Mukhopadhyay R, Dey S, Xu N, Gage D, Lightbody J, Ouellette M, Rosen BP.; 1996 Sep 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38393
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Uptake Kinetics of Arsenic Species in Rice Plants. by Abedin MJ, Feldmann J, Meharg AA.; 2002 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152223
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Virulence and arsenic resistance in Yersiniae. by Neyt C, Iriarte M, Thi VH, Cornelis GR.; 1997 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=178738
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 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
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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 arsenic, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “arsenic” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for arsenic (hyperlinks lead to article summaries): •
A major human arsenic metabolite, dimethylarsinic acid, requires reduced glutathione to induce apoptosis. Author(s): Sakurai T, Qu W, Sakurai MH, Waalkes MP. Source: Chemical Research in Toxicology. 2002 May; 15(5): 629-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12018983&dopt=Abstract
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A review of animal models for the study of arsenic carcinogenesis. Author(s): Wang JP, Qi L, Moore MR, Ng JC. Source: Toxicology Letters. 2002 July 7; 133(1): 17-31. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076507&dopt=Abstract
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Arsenic and heavy metal poisons. Author(s): Rouss P Jr. Source: Southern Medical Journal. 2003 June; 96(6): 633-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938800&dopt=Abstract
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Arsenic and old lace: end-of-life care in the postoperative period. Author(s): Jones JW, McCullough LB. Source: Surgery. 2002 May; 131(5): 583-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12019415&dopt=Abstract
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Arsenic contamination in Bangladesh groundwater: a major environmental and social disaster. Author(s): Alam MG, Allinson G, Stagnitti F, Tanaka A, Westbrooke M. Source: International Journal of Environmental Health Research. 2002 September; 12(3): 235-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12396524&dopt=Abstract
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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Arsenic contamination in ground water: Indian scenario. Author(s): Jain CK. Source: Indian J Environ Health. 2002 July; 44(3): 238-43. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14503449&dopt=Abstract
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Arsenic hazards to humans, plants, and animals from gold mining. Author(s): Eisler R. Source: Rev Environ Contam Toxicol. 2004; 180: 133-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14561078&dopt=Abstract
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Arsenic induces tumor necrosis factor alpha release and tumor necrosis factor receptor 1 signaling in T helper cell apoptosis. Author(s): Yu HS, Liao WT, Chang KL, Yu CL, Chen GS. Source: The Journal of Investigative Dermatology. 2002 October; 119(4): 812-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12406325&dopt=Abstract
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Arsenic levels in cooked food and assessment of adult dietary intake of arsenic in the Region Lagunera, Mexico. Author(s): Del Razo LM, Garcia-Vargas GG, Garcia-Salcedo J, Sanmiguel MF, Rivera M, Hernandez MC, Cebrian ME. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 2002 October; 40(10): 1423-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12387304&dopt=Abstract
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Arsenic poisoning in a family. Author(s): Jha S, Dhanuka AK, Singh MN. Source: Neurology India. 2002 September; 50(3): 364-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391471&dopt=Abstract
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Arsenic pollution in groundwater: a self-organizing complex geochemical process in the deltaic sedimentary environment, Bangladesh. Author(s): Tareq SM, Safiullah S, Anawar HM, Rahman MM, Ishizuka T. Source: The Science of the Total Environment. 2003 September 1; 313(1-3): 213-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12922072&dopt=Abstract
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Arsenic remobilization in a shallow lake: the role of sediment resuspension. Author(s): Linge KL, Oldham CE. Source: J Environ Qual. 2002 May-June; 31(3): 822-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12026085&dopt=Abstract
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Arsenic toxicity and potential mechanisms of action. Author(s): Hughes MF. Source: Toxicology Letters. 2002 July 7; 133(1): 1-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076506&dopt=Abstract
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Arsenic trioxide and breast cancer: analysis of the apoptotic, differentiative and immunomodulatory effects. Author(s): Baj G, Arnulfo A, Deaglio S, Mallone R, Vigone A, De Cesaris MG, Surico N, Malavasi F, Ferrero E. Source: Breast Cancer Research and Treatment. 2002 May; 73(1): 61-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12083632&dopt=Abstract
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Arsenic trioxide in the mechanism of drug resistance reversal in MCF-7/ADM cell line of human breast cancer. Author(s): Wang X, Kong L, Zhao J, Yang P. Source: Zhonghua Zhong Liu Za Zhi. 2002 July; 24(4): 339-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12408759&dopt=Abstract
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Arsenic trioxide promotes histone H3 phosphoacetylation at the chromatin of CASPASE-10 in acute promyelocytic leukemia cells. Author(s): Li J, Chen P, Sinogeeva N, Gorospe M, Wersto RP, Chrest FJ, Barnes J, Liu Y. Source: The Journal of Biological Chemistry. 2002 December 20; 277(51): 49504-10. Epub 2002 October 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12388546&dopt=Abstract
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Arsenic trioxide: acute promyelocytic leukemia and beyond. Author(s): Bachleitner-Hofmann T, Kees M, Gisslinger H. Source: Leukemia & Lymphoma. 2002 August; 43(8): 1535-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400595&dopt=Abstract
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Assessment of cancer risk and environmental levels of arsenic in New Hampshire. Author(s): Karagas MR, Stukel TA, Tosteson TD. Source: International Journal of Hygiene and Environmental Health. 2002 March; 205(12): 85-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12018020&dopt=Abstract
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Assessment of environmental arsenic levels in Prievidza district. Author(s): Keegan T, Hong B, Thornton I, Farago M, Jakubis P, Jakubis M, Pesch B, Ranft U, Nieuwenhuijsen MJ; EXPASCAN Study Group. Source: Journal of Exposure Analysis and Environmental Epidemiology. 2002 May; 12(3): 179-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12032814&dopt=Abstract
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Assessment of human health risks for arsenic bioaccumulation in tilapia (Oreochromis mossambicus) and large-scale mullet (Liza macrolepis) from blackfoot disease area in Taiwan. Author(s): Liao CM, Ling MP. Source: Archives of Environmental Contamination and Toxicology. 2003 August; 45(2): 264-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14565585&dopt=Abstract
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Backing into cancer: effects of arsenic on cell differentiation. Author(s): Salnikow K, Cohen MD. Source: Toxicological Sciences : an Official Journal of the Society of Toxicology. 2002 February; 65(2): 161-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11812918&dopt=Abstract
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Bangladesh. Agricultural pumping linked to arsenic. Author(s): Stokstad E. Source: Science. 2002 November 22; 298(5598): 1535-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446879&dopt=Abstract
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Bangladeshis to sue over arsenic poisoning. Author(s): Clarke T. Source: Nature. 2001 October 11; 413(6856): 556. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11595905&dopt=Abstract
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Basal cell carcinoma in chronic arsenicism occurring in Queensland, Australia, after ingestion of an asthma medication. Author(s): Boonchai W, Green A, Ng J, Dicker A, Chenevix-Trench G. Source: Journal of the American Academy of Dermatology. 2000 October; 43(4): 664-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11004623&dopt=Abstract
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Batch-mixed iron treatment of high arsenic waters. Author(s): Ramaswami A, Tawachsupa S, Isleyen M. Source: Water Research. 2001 December; 35(18): 4474-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11763050&dopt=Abstract
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BCR-ABL mediates arsenic trioxide-induced apoptosis independently of its aberrant kinase activity. Author(s): Puccetti E, Guller S, Orleth A, Bruggenolte N, Hoelzer D, Ottmann OG, Ruthardt M. Source: Cancer Research. 2000 July 1; 60(13): 3409-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10910048&dopt=Abstract
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Bilateral oroantral fistulas following devitalization of teeth by arsenic trioxide: a case report. Author(s): Yalcin S, Aybar B, Haznedaroglu F, Yucel E. Source: Journal of Endodontics. 2003 March; 29(3): 205-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12669882&dopt=Abstract
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Biochemistry of arsenic detoxification. Author(s): Rosen BP. Source: Febs Letters. 2002 October 2; 529(1): 86-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12354618&dopt=Abstract
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Biological gradient between long-term arsenic exposure and carotid atherosclerosis. Author(s): Wang CH, Jeng JS, Yip PK, Chen CL, Hsu LI, Hsueh YM, Chiou HY, Wu MM, Chen CJ. Source: Circulation. 2002 April 16; 105(15): 1804-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11956123&dopt=Abstract
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Biological monitoring of occupational exposure to arsenic by determining urinary content of inorganic arsenic and its methylated metabolites. Author(s): Jakubowski M, Trzcinka-Ochocka M, Razniewska G, Matczak W. Source: International Archives of Occupational and Environmental Health. 1998 September; 71 Suppl: S29-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9827876&dopt=Abstract
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Biological monitoring of occupational exposure to inorganic arsenic. Author(s): Apostoli P, Bartoli D, Alessio L, Buchet JP. Source: Occupational and Environmental Medicine. 1999 December; 56(12): 825-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10658539&dopt=Abstract
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Blockage of multidrug resistance-associated proteins potentiates the inhibitory effects of arsenic trioxide on CYP1A1 induction by polycyclic aromatic hydrocarbons. Author(s): Vernhet L, Allain N, Le Vee M, Morel F, Guillouzo A, Fardel O. Source: The Journal of Pharmacology and Experimental Therapeutics. 2003 January; 304(1): 145-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490585&dopt=Abstract
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Broadsheet number 48: Mercury, cadmium and arsenic: toxicology and laboratory investigation. Author(s): Campbell BG. Source: Pathology. 1999 February; 31(1): 17-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10212916&dopt=Abstract
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Buerger disease or arsenic intoxication? Author(s): Noel B. Source: Archives of Internal Medicine. 2001 April 9; 161(7): 1016. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11295977&dopt=Abstract
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Cancer risk assessment for arsenic exposure through oyster consumption. Author(s): Guo HR. Source: Environmental Health Perspectives. 2002 February; 110(2): 123-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11836137&dopt=Abstract
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Carcinogenic risks of inorganic arsenic in perspective. Author(s): Byrd DM, Roegner ML, Griffiths JC, Lamm SH, Grumski KS, Wilson R, Lai S. Source: International Archives of Occupational and Environmental Health. 1996; 68(6): 484-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8891790&dopt=Abstract
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Caveats in hair analysis in chronic arsenic poisoning. Author(s): Hindmarsh JT. Source: Clinical Biochemistry. 2002 February; 35(1): 1-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11937073&dopt=Abstract
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Childhood cancer incidence and arsenic exposure in drinking water in Nevada. Author(s): Moore LE, Lu M, Smith AH. Source: Archives of Environmental Health. 2002 May-June; 57(3): 201-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12507173&dopt=Abstract
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Chromosomal aberrations and sister chromatid exchanges in individuals exposed to arsenic through drinking water in West Bengal, India. Author(s): Mahata J, Basu A, Ghoshal S, Sarkar JN, Roy AK, Poddar G, Nandy AK, Banerjee A, Ray K, Natarajan AT, Nilsson R, Giri AK. Source: Mutation Research. 2003 January 10; 534(1-2): 133-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12504762&dopt=Abstract
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Chronic arsenic poisoning mimicking Gottron's rash. Author(s): Wakhlu A, Aggarwal A, Misra R. Source: The Journal of Rheumatology. 2003 February; 30(2): 415-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563706&dopt=Abstract
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Chronic arsenic poisoning. Author(s): Hall AH. Source: Toxicology Letters. 2002 March 10; 128(1-3): 69-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11869818&dopt=Abstract
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Chronic arsenic-exposed human prostate epithelial cells exhibit stable arsenic tolerance: mechanistic implications of altered cellular glutathione and glutathione Stransferase. Author(s): Brambila EM, Achanzar WE, Qu W, Webber MM, Waalkes MP. Source: Toxicology and Applied Pharmacology. 2002 September 1; 183(2): 99-107. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12387749&dopt=Abstract
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Clinical activity of arsenic trioxide for the treatment of multiple myeloma. Author(s): Munshi NC, Tricot G, Desikan R, Badros A, Zangari M, Toor A, Morris C, Anaissie E, Barlogie B. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 September; 16(9): 1835-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12200700&dopt=Abstract
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Clinical activity of arsenic trioxide in Burkitt-like lymphoma. Author(s): Ravandi F, van Besien K. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 January; 17(1): 271-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529694&dopt=Abstract
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Clinical usefulness of arsenic trioxide in the treatment of acute promyelocytic leukemia. Author(s): Lo Coco F. Source: Haematologica. 2002 May; 87(5): 452-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12010655&dopt=Abstract
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Cocaine and arsenic-induced Raynaud's phenomenon. Author(s): Noel B. Source: Clinical Rheumatology. 2002 August; 21(4): 343-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12296288&dopt=Abstract
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Combined arsenic trioxide and all-trans retinoic acid treatment for acute promyelocytic leukaemia recurring from previous relapses successfully treated using arsenic trioxide. Author(s): Au WY, Chim CS, Lie AK, Liang R, Kwong YL. Source: British Journal of Haematology. 2002 April; 117(1): 130-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11918543&dopt=Abstract
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Combined treatment with arsenic trioxide and all-trans-retinoic acid in patients with relapsed acute promyelocytic leukemia. Author(s): Raffoux E, Rousselot P, Poupon J, Daniel MT, Cassinat B, Delarue R, Taksin AL, Rea D, Buzyn A, Tibi A, Lebbe G, Cimerman P, Chomienne C, Fermand JP, de The H, Degos L, Hermine O, Dombret H. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 15; 21(12): 2326-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12805334&dopt=Abstract
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Concentrations of arsenic, cadmium, mercury, and lead in common foods and estimated daily intake by children, adolescents, adults, and seniors of Catalonia, Spain. Author(s): Llobet JM, Falco G, Casas C, Teixido A, Domingo JL. Source: Journal of Agricultural and Food Chemistry. 2003 January 29; 51(3): 838-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12537467&dopt=Abstract
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Consumption of arsenic through cooked rice. Author(s): Misbahuddin M. Source: Lancet. 2003 February 1; 361(9355): 435-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573413&dopt=Abstract
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Contact hypersensitivity to arsenic in a crystal factory worker. Author(s): Barbaud A, Mougeolle JM, Schmutz JL. Source: Contact Dermatitis. 1995 October; 33(4): 272-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8654085&dopt=Abstract
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Cytotoxicity of arsenic trioxide to transitional carcinoma cells. Author(s): Pu YS, Hour TC, Chen J, Huang CY, Guan JY, Lu SH. Source: Urology. 2002 August; 60(2): 346-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12137851&dopt=Abstract
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Decreased DNA repair gene expression among individuals exposed to arsenic in United States drinking water. Author(s): Andrew AS, Karagas MR, Hamilton JW. Source: International Journal of Cancer. Journal International Du Cancer. 2003 April 10; 104(3): 263-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12569548&dopt=Abstract
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Detection of excess arsenic-related cancer risks. Author(s): Frost F, Craun G, Brown KG. Source: Environmental Health Perspectives. 2002 January; 110(1): A12-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11813697&dopt=Abstract
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Determinants of inorganic arsenic methylation capability among residents of the Lanyang Basin, Taiwan: arsenic and selenium exposure and alcohol consumption. Author(s): Hsueh YM, Ko YF, Huang YK, Chen HW, Chiou HY, Huang YL, Yang MH, Chen CJ. Source: Toxicology Letters. 2003 January 31; 137(1-2): 49-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505432&dopt=Abstract
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Determination of arsenic metabolic complex excreted in human urine after administration of sodium 2,3-dimercapto-1-propane sulfonate. Author(s): Gong Z, Jiang G, Cullen WR, Aposhian HV, Le XC. Source: Chemical Research in Toxicology. 2002 October; 15(10): 1318-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12387631&dopt=Abstract
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Determination of urinary beryllium, arsenic, and selenium in steel production workers. Author(s): Horng CJ, Horng PH, Lin SC, Tsai JL, Lin SR, Tzeng CC. Source: Biological Trace Element Research. 2002 September; 88(3): 235-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12350133&dopt=Abstract
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Development and application of a robust speciation method for determination of six arsenic compounds present in human urine. Author(s): Milstein LS, Essader A, Pellizzari ED, Fernando RA, Raymer JH, Levine KE, Akinbo O. Source: Environmental Health Perspectives. 2003 March; 111(3): 293-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12611657&dopt=Abstract
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Diabetes mellitus and arsenic exposure: a second look at case-control data from a Swedish copper smelter. Author(s): Rahman M, Axelson O. Source: Occupational and Environmental Medicine. 1995 November; 52(11): 773-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8535499&dopt=Abstract
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Diagnosis of arsenicosis. Author(s): Saha KC. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 255-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635831&dopt=Abstract
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Dietary reference intakes: vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Author(s): Trumbo P, Yates AA, Schlicker S, Poos M. Source: Journal of the American Dietetic Association. 2001 March; 101(3): 294-301. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11269606&dopt=Abstract
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Differential activation of AP-1 in human bladder epithelial cells by inorganic and methylated arsenicals. Author(s): Drobna Z, Jaspers I, Thomas DJ, Styblo M. Source: The Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology. 2003 January; 17(1): 67-9. Epub 2002 November 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475910&dopt=Abstract
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Differential effects of trivalent and pentavalent arsenicals on cell proliferation and cytokine secretion in normal human epidermal keratinocytes. Author(s): Vega L, Styblo M, Patterson R, Cullen W, Wang C, Germolec D. Source: Toxicology and Applied Pharmacology. 2001 May 1; 172(3): 225-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11312651&dopt=Abstract
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Dislodgeable copper, chromium and arsenic from CCA-treated wood surfaces. Author(s): Stilwell D, Toner M, Sawhney B. Source: The Science of the Total Environment. 2003 August 1; 312(1-3): 123-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873405&dopt=Abstract
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Distribution and accumulation of a mixture of arsenic, cadmium, chromium, nickel, and vanadium in mouse small intestine, kidneys, pancreas, and femur following oral administration in water or feed. Author(s): Radike M, Warshawsky D, Caruso J, Goth-Goldstein R, Reilman R, Collins T, Yaeger M, Wang J, Vela N, Olsen L, Schneider J. Source: Journal of Toxicology and Environmental Health. Part A. 2002 December 13; 65(23): 2029-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490046&dopt=Abstract
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DNA damage by cadmium and arsenic salts assessed by the single cell gel electrophoresis assay. Author(s): Mouron SA, Golijow CD, Dulout FN. Source: Mutation Research. 2001 November 15; 498(1-2): 47-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11673070&dopt=Abstract
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DNA damage in buccal epithelial cells from individuals chronically exposed to arsenic via drinking water in Inner Mongolia, China. Author(s): Feng Z, Xia Y, Tian D, Wu K, Schmitt M, Kwok RK, Mumford JL. Source: Anticancer Res. 2001 January-February; 21(1A): 51-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11299789&dopt=Abstract
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DNA damage induced by methylated trivalent arsenicals is mediated by reactive oxygen species. Author(s): Nesnow S, Roop BC, Lambert G, Kadiiska M, Mason RP, Cullen WR, Mass MJ. Source: Chemical Research in Toxicology. 2002 December; 15(12): 1627-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12482246&dopt=Abstract
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DNA repair gene XPD and susceptibility to arsenic-induced hyperkeratosis. Author(s): Ahsan H, Chen Y, Wang Q, Slavkovich V, Graziano JH, Santella RM. Source: Toxicology Letters. 2003 July 20; 143(2): 123-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749816&dopt=Abstract
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Dose-response relationship between peripheral vascular disease and ingested inorganic arsenic among residents in blackfoot disease endemic villages in Taiwan. Author(s): Tseng CH, Chong CK, Chen CJ, Tai TY. Source: Atherosclerosis. 1996 February; 120(1-2): 125-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8645353&dopt=Abstract
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Down-regulation of human papillomavirus E6/E7 oncogene by arsenic trioxide in cervical carcinoma cells. Author(s): Um SJ, Lee SY, Kim EJ, Myoung J, Namkoong SE, Park JS. Source: Cancer Letters. 2002 July 8; 181(1): 11-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12430174&dopt=Abstract
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Dual effects of arsenic trioxide (As2O3) on non-acute promyelocytic leukaemia myeloid cell lines: induction of apoptosis and inhibition of proliferation. Author(s): Rojewski MT, Baldus C, Knauf W, Thiel E, Schrezenmeier H. Source: British Journal of Haematology. 2002 March; 116(3): 555-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11849211&dopt=Abstract
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Effect of arsenic and cadmium on the persistence of mutagen-induced DNA lesions in human cells. Author(s): Hartmann A, Speit G. Source: Environmental and Molecular Mutagenesis. 1996; 27(2): 98-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8603672&dopt=Abstract
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Effect of arsenic and mercury speciation on inhibition of respiration rate in activated sludge systems. Author(s): Stasinakis AS, Thomaidis NS, Giannes AS, Lekkas TD. Source: Environ Sci Pollut Res Int. 2003; 10(3): 177-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846379&dopt=Abstract
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Effect of arsenic on transcription factor AP-1 and NF-kappaB DNA binding activity and related gene expression. Author(s): Hu Y, Jin X, Snow ET. Source: Toxicology Letters. 2002 July 7; 133(1): 33-45. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076508&dopt=Abstract
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Effect of arsenic trioxide on different cell lines derived from chronic myeloid leukemia. Author(s): Jing HM, Yukihiro S, Ke XY, Yoshiro K, Akiharu W. Source: Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2002 October; 10(5): 413-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12513739&dopt=Abstract
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Effect of arsenic trioxide on QT interval in patients with advanced malignancies. Author(s): Barbey JT, Pezzullo JC, Soignet SL. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 October 1; 21(19): 3609-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512391&dopt=Abstract
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Effect of arsenic, cadmium and lead on the induction of apoptosis of normal human mononuclear cells. Author(s): de la Fuente H, Portales-Perez D, Baranda L, Diaz-Barriga F, Saavedra-Alanis V, Layseca E, Gonzalez-Amaro R. Source: Clinical and Experimental Immunology. 2002 July; 129(1): 69-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12100024&dopt=Abstract
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Effects of arsenic on human keratinocytes: morphological, physiological, and precursor incorporation studies. Author(s): Bernstam L, Lan CH, Lee J, Nriagu JO. Source: Environmental Research. 2002 July; 89(3): 220-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12176006&dopt=Abstract
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Effects of arsenic on younger generations. Author(s): Watanabe C, Inaoka T, Matsui T, Ishigaki K, Murayama N, Ohtsuka R. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 129-39. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635823&dopt=Abstract
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Electrothermal atomization of arsenic, antimony and thallium using a graphite atomizer with refractory metal platforms. Author(s): Detcheva A, Havezov I, Gentscheva G, Ivanova E. Source: Ann Chim. 2002 May-June; 92(5-6): 595-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12125464&dopt=Abstract
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Elevated mortality from lung cancer associated with arsenic exposure for a limited duration. Author(s): Nakadaira H, Endoh K, Katagiri M, Yamamoto M. Source: Journal of Occupational and Environmental Medicine / American College of Occupational and Environmental Medicine. 2002 March; 44(3): 291-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11911031&dopt=Abstract
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Endonuclease III, formamidopyrimidine-DNA glycosylase, and proteinase K additively enhance arsenic-induced DNA strand breaks in human cells. Author(s): Wang TS, Chung CH, Wang AS, Bau DT, Samikkannu T, Jan KY, Cheng YM, Lee TC. Source: Chemical Research in Toxicology. 2002 October; 15(10): 1254-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12387622&dopt=Abstract
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Enhanced frequency of micronuclei in individuals exposed to arsenic through drinking water in West Bengal, India. Author(s): Basu A, Mahata J, Roy AK, Sarkar JN, Poddar G, Nandy AK, Sarkar PK, Dutta PK, Banerjee A, Das M, Ray K, Roychaudhury S, Natarajan AT, Nilsson R, Giri AK. Source: Mutation Research. 2002 April 26; 516(1-2): 29-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11943608&dopt=Abstract
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Enhancement of platelet aggregation and thrombus formation by arsenic in drinking water: a contributing factor to cardiovascular disease. Author(s): Lee MY, Bae ON, Chung SM, Kang KT, Lee JY, Chung JH. Source: Toxicology and Applied Pharmacology. 2002 March 1; 179(2): 83-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11884240&dopt=Abstract
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Enhancement of radiation response in human cervical cancer cells in vitro and in vivo by arsenic trioxide (As2O3). Author(s): Chun YJ, Park IC, Park MJ, Woo SH, Hong SI, Chung HY, Kim TH, Lee YS, Rhee CH, Lee SJ. Source: Febs Letters. 2002 May 22; 519(1-3): 195-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12023044&dopt=Abstract
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Environmental arsenic exposure from a coal-burning power plant as a potential risk factor for nonmelanoma skin carcinoma: results from a case-control study in the district of Prievidza, Slovakia. Author(s): Pesch B, Ranft U, Jakubis P, Nieuwenhuijsen MJ, Hergemoller A, Unfried K, Jakubis M, Miskovic P, Keegan T. Source: American Journal of Epidemiology. 2002 May 1; 155(9): 798-809. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11978583&dopt=Abstract
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Epidemiologic evidence of diabetogenic effect of arsenic. Author(s): Tseng CH, Tseng CP, Chiou HY, Hsueh YM, Chong CK, Chen CJ. Source: Toxicology Letters. 2002 July 7; 133(1): 69-76. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076511&dopt=Abstract
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Established practice in the treatment of patients with acute promyleocytic leukemia and the introduction of arsenic trioxide as a novel therapy. Author(s): Dombret H, Fenaux P, Soignet SL, Tallman MS. Source: Semin Hematol. 2002 April; 39(2 Suppl 1): 8-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12012316&dopt=Abstract
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Evidence for induction of oxidative stress caused by chronic exposure of Chinese residents to arsenic contained in drinking water. Author(s): Pi J, Yamauchi H, Kumagai Y, Sun G, Yoshida T, Aikawa H, Hopenhayn-Rich C, Shimojo N. Source: Environmental Health Perspectives. 2002 April; 110(4): 331-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11940449&dopt=Abstract
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Expanding the use of arsenic trioxide: leukemias and beyond. Author(s): Chen Z, Chen GQ, Shen ZX, Sun GL, Tong JH, Wang ZY, Chen SJ. Source: Semin Hematol. 2002 April; 39(2 Suppl 1): 22-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12012319&dopt=Abstract
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Factors affecting lead, cadmium, and arsenic levels in house dust in a smelter town in eastern Germany. Author(s): Meyer I, Heinrich J, Lippold U. Source: Environmental Research. 1999 July; 81(1): 32-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10361024&dopt=Abstract
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Family correlations of arsenic methylation patterns in children and parents exposed to high concentrations of arsenic in drinking water. Author(s): Chung JS, Kalman DA, Moore LE, Kosnett MJ, Arroyo AP, Beeris M, Mazumder DN, Hernandez AL, Smith AH. Source: Environmental Health Perspectives. 2002 July; 110(7): 729-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12117651&dopt=Abstract
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Fatal rhabdomyolysis in arsenic trioxide poisoning. Author(s): Fanton L, Duperret S, Guillaumee F, Miras A, Vallon JJ, Malicier D. Source: Human & Experimental Toxicology. 1999 October; 18(10): 640-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10557017&dopt=Abstract
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Feasibility and correlates of arsenic trioxide combined with ascorbic acid-mediated depletion of intracellular glutathione for the treatment of relapsed/refractory multiple myeloma. Author(s): Bahlis NJ, McCafferty-Grad J, Jordan-McMurry I, Neil J, Reis I, KharfanDabaja M, Eckman J, Goodman M, Fernandez HF, Boise LH, Lee KP. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2002 December; 8(12): 3658-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12473574&dopt=Abstract
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Field kits fail to provide accurate measure of arsenic in groundwater. Author(s): Erickson BE. Source: Environmental Science & Technology. 2003 January 1; 37(1): 35A-38A. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12542282&dopt=Abstract
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Fighting arsenic at the grassroots: experience of BRAC's community awareness initiative in Bangladesh. Author(s): Hadi A. Source: Health Policy and Planning. 2003 March; 18(1): 93-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582112&dopt=Abstract
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Fish arsenic may influence human blood arsenic, selenium, and T4:T3 ratio. Author(s): Meltzer HM, Maage A, Ydersbond TA, Haug E, Glattre E, Holm H. Source: Biological Trace Element Research. 2002 Winter; 90(1-3): 83-98. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666828&dopt=Abstract
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Follow up of water use in a tin mining area affected with arsenic poisoning. Author(s): Chongsuvivatwong V, Lim A, Dueravee M, Geater A, Ritsamitchai S, Oshikawa S. Source: Southeast Asian J Trop Med Public Health. 2000 December; 31(4): 769-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11414427&dopt=Abstract
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Food chain aspects of arsenic contamination in Bangladesh: effects on quality and productivity of rice. Author(s): Duxbury JM, Mayer AB, Lauren JG, Hassan N. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 61-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635819&dopt=Abstract
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Food surveillance in the Basque Country (Spain). II. Estimation of the dietary intake of organochlorine pesticides, heavy metals, arsenic, aflatoxin M1, iron and zinc through the Total Diet Study, 1990/91. Author(s): Urieta I, Jalon M, Eguilero I. Source: Food Additives and Contaminants. 1996 January; 13(1): 29-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8647305&dopt=Abstract
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Formamidopyrimidine-DNA glycosylase enhances arsenic-induced DNA strand breaks in PHA-stimulated and unstimulated human lymphocytes. Author(s): Li D, Morimoto K, Takeshita T, Lu Y. Source: Environmental Health Perspectives. 2001 May; 109(5): 523-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11401765&dopt=Abstract
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From durum wheat to pasta: effect of technological processing on the levels of arsenic, cadmium, lead and nickel--a pilot study. Author(s): Cubadda F, Raggi A, Zanasi F, Carcea M. Source: Food Additives and Contaminants. 2003 April; 20(4): 353-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775477&dopt=Abstract
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Fulminant malignant arrythmia and multiorgan failure in acute arsenic poisoning. Author(s): Civantos DP, Lopez Rodriguez A, Aguado-Borruey JM, Narvaez JA. Source: Chest. 1995 December; 108(6): 1774-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7497814&dopt=Abstract
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Functional repression of estrogen receptor a by arsenic trioxide in human breast cancer cells. Author(s): Chen GC, Guan LS, Hu WL, Wang ZY. Source: Anticancer Res. 2002 March-April; 22(2A): 633-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12014631&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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Genetic events associated with arsenic-induced malignant transformation: applications of cDNA microarray technology. Author(s): Chen H, Liu J, Merrick BA, Waalkes MP. Source: Molecular Carcinogenesis. 2001 February; 30(2): 79-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11241755&dopt=Abstract
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Genetic polymorphism in the biotransformation of inorganic arsenic and its role in toxicity. Author(s): Vahter M. Source: Toxicology Letters. 2000 March 15; 112-113: 209-17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10720733&dopt=Abstract
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Genetic toxicology of a paradoxical human carcinogen, arsenic: a review. Author(s): Basu A, Mahata J, Gupta S, Giri AK. Source: Mutation Research. 2001 May; 488(2): 171-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11344043&dopt=Abstract
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Genotoxicity of arsenical compounds. Author(s): Gebel TW. Source: International Journal of Hygiene and Environmental Health. 2001 March; 203(3): 249-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11279822&dopt=Abstract
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Geographical and temporal differences in the urinary excretion of inorganic arsenic: a Belgian population study. Author(s): Buchet JP, Staessen J, Roels H, Lauwerys R, Fagard R. Source: Occupational and Environmental Medicine. 1996 May; 53(5): 320-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8673179&dopt=Abstract
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Global alteration of gene expression in human keratinocytes by inorganic arsenic. Author(s): Rea MA, Gregg JP, Qin Q, Phillips MA, Rice RH. Source: Carcinogenesis. 2003 April; 24(4): 747-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727804&dopt=Abstract
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Glutathione depletion overcomes resistance to arsenic trioxide in arsenic-resistant cell lines. Author(s): Davison K, Cote S, Mader S, Miller WH. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 May; 17(5): 931-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750708&dopt=Abstract
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Groundwater arsenic contamination in Bangladesh and West Bengal, India. Author(s): Chowdhury UK, Biswas BK, Chowdhury TR, Samanta G, Mandal BK, Basu GC, Chanda CR, Lodh D, Saha KC, Mukherjee SK, Roy S, Kabir S, Quamruzzaman Q, Chakraborti D. Source: Environmental Health Perspectives. 2000 May; 108(5): 393-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10811564&dopt=Abstract
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Groundwater arsenic contamination, its health impact and mitigation program in Nepal. Author(s): Shrestha RR, Shrestha MP, Upadhyay NP, Pradhan R, Khadka R, Maskey A, Maharjan M, Tuladhar S, Dahal BM, Shrestha K. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 185-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635826&dopt=Abstract
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Hair and toenail arsenic concentrations of residents living in areas with high environmental arsenic concentrations. Author(s): Hinwood AL, Sim MR, Jolley D, de Klerk N, Bastone EB, Gerostamoulos J, Drummer OH. Source: Environmental Health Perspectives. 2003 February; 111(2): 187-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573904&dopt=Abstract
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Half of Bangladesh population at risk of arsenic poisoning. Author(s): Mudur G. Source: Bmj (Clinical Research Ed.). 2000 March 25; 320(7238): 822. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10731160&dopt=Abstract
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Health cancer risk assessment for arsenic exposure in potentially contaminated areas by fertilizer plants: a possible regulatory approach applied to a case study in Moscow region-Russia. Author(s): Zakharova T, Tatano F, Menshikov V. Source: Regulatory Toxicology and Pharmacology : Rtp. 2002 August; 36(1): 22-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12383715&dopt=Abstract
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Health effects and risk assessment of arsenic. Author(s): Abernathy CO, Thomas DJ, Calderon RL. Source: The Journal of Nutrition. 2003 May; 133(5 Suppl 1): 1536S-8S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12730460&dopt=Abstract
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Health risk assessment for inhalation exposure to arsenic. Author(s): Fabianova E, Hettychova L, Koppova K, Hruba F, Marko M, Maroni M, Grech G, Bencko V. Source: Cent Eur J Public Health. 2000 February; 8(1): 28-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10761624&dopt=Abstract
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Health status of workers of a thermal power station exposed for prolonged periods to arsenic and other elements from fuel. Author(s): Buchancova J, Klimentova G, Knizkova M, Mesko D, Galikova E, Kubik J, Fabianova E, Jakubis M. Source: Cent Eur J Public Health. 1998 February; 6(1): 29-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9524739&dopt=Abstract
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Hemostatic abnormalities associated with acute promyelocytic leukemia and corrective effects of all-trans-retinoic acid or arsenic trioxide treatment. Author(s): Zhao W, Wang X, Guo W, Qu B, Wang H, Shen Z, Chen Z, Wang Z. Source: Chinese Medical Journal. 2000 March; 113(3): 236-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11775254&dopt=Abstract
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Hepatic manifestations in chronic arsenic toxicity. Author(s): Santra A, Das Gupta J, De BK, Roy B, Guha Mazumder DN. Source: Indian J Gastroenterol. 1999 October-November; 18(4): 152-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10531716&dopt=Abstract
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Heterogeneity of the DNA damage provoked by antimony and arsenic. Author(s): Schaumloffel N, Gebel T. Source: Mutagenesis. 1998 May; 13(3): 281-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9643588&dopt=Abstract
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Histone deacetylase inhibitor but not arsenic trioxide differentiates acute promyelocytic leukaemia cells with t(11;17) in combination with all-trans retinoic acid. Author(s): Kitamura K, Hoshi S, Koike M, Kiyoi H, Saito H, Naoe T. Source: British Journal of Haematology. 2000 March; 108(4): 696-702. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10792271&dopt=Abstract
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Histopathology of skin lesions in chronic arsenic toxicity--grading of changes and study of proliferative markers. Author(s): Paul PC, Chattopadhyay A, Dutta SK, Mazumder DN, Santra A. Source: Indian J Pathol Microbiol. 2000 July; 43(3): 257-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11218669&dopt=Abstract
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How acute promyelocytic leukaemia revived arsenic. Author(s): Zhu J, Chen Z, Lallemand-Breitenbach V, de The H. Source: Nature Reviews. Cancer. 2002 September; 2(9): 705-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12209159&dopt=Abstract
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Human exposures to arsenic from consumption of well water in West Bengal, India. Author(s): Subramanian KS, Kosnett MJ. Source: International Journal of Occupational and Environmental Health : Official Journal of the International Commission on Occupational Health. 1998 OctoberDecember; 4(4): 217-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9876630&dopt=Abstract
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Human lymphocyte heme oxygenase 1 as a response biomarker to inorganic arsenic. Author(s): Menzel DB, Rasmussen RE, Lee E, Meacher DM, Said B, Hamadeh H, Vargas M, Greene H, Roth RN. Source: Biochemical and Biophysical Research Communications. 1998 September 29; 250(3): 653-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9784401&dopt=Abstract
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Human sperm immobilizing activity of aminophenyl arsenic acid and its Nsubstituted quinazoline, pyrimidine, and purine derivatives: protective effect of glutathione. Author(s): Uckun FM, Liu XP, D'Cruz OJ. Source: Reproductive Toxicology (Elmsford, N.Y.). 2002 January-February; 16(1): 57-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11934532&dopt=Abstract
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Human urine certified reference material for arsenic speciation. Author(s): Yoshinaga J, Chatterjee A, Shibata Y, Morita M, Edmonds JS. Source: Clinical Chemistry. 2000 November; 46(11): 1781-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11067813&dopt=Abstract
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Hydrogeological investigation of ground water arsenic contamination in south Calcutta. Author(s): Chatterjee A, Mukherjee A. Source: The Science of the Total Environment. 1999 January 26; 225(3): 249-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10063652&dopt=Abstract
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Hyperleukocytosis during induction therapy with arsenic trioxide for relapsed acute promyelocytic leukemia associated with central nervous system infarction. Author(s): Roberts TF, Sprague K, Schenkein D, Miller KB, Relias V. Source: Blood. 2000 December 1; 96(12): 4000-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11186272&dopt=Abstract
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Hypertension and arsenic exposure in Bangladesh. Author(s): Rahman M, Tondel M, Ahmad SA, Chowdhury IA, Faruquee MH, Axelson O. Source: Hypertension. 1999 January; 33(1): 74-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9931084&dopt=Abstract
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Identification of dimethylarsinous and monomethylarsonous acids in human urine of the arsenic-affected areas in West Bengal, India. Author(s): Mandal BK, Ogra Y, Suzuki KT. Source: Chemical Research in Toxicology. 2001 April; 14(4): 371-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11304125&dopt=Abstract
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Identification of galectin I and thioredoxin peroxidase II as two arsenic-binding proteins in Chinese hamster ovary cells. Author(s): Chang KN, Lee TC, Tam MF, Chen YC, Lee LW, Lee SY, Lin PJ, Huang RN. Source: The Biochemical Journal. 2003 April 15; 371(Pt 2): 495-503. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519079&dopt=Abstract
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Immunosuppression by arsenic: a comparison of cathepsin L inhibition and apoptosis. Author(s): Harrison MT, McCoy KL. Source: International Immunopharmacology. 2001 April; 1(4): 647-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11357877&dopt=Abstract
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In vitro studies of the combination of imatinib mesylate (Gleevec) and arsenic trioxide (Trisenox) in chronic myelogenous leukemia. Author(s): La Rosee P, Johnson K, O'Dwyer ME, Druker BJ. Source: Experimental Hematology. 2002 July; 30(7): 729-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12135670&dopt=Abstract
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Incidence of transitional cell carcinoma and arsenic in drinking water: a follow-up study of 8,102 residents in an arseniasis-endemic area in northeastern Taiwan. Author(s): Chiou HY, Chiou ST, Hsu YH, Chou YL, Tseng CH, Wei ML, Chen CJ. Source: American Journal of Epidemiology. 2001 March 1; 153(5): 411-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11226969&dopt=Abstract
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Increasing awareness of arsenic in Bangladesh: lessons from a public education programme. Author(s): Hanchett S, Nahar Q, Van Agthoven A, Geers C, Rezvi MD. Source: Health Policy and Planning. 2002 December; 17(4): 393-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12424211&dopt=Abstract
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Induction of autophagic cell death in malignant glioma cells by arsenic trioxide. Author(s): Kanzawa T, Kondo Y, Ito H, Kondo S, Germano I. Source: Cancer Research. 2003 May 1; 63(9): 2103-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727826&dopt=Abstract
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Induction of oxyradicals by arsenic: implication for mechanism of genotoxicity. Author(s): Liu SX, Athar M, Lippai I, Waldren C, Hei TK. Source: Proceedings of the National Academy of Sciences of the United States of America. 2001 February 13; 98(4): 1643-8. Epub 2001 Feb 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11172004&dopt=Abstract
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Inhibition of growth of human nasopharyngeal cancer xenografts in SCID mice by arsenic trioxide. Author(s): Li D, Du C, Lin Y, Wu M. Source: Tumori. 2002 November-December; 88(6): 522-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12597150&dopt=Abstract
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Inhibition of human plasmin activity using humic acids with arsenic. Author(s): Hseu YC, Chang WC, Yang HL. Source: The Science of the Total Environment. 2001 June 12; 273(1-3): 93-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11419606&dopt=Abstract
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Inhibition of NF-kappaB essentially contributes to arsenic-induced apoptosis. Author(s): Mathas S, Lietz A, Janz M, Hinz M, Jundt F, Scheidereit C, Bommert K, Dorken B. Source: Blood. 2003 August 1; 102(3): 1028-34. Epub 2003 April 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12676792&dopt=Abstract
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Inorganic and dimethylated arsenic species induce cellular p53. Author(s): Filippova M, Duerksen-Hughes PJ. Source: Chemical Research in Toxicology. 2003 March; 16(3): 423-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12641444&dopt=Abstract
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Intentional overdose of dimercaptosuccinic acid in the course of treatment for arsenic poisoning. Author(s): Buchwald AL. Source: Journal of Toxicology. Clinical Toxicology. 2001; 39(1): 113-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11327220&dopt=Abstract
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Interactions of arsenic with human metallothionein-2. Author(s): Toyama M, Yamashita M, Hirayama N, Murooka Y. Source: Journal of Biochemistry. 2002 August; 132(2): 217-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12153718&dopt=Abstract
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Intra-individual variation in the metabolism of inorganic arsenic. Author(s): Concha G, Vogler G, Nermell B, Vahter M. Source: International Archives of Occupational and Environmental Health. 2002 October; 75(8): 576-80. Epub 2002 July 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12373320&dopt=Abstract
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Introduction: the history of arsenic trioxide in cancer therapy. Author(s): Antman KH. Source: The Oncologist. 2001; 6 Suppl 2: 1-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11331433&dopt=Abstract
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Investigation of skin manifestations of arsenicism due to intake of arseniccontaminated groundwater in residents of Samta, Jessore, Bangladesh. Author(s): Kurokawa M, Ogata K, Idemori M, Tsumori S, Miyaguni H, Inoue S, Hotta N. Source: Archives of Dermatology. 2001 January; 137(1): 102-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11176681&dopt=Abstract
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Invited commentary: arsenic and cancer of the urinary tract. Author(s): Cantor KP. Source: American Journal of Epidemiology. 2001 March 1; 153(5): 422-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11226972&dopt=Abstract
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Is ingested inorganic arsenic a “threshold” carcinogen? Author(s): Abernathy CO, Chappell WR, Meek ME, Gibb H, Guo HR. Source: Fundamental and Applied Toxicology : Official Journal of the Society of Toxicology. 1996 February; 29(2): 168-75. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8742312&dopt=Abstract
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Keratinocyte differentiation marker suppression by arsenic: mediation by AP1 response elements and antagonism by tetradecanoylphorbol acetate. Author(s): Jessen BA, Qin Q, Phillips MA, Phillips DL, Rice RH. Source: Toxicology and Applied Pharmacology. 2001 August 1; 174(3): 302-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11485391&dopt=Abstract
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Laboratory and field assessment of arsenic testing field kits in Bangladesh and West Bengal, India. Author(s): Pande SP, Deshpande LS, Kaul SN. Source: Environmental Monitoring and Assessment. 2001 April; 68(1): 1-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11336408&dopt=Abstract
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Laboratory case identification of arsenic in Ronpibul village, Thailand (2000-2002). Author(s): Pavittranon S, Sripaoraya K, Ramchuen S, Kachamatch S, Puttaprug W, Pamornpusirikul N, Thaicharuen S, Rujiwanitchkul S, Walueng W. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 213-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635828&dopt=Abstract
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Lack of clinical symptoms in an acute arsenic poisoning: an unusual case. Author(s): Hernandez AF, Schiaffino S, Ballesteros JL, Gil F, Pla A, Villanueva E. Source: Vet Hum Toxicol. 1998 December; 40(6): 344-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9830695&dopt=Abstract
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Leukocytosis and the retinoic acid syndrome in patients with acute promyelocytic leukemia treated with arsenic trioxide. Author(s): Camacho LH, Soignet SL, Chanel S, Ho R, Heller G, Scheinberg DA, Ellison R, Warrell RP Jr. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2000 July; 18(13): 2620-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10893295&dopt=Abstract
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Localized alveolar bone necrosis following the use of an arsenical paste: a case report. Author(s): Ozmeric N. Source: International Endodontic Journal. 2002 March; 35(3): 295-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11993440&dopt=Abstract
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Longitudinal investigation of exposure to arsenic, cadmium, and lead in drinking water. Author(s): Ryan PB, Huet N, MacIntosh DL. Source: Environmental Health Perspectives. 2000 August; 108(8): 731-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10964793&dopt=Abstract
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Longitudinal investigation of exposure to arsenic, cadmium, chromium and lead via beverage consumption. Author(s): MacIntosh DL, Kabiru C, Scanlon KA, Ryan PB. Source: Journal of Exposure Analysis and Environmental Epidemiology. 2000 MarchApril; 10(2): 196-205. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10791600&dopt=Abstract
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Long-term arsenic exposure and incidence of non-insulin-dependent diabetes mellitus: a cohort study in arseniasis-hyperendemic villages in Taiwan. Author(s): Tseng CH, Tai TY, Chong CK, Tseng CP, Lai MS, Lin BJ, Chiou HY, Hsueh YM, Hsu KH, Chen CJ. Source: Environmental Health Perspectives. 2000 September; 108(9): 847-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11017889&dopt=Abstract
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Long-term arsenic exposure and ischemic heart disease in arseniasis-hyperendemic villages in Taiwan. Author(s): Tseng CH, Chong CK, Tseng CP, Hsueh YM, Chiou HY, Tseng CC, Chen CJ. Source: Toxicology Letters. 2003 January 31; 137(1-2): 15-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505429&dopt=Abstract
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Low serum carotene level and increased risk of ischemic heart disease related to longterm arsenic exposure. Author(s): Hsueh YM, Wu WL, Huang YL, Chiou HY, Tseng CH, Chen CJ. Source: Atherosclerosis. 1998 December; 141(2): 249-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9862173&dopt=Abstract
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Low-level arsenic excretion in breast milk of native Andean women exposed to high levels of arsenic in the drinking water. Author(s): Concha G, Vogler G, Nermell B, Vahter M. Source: International Archives of Occupational and Environmental Health. 1998 February; 71(1): 42-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9523248&dopt=Abstract
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Lung and kidney cancer mortality associated with arsenic in drinking water in Cordoba, Argentina. Author(s): Hopenhayn-Rich C, Biggs ML, Smith AH. Source: International Journal of Epidemiology. 1998 August; 27(4): 561-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9758107&dopt=Abstract
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Lung cancer and arsenic concentrations in drinking water in Chile. Author(s): Ferreccio C, Gonzalez C, Milosavjlevic V, Marshall G, Sancha AM, Smith AH. Source: Epidemiology (Cambridge, Mass.). 2000 November; 11(6): 673-9. Erratum In: Epidemiology 2001 March; 12(2): 283. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11055628&dopt=Abstract
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Lung cancer and arsenic exposure in drinking water: a case-control study in northern Chile. Author(s): Ferreccio C, Gonzalez Psych C, Milosavjlevic Stat V, Marshall Gredis G, Sancha AM. Source: Cadernos De Saude Publica / Ministerio Da Saude, Fundacao Oswaldo Cruz, Escola Nacional De Saude Publica. 1998; 14 Suppl 3: 193-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9819479&dopt=Abstract
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Lung cancer risks among lead smelter workers also exposed to arsenic. Author(s): Englyst V, Lundstrom NG, Gerhardsson L, Rylander L, Nordberg G. Source: The Science of the Total Environment. 2001 June 12; 273(1-3): 77-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11419604&dopt=Abstract
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Lymphocyte replicating ability in individuals exposed to arsenic via drinking water. Author(s): Gonsebatt ME, Vega L, Montero R, Garcia-Vargas G, Del Razo LM, Albores A, Cebrian ME, Ostrosky-Wegman P. Source: Mutation Research. 1994 October-December; 313(2-3): 293-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7523914&dopt=Abstract
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Magnitude of arsenic toxicity in tube-well drinking water in Bangladesh and its adverse effects on human health including cancer: evidence from a review of the literature. Author(s): Khan MM, Sakauchi F, Sonoda T, Washio M, Mori M. Source: Asian Pac J Cancer Prev. 2003 January-March; 4(1): 7-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12718695&dopt=Abstract
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Male reproductive effect of arsenic in mice. Author(s): Pant N, Kumar R, Murthy RC, Srivastava SP. Source: Biometals : an International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine. 2001 June; 14(2): 113-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11508843&dopt=Abstract
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Males in rural Bangladeshi communities are more susceptible to chronic arsenic poisoning than females: analyses based on urinary arsenic. Author(s): Watanabe C, Inaoka T, Kadono T, Nagano M, Nakamura S, Ushijima K, Murayama N, Miyazaki K, Ohtsuka R. Source: Environmental Health Perspectives. 2001 December; 109(12): 1265-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11748034&dopt=Abstract
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Markers of low level arsenic exposure for evaluating human cancer risks in a US population. Author(s): Karagas MR, Le CX, Morris S, Blum J, Lu X, Spate V, Carey M, Stannard V, Klaue B, Tosteson TD. Source: International Journal of Occupational Medicine and Environmental Health. 2001; 14(2): 171-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11548067&dopt=Abstract
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Market basket and duplicate portion estimation of dietary intakes of cadmium, mercury, arsenic, copper, manganese, and zinc by Japanese adults. Author(s): Tsuda T, Inoue T, Kojima M, Aoki S. Source: J Aoac Int. 1995 November-December; 78(6): 1363-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8664571&dopt=Abstract
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Mechanism of action of all-trans retinoic acid and arsenic trioxide in the treatment of acute promyelocytic leukemia. Author(s): Wang ZY. Source: Gan to Kagaku Ryoho. 2002 February; 29 Suppl 1: 214-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11890109&dopt=Abstract
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Mechanisms of action of arsenic trioxide. Author(s): Miller WH Jr, Schipper HM, Lee JS, Singer J, Waxman S. Source: Cancer Research. 2002 July 15; 62(14): 3893-903. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12124315&dopt=Abstract
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Mechanisms of arsenic biotransformation. Author(s): Vahter M. Source: Toxicology. 2002 December 27; 181-182: 211-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505313&dopt=Abstract
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Mees' lines in a patient following acute arsenic intoxication. Author(s): Seavolt MB, Sarro RA, Levin K, Camisa C. Source: International Journal of Dermatology. 2002 July; 41(7): 399-401. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12121552&dopt=Abstract
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Mercury and arsenic levels among Lebanese dentists: a call for action. Author(s): Harakeh S, Sabra N, Kassak K, Doughan B, Sukhn C. Source: Bulletin of Environmental Contamination and Toxicology. 2003 April; 70(4): 62935. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12677371&dopt=Abstract
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Mercury, arsenic, lead and cadmium in fish and shellfish from the Adriatic Sea. Author(s): Juresa D, Blanusa M. Source: Food Additives and Contaminants. 2003 March; 20(3): 241-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623648&dopt=Abstract
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Methylarsonic and dimethylarsinic acids toxicity and total arsenic accumulation in edible bush beans, Phaseolus vulgaris. Author(s): Lario Y, Burlo F, Aracil P, Martinez-Romero D, Castillo S, Valero D, Carbonell-Barrachina AA. Source: Food Additives and Contaminants. 2002 May; 19(5): 417-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12028641&dopt=Abstract
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Methylated metabolites of arsenic trioxide are more potent than arsenic trioxide as apoptotic but not differentiation inducers in leukemia and lymphoma cells. Author(s): Chen GQ, Zhou L, Styblo M, Walton F, Jing Y, Weinberg R, Chen Z, Waxman S. Source: Cancer Research. 2003 April 15; 63(8): 1853-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12702573&dopt=Abstract
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Millions more at risk of arsenic poisoning than previously thought. Author(s): Kumar S. Source: Bmj (Clinical Research Ed.). 2003 March 1; 326(7387): 466. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12609925&dopt=Abstract
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Molecular pathology of skin carcinogenesis due to arsenicalism from coal-burning. Author(s): Hu CJ, Zhang AH, Huang HH. Source: Archives of Environmental Health. 2003 February; 58(2): 92-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12899209&dopt=Abstract
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Molecular remission and reconstitution of a full chimera with arsenic trioxide in a patient with acute promyelocytic leukemia relapsed after allogeneic bone marrow transplantation. Author(s): Tedeschi A, Cairoli R, Marenco P, Nosari A, Tresoldi E, Di Bona E, Montillo M, Morra E. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 December; 16(12): 2455-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454753&dopt=Abstract
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Molecular targets of arsenic trioxide in malignant cells. Author(s): Miller WH Jr. Source: The Oncologist. 2002; 7 Suppl 1: 14-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11961205&dopt=Abstract
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Monitoring of arsenic exposure with speciated urinary inorganic arsenic metabolites for ion implanter maintenance engineers. Author(s): Hwang YH, Lee ZY, Wang JD, Hsueh YM, Lu IC, Yao WL. Source: Environmental Research. 2002 November; 90(3): 207-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12477466&dopt=Abstract
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Morphological and functional changes of mitochondria in apoptotic esophageal carcinoma cells induced by arsenic trioxide. Author(s): Shen ZY, Shen J, Li QS, Chen CY, Chen JY, Yi Z. Source: World Journal of Gastroenterology : Wjg. 2002 February; 8(1): 31-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11833066&dopt=Abstract
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National Human Exposure Assessment Survey (NHEXAS): distributions and associations of lead, arsenic and volatile organic compounds in EPA region 5. Author(s): Clayton CA, Pellizzari ED, Whitmore RW, Perritt RL, Quackenboss JJ. Source: Journal of Exposure Analysis and Environmental Epidemiology. 1999 September-October; 9(5): 381-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10554141&dopt=Abstract
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National Human Exposure Assessment Survey: analysis of exposure pathways and routes for arsenic and lead in EPA Region 5. Author(s): Clayton CA, Pellizzari ED, Quackenboss JJ. Source: Journal of Exposure Analysis and Environmental Epidemiology. 2002 JanuaryFebruary; 12(1): 29-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11859431&dopt=Abstract
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Natural contamination with arsenic and other trace elements in ground waters of Argentine Pampean Plain. Author(s): Farias SS, Casa VA, Vazquez C, Ferpozzi L, Pucci GN, Cohen IM. Source: The Science of the Total Environment. 2003 June 20; 309(1-3): 187-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12798103&dopt=Abstract
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Neurological effects of environmental exposure to arsenic in dust and soil among humans. Author(s): Gerr F, Letz R, Ryan PB, Green RC. Source: Neurotoxicology. 2000 August; 21(4): 475-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11022857&dopt=Abstract
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Neuropathy in arsenic toxicity from groundwater arsenic contamination in West Bengal, India. Author(s): Mukherjee SC, Rahman MM, Chowdhury UK, Sengupta MK, Lodh D, Chanda CR, Saha KC, Chakraborti D. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 165-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635825&dopt=Abstract
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Never on a Saturday (or a Sunday): the case against using weekend urine specimens to assess arsenic exposure. Author(s): Knobeloch L, Korthof S, Anderson H. Source: Wmj. 1998 October; 97(9): 46-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9810258&dopt=Abstract
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New perspectives in arsenic-induced cell signal transduction. Author(s): Qian Y, Castranova V, Shi X. Source: Journal of Inorganic Biochemistry. 2003 August 1; 96(2-3): 271-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888263&dopt=Abstract
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New retinoids and arsenic compounds for the treatment of refractory acute promyelocytic leukemia: clinical and basic studies for the next generation. Author(s): Kitamura K, Kiyoi H, Yoshida H, Tobita T, Takeshita A, Ohno R, Naoe T. Source: Cancer Chemotherapy and Pharmacology. 1997; 40 Suppl: S36-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9272132&dopt=Abstract
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Non-cancer effects of chronic arsenicosis in Bangladesh: preliminary results. Author(s): Milton AH, Hasan Z, Rahman A, Rahman M. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 301-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635834&dopt=Abstract
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Nonlinearity in the lung cancer dose-response for airborne arsenic: apparent confounding by year of hire in evaluating lung cancer risks from arsenic exposure in Tacoma smelter workers. Author(s): Viren J, Silvers A. Source: Regulatory Toxicology and Pharmacology : Rtp. 1999 October; 30(2 Pt 1): 117-29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10536107&dopt=Abstract
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Normal values for arsenic and selenium concentrations in human lung tissue. Author(s): Kraus T, Quidenus G, Schaller KH. Source: Archives of Environmental Contamination and Toxicology. 2000 April; 38(3): 384-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10667938&dopt=Abstract
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Nuclear matrix associated protein PML: an arsenic trioxide apoptosis therapeutic target protein in HepG2 cells. Author(s): Yu D, Wang Z, Zhu L, Chew EC. Source: Chinese Medical Journal. 2003 January; 116(1): 93-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12667397&dopt=Abstract
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Numerous erythematous truncal plaques. Multiple basal cell carcinomas associated with arsenic ingestion. Author(s): Mowad CM, Jaworsky C, Werth VP. Source: Archives of Dermatology. 1996 September; 132(9): 1105-6, 1108-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8795554&dopt=Abstract
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Occupational arsenic exposure and glycosylated haemoglobin. Author(s): Jensen GE, Hansen ML. Source: The Analyst. 1998 January; 123(1): 77-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9581024&dopt=Abstract
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Occupational contact dermatitis from arsenic in a tin-smelting factory. Author(s): Mohamed KB. Source: Contact Dermatitis. 1998 April; 38(4): 224-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9565305&dopt=Abstract
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Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Author(s): Aposhian HV, Gurzau ES, Le XC, Gurzau A, Healy SM, Lu X, Ma M, Yip L, Zakharyan RA, Maiorino RM, Dart RC, Tircus MG, Gonzalez-Ramirez D, Morgan DL, Avram D, Aposhian MM. Source: Chemical Research in Toxicology. 2000 August; 13(8): 693-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10956055&dopt=Abstract
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On-column formation of arsenic-glutathione species detected by size-exclusion chromatography in conjunction with arsenic-specific detectors. Author(s): Gailer J, Lindner W. Source: J Chromatogr B Biomed Sci Appl. 1998 September 25; 716(1-2): 83-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9824221&dopt=Abstract
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On-line reversed-phase liquid chromatography hydride generation emission spectrometry: speciation of arsenic in urine of patients intravenously treated with As2O3. Author(s): Do B, Alet P, Pradeau D, Poupon J, Guilley-Gaillot M, Guyon F. Source: J Chromatogr B Biomed Sci Appl. 2000 April 14; 740(2): 179-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10821403&dopt=Abstract
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Opportunities for Trisenox (arsenic trioxide) in the treatment of myelodysplastic syndromes. Author(s): List A, Beran M, DiPersio J, Slack J, Vey N, Rosenfeld CS, Greenberg P. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 August; 17(8): 1499-507. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886236&dopt=Abstract
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Opposite biological effects of arsenic trioxide and arsacetin involve a different regulation of signaling in human gastric cancer MGC-803 cells. Author(s): Zhang TC, Cao EH, Qin JF. Source: Pharmacology. 2002; 64(3): 160-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11834893&dopt=Abstract
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Oral arsenic trioxide in the treatment of relapsed acute promyelocytic leukemia. Author(s): Au WY, Kumana CR, Kou M, Mak R, Chan GC, Lam CW, Kwong YL. Source: Blood. 2003 July 1; 102(1): 407-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814916&dopt=Abstract
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Organic arsenic intoxication from bird's nest soup. Author(s): Luong KV, Nguyen LT. Source: The American Journal of the Medical Sciences. 1999 April; 317(4): 269-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10210366&dopt=Abstract
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Overexpression of Bcl-2 partly inhibits apoptosis of human cervical cancer SiHa cells induced by arsenic trioxide. Author(s): Deng Y, Lin C, Zheng J, Fu M, Liang X, Chen J, Xiao P, Wu M. Source: Chinese Medical Journal. 2000 January; 113(1): 84-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11775218&dopt=Abstract
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Oxidative stress as a possible mode of action for arsenic carcinogenesis. Author(s): Kitchin KT, Ahmad S. Source: Toxicology Letters. 2003 January 31; 137(1-2): 3-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12505428&dopt=Abstract
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Paget's disease of bone in Lancashire and arsenic pesticide in cotton mill wastewater: a speculative hypothesis. Author(s): Lever JH. Source: Bone. 2002 September; 31(3): 434-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12231419&dopt=Abstract
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Pathology related to chronic arsenic exposure. Author(s): Centeno JA, Mullick FG, Martinez L, Page NP, Gibb H, Longfellow D, Thompson C, Ladich ER. Source: Environmental Health Perspectives. 2002 October; 110 Suppl 5: 883-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12426152&dopt=Abstract
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Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission. Author(s): Zhu J, Lallemand-Breitenbach V, de The H. Source: Oncogene. 2001 October 29; 20(49): 7257-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11704854&dopt=Abstract
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Patterns of gene expressions induced by arsenic trioxide in cultured human fibroblasts. Author(s): Burnichon V, Jean S, Bellon L, Maraninchi M, Bideau C, Orsiere T, Margotat A, Gerolami V, Botta A, Berge-Lefranc JL. Source: Toxicology Letters. 2003 July 20; 143(2): 155-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749819&dopt=Abstract
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Peripheral vascular diseases resulting from chronic arsenical poisoning. Author(s): Yu HS, Lee CH, Chen GS. Source: The Journal of Dermatology. 2002 March; 29(3): 123-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11990246&dopt=Abstract
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P-glycoprotein (P-gp) and multidrug resistance-associated protein 1 (MRP1) are induced by arsenic trioxide (As(2)O(3)), but are not the main mechanism of As(2)O(3)resistance in acute promyelocytic leukemia cells. Author(s): Takeshita A, Shinjo K, Naito K, Matsui H, Shigeno K, Nakamura S, Horii T, Maekawa M, Kitamura K, Naoe T, Ohnishi K, Ohno R. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 March; 17(3): 648-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646961&dopt=Abstract
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Pharmacokinetics of intravenous arsenic trioxide in the treatment of acute promyelocytic leukemia. Author(s): Ni J, Chen G, Shen Z, Li X, Liu H, Huang Y, Fang Z, Chen S, Wang Z, Chen Z. Source: Chinese Medical Journal. 1998 December; 111(12): 1107-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11263375&dopt=Abstract
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Pharmacokinetics, metabolism, and carcinogenicity of arsenic. Author(s): Pott WA, Benjamin SA, Yang RS. Source: Rev Environ Contam Toxicol. 2001; 169: 165-214. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11330077&dopt=Abstract
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Phase II trial of arsenic trioxide in patients with metastatic renal cell carcinoma. Author(s): Vuky J, Yu R, Schwartz L, Motzer RJ. Source: Investigational New Drugs. 2002 August; 20(3): 327-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12201495&dopt=Abstract
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Physical injury risks associated with drinking water arsenic treatment. Author(s): Frost FJ, Chwirka J, Craun GF, Thomson B, Stomps J. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 2002 April; 22(2): 235-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12022673&dopt=Abstract
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Pink-eyed dilution protein modulates arsenic sensitivity and intracellular glutathione metabolism. Author(s): Staleva L, Manga P, Orlow SJ. Source: Molecular Biology of the Cell. 2002 December; 13(12): 4206-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475946&dopt=Abstract
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Plasmid DNA damage caused by methylated arsenicals, ascorbic acid and human liver ferritin. Author(s): Ahmad S, Kitchin KT, Cullen WR. Source: Toxicology Letters. 2002 July 7; 133(1): 47-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076509&dopt=Abstract
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Population-based biomonitoring in the Czech Republic: urinary arsenic. Author(s): Spevacova V, Cejchanova M, Cerna M, Spevacek V, Smid J, Benes B. Source: Journal of Environmental Monitoring : Jem. 2002 October; 4(5): 796-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400934&dopt=Abstract
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Porphyrins as early biomarkers for arsenic exposure in animals and humans. Author(s): Wang JP, Qi L, Zheng B, Liu F, Moore MR, Ng JC. Source: Cell Mol Biol (Noisy-Le-Grand). 2002 December; 48(8): 835-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699241&dopt=Abstract
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Potential exposure to arsenic and other highly toxic chemicals when handling museum artifacts. Author(s): Smith B, Coulehan B. Source: Applied Occupational and Environmental Hygiene. 2002 November; 17(11): 7413. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419100&dopt=Abstract
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Potential role of caspase-3 and -9 in arsenic trioxide-mediated apoptosis in PCI-1 head and neck cancer cells. Author(s): Seol JG, Park WH, Kim ES, Jung CW, Hyun JM, Lee YY, Kim BK. Source: International Journal of Oncology. 2001 February; 18(2): 249-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11172589&dopt=Abstract
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Prolongation of the QT interval and ventricular tachycardia in patients treated with arsenic trioxide for acute promyelocytic leukemia. Author(s): Barbey JT, Soignet S. Source: Annals of Internal Medicine. 2001 November 6; 135(9): 842-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11694116&dopt=Abstract
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Prolonged molecular remission after arsenic trioxide and all-trans retinoic acid for acute promyelocytic leukemia relapsed after allogeneic stem cell transplantation. Author(s): Grigg A, Kimber R, Szer J. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1916-7; Author Reply 1918. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970801&dopt=Abstract
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Promotion of well-switching to mitigate the current arsenic crisis in Bangladesh. Author(s): Van Geen A, Ahsan H, Horneman AH, Dhar RK, Zheng Y, Hussain I, Ahmed KM, Gelman A, Stute M, Simpson HJ, Wallace S, Small C, Parvez F, Slavkovich V, Loiacono NJ, Becker M, Cheng Z, Momotaj H, Shahnewaz M, Seddique AA, Graziano JH. Source: Bulletin of the World Health Organization. 2002; 80(9): 732-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12378292&dopt=Abstract
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Public health. Arsenic epidemiology and drinking water standards. Author(s): Smith AH, Lopipero PA, Bates MN, Steinmaus CM. Source: Science. 2002 June 21; 296(5576): 2145-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12077388&dopt=Abstract
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Radiation recall phenomenon associated with arsenic trioxide. Author(s): Keung YK, Lyerly ES, Powell BL. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1417-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835734&dopt=Abstract
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Radon and its daughter products behaviour in the air of an underground tourist route in the former arsenic and gold mine in Zloty Stok (Sudety Mountains, SW Poland). Author(s): Przylibski TA. Source: Journal of Environmental Radioactivity. 2001; 57(2): 87-103. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11545384&dopt=Abstract
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Re: “Does arsenic exposure increase the risk for circulatory disease?”. Author(s): Lubin JH, Fraumeni JF Jr. Source: American Journal of Epidemiology. 2000 August 1; 152(3): 290-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10933278&dopt=Abstract
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Re: risk assessment of internal cancers from arsenic in drinking water. Author(s): Stohrer G. Source: Environmental Health Perspectives. 2001 December; 109(12): A571. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11776955&dopt=Abstract
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Reactive oxygen species are involved in arsenic trioxide inhibition of pyruvate dehydrogenase activity. Author(s): Samikkannu T, Chen CH, Yih LH, Wang AS, Lin SY, Chen TC, Jan KY. Source: Chemical Research in Toxicology. 2003 March; 16(3): 409-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12641442&dopt=Abstract
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Real-time quantification of the multidrug resistance-1 gene expression in relapsed acute promyelocytic leukemia treated with arsenic trioxide. Author(s): Au WY, Chim CS, Wai Lie AK, Pang A, Kwong YL. Source: Haematologica. 2002 October; 87(10): 1109-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368167&dopt=Abstract
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Recent advances in arsenic carcinogenesis: modes of action, animal model systems, and methylated arsenic metabolites. Author(s): Kitchin KT. Source: Toxicology and Applied Pharmacology. 2001 May 1; 172(3): 249-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11312654&dopt=Abstract
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Recommendations for water supply in arsenic mitigation: a case study from Bangladesh. Author(s): Hoque BA, Mahmood AA, Quadiruzzaman M, Khan F, Ahmed SA, Shafique SA, Rahman M, Morshed G, Chowdhury T, Rahman MM, Khan FH, Shahjahan M, Begum M, Hoque MM. Source: Public Health. 2000 November; 114(6): 488-94. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11114764&dopt=Abstract
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Recovery from severe arsenic-induced peripheral neuropathy with 2,3-dimercapto-1propanesulphonic acid. Author(s): Wax PM, Thornton CA. Source: Journal of Toxicology. Clinical Toxicology. 2000; 38(7): 777-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11192465&dopt=Abstract
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Relation of a seafood diet to mercury, selenium, arsenic, and polychlorinated biphenyl and other organochlorine concentrations in human milk. Author(s): Grandjean P, Weihe P, Needham LL, Burse VW, Patterson DG Jr, Sampson EJ, Jorgensen PJ, Vahter M. Source: Environmental Research. 1995 October; 71(1): 29-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8757236&dopt=Abstract
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Repetitive endoscopy and continuous alkaline gastric irrigation in a case of arsenic poisoning. Author(s): Michaux I, Haufroid V, Dive A, Buchet JP, Bulpa P, Mahieu P, Installe E. Source: Journal of Toxicology. Clinical Toxicology. 2000; 38(5): 471-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10981956&dopt=Abstract
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Resistance of human multidrug resistance-associated protein 1-overexpressing lung tumor cells to the anticancer drug arsenic trioxide. Author(s): Vernhet L, Allain N, Payen L, Anger JP, Guillouzo A, Fardel O. Source: Biochemical Pharmacology. 2001 June 1; 61(11): 1387-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11331074&dopt=Abstract
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Respiratory effects and arsenic contaminated well water in Bangladesh. Author(s): Milton AH, Rahman M. Source: International Journal of Environmental Health Research. 2002 June; 12(2): 175-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400554&dopt=Abstract
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Retinoic acid syndrome induced by arsenic trioxide in treating recurrent all-trans retinoic acid resistant acute promyelocytic leukemia. Author(s): Che-Pin Lin, Huang MJ, Chang IY, Lin WY, Sheu YT. Source: Leukemia & Lymphoma. 2000 June; 38(1-2): 195-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10811463&dopt=Abstract
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Risk assessment and pathway study of arsenic in industrially contaminated sites of Hyderabad: a case study. Author(s): Chandra Sekhar K, Chary NS, Kamala CT, Venkateswara Rao J, Balaram V, Anjaneyulu Y. Source: Environment International. 2003 August; 29(5): 601-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742403&dopt=Abstract
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Risk of arsenic transfer to a semi-confined aquifer and the effect of water level fluctuation in North Mortagne, France at a former industrial site. Author(s): Charlet L, Ansari AA, Lespagnol G, Musso M. Source: The Science of the Total Environment. 2001 September 28; 277(1-3): 133-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11589393&dopt=Abstract
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Risk of internal cancers from arsenic in drinking water. Author(s): Morales KH, Ryan L, Kuo TL, Wu MM, Chen CJ. Source: Environmental Health Perspectives. 2000 July; 108(7): 655-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10903620&dopt=Abstract
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Risk/benefit profile of arsenic trioxide. Author(s): Rust DM, Soignet SL. Source: The Oncologist. 2001; 6 Suppl 2: 29-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11331438&dopt=Abstract
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Role of metabolism in arsenic toxicity. Author(s): Vahter M, Concha G. Source: Pharmacology & Toxicology. 2001 July; 89(1): 1-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11484904&dopt=Abstract
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Safety evaluation of organoarsenical species in edible Porphyra from the China Sea. Author(s): Wei C, Li W, Zhang C, Van Hulle M, Cornelis R, Zhang X. Source: Journal of Agricultural and Food Chemistry. 2003 August 13; 51(17): 5176-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12903988&dopt=Abstract
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Sampling private wells at past homes to estimate arsenic exposure: a methodologic study in New England. Author(s): Colt JS, Baris D, Clark SF, Ayotte JD, Ward M, Nuckols JR, Cantor KP, Silverman DT, Karagas M. Source: Journal of Exposure Analysis and Environmental Epidemiology. 2002 September; 12(5): 329-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12198581&dopt=Abstract
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Searching for an optimum solution to the Bangladesh arsenic crisis. Author(s): Caldwell BK, Caldwell JC, Mitra SN, Smith W. Source: Social Science & Medicine (1982). 2003 May; 56(10): 2089-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12697199&dopt=Abstract
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Silicon, aluminium, arsenic and lithium: essentiality and human health implications. Author(s): Perez-Granados AM, Vaquero MP. Source: J Nutr Health Aging. 2002; 6(2): 154-62. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12166372&dopt=Abstract
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Skin cancer induced by arsenic in the water. Author(s): Cabrera HN, Gomez ML. Source: Journal of Cutaneous Medicine and Surgery. 2003 March-April; 7(2): 106-11. Epub 2002 November 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12447618&dopt=Abstract
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Skin manifestations of arsenicosis in two villages in Bangladesh. Author(s): Kadono T, Inaoka T, Murayama N, Ushijima K, Nagano M, Nakamura S, Watanabe C, Tamaki K, Ohtsuka R. Source: International Journal of Dermatology. 2002 December; 41(12): 841-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492966&dopt=Abstract
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Some aspects of arsenic toxicity and carcinogenicity in living organism with special regard to its influence on cardiovascular system, blood and bone marrow. Author(s): Szymanska-Chabowska A, Antonowicz-Juchniewicz J, Andrzejak R. Source: International Journal of Occupational Medicine and Environmental Health. 2002; 15(2): 101-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12216766&dopt=Abstract
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Speciation of arsenic in human nail and hair from arsenic-affected area by HPLCinductively coupled argon plasma mass spectrometry. Author(s): Mandal BK, Ogra Y, Suzuki KT. Source: Toxicology and Applied Pharmacology. 2003 June 1; 189(2): 73-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781625&dopt=Abstract
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Speciation of arsenic metabolite intermediates in human urine by ion-exchange chromatography and flow injection hydride generation atomic absorption spectrometry. Author(s): Alauddin M, Alauddin ST, Bhattacharjee M, Sultana S, Chowdhury D, Bibi H, Rabbani GH. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 115-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635822&dopt=Abstract
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Stability of arsenic species and insoluble arsenic in human urine. Author(s): Chen YC, Amarasiriwardena CJ, Hsueh YM, Christiani DC. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2002 November; 11(11): 1427-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12433722&dopt=Abstract
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Subacute arsenical neuropathy leading to Gullian-Barre-like syndrome and respiratory failure. Author(s): Singh S, Reddy SR, Sud A, Wanchu A, Bambery P, Gill KD. Source: J Assoc Physicians India. 2002 June; 50: 853-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12240865&dopt=Abstract
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Survey of arsenic and other heavy metals in food composites and drinking water and estimation of dietary intake by the villagers from an arsenic-affected area of West Bengal, India. Author(s): Roychowdhury T, Tokunaga H, Ando M. Source: The Science of the Total Environment. 2003 June 1; 308(1-3): 15-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738198&dopt=Abstract
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Survey of arsenic in food composites from an arsenic-affected area of West Bengal, India. Author(s): Roychowdhury T, Uchino T, Tokunaga H, Ando M. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 2002 November; 40(11): 1611-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12176088&dopt=Abstract
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Synergistic effect of cell differential agent-II and arsenic trioxide on induction of cell cycle arrest and apoptosis in hepatoma cells. Author(s): Liu JW, Tang Y, Shen Y, Zhong XY. Source: World Journal of Gastroenterology : Wjg. 2003 January; 9(1): 65-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508353&dopt=Abstract
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Systemic availability of arsenic from oral arsenic-trioxide used to treat patients with hematological malignancies. Author(s): Kumana CR, Au WY, Lee NS, Kou M, Mak RW, Lam CW, Kwong YL. Source: European Journal of Clinical Pharmacology. 2002 November; 58(8): 521-6. Epub 2002 October 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12451429&dopt=Abstract
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The absorption and excretion of fluoride and arsenic in humans. Author(s): Zheng Y, Wu J, Ng JC, Wang G, Lian W. Source: Toxicology Letters. 2002 July 7; 133(1): 77-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076512&dopt=Abstract
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The concentrations of arsenic and other toxic elements in Bangladesh's drinking water. Author(s): Frisbie SH, Ortega R, Maynard DM, Sarkar B. Source: Environmental Health Perspectives. 2002 November; 110(11): 1147-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12417487&dopt=Abstract
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The ecology of arsenic. Author(s): Oremland RS, Stolz JF. Source: Science. 2003 May 9; 300(5621): 939-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738852&dopt=Abstract
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The effects of arsenic exposure on the nervous system. Author(s): Rodriguez VM, Jimenez-Capdeville ME, Giordano M. Source: Toxicology Letters. 2003 November 1; 145(1): 1-18. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12962969&dopt=Abstract
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The effects of chronic arsenic exposure from drinking water on the neurobehavioral development in adolescence. Author(s): Tsai SY, Chou HY, The HW, Chen CM, Chen CJ. Source: Neurotoxicology. 2003 August; 24(4-5): 747-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12900089&dopt=Abstract
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The molecular mechanism of arsenic trioxide-induced apoptosis and oncosis in leukemia/lymphoma cell lines. Author(s): Zhu J, Okumura H, Ohtake S, Nakamura S, Nakao S. Source: Acta Haematologica. 2003; 110(1): 1-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975549&dopt=Abstract
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The MRP1-mediated effluxes of arsenic and antimony do not require arsenicglutathione and antimony-glutathione complex formation. Author(s): Salerno M, Petroutsa M, Garnier-Suillerot A. Source: Journal of Bioenergetics and Biomembranes. 2002 April; 34(2): 135-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12018890&dopt=Abstract
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The prevalence of subjective symptoms after exposure to arsenic in drinking water in Inner Mongolia, China. Author(s): Guo X, Fujino Y, Chai J, Wu K, Xia Y, Li Y, Lv J, Sun Z, Yoshimura T. Source: J Epidemiol. 2003 July; 13(4): 211-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934964&dopt=Abstract
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Toxicology. Arsenic victims to take British science body to court. Author(s): Bachtold D. Source: Science. 2003 May 16; 300(5622): 1066. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750486&dopt=Abstract
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Treatment of acute promyelocytic leukemia and other hematologic malignancies with arsenic trioxide: review of clinical and basic studies. Author(s): Liu P, Han ZC. Source: International Journal of Hematology. 2003 July; 78(1): 32-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894848&dopt=Abstract
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Unanswered questions in arsenic toxicology. Author(s): Gebel TW. Source: Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer. 2001; 20(4): 299309. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11797839&dopt=Abstract
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United States multicenter study of arsenic trioxide in relapsed acute promyelocytic leukemia. Author(s): Soignet SL, Frankel SR, Douer D, Tallman MS, Kantarjian H, Calleja E, Stone RM, Kalaycio M, Scheinberg DA, Steinherz P, Sievers EL, Coutre S, Dahlberg S, Ellison R, Warrell RP Jr. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2001 September 15; 19(18): 3852-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11559723&dopt=Abstract
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Unusual manifestations of acute leukemia. Case 1. CNS extramedullary relapse of acute promyelocytic leukemia after arsenic trioxide-induced remission. Author(s): Au WY, Ma SK, Ooi C, Liang R, Kwong YL. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2000 October 1; 18(19): 3435-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11013284&dopt=Abstract
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Unusual sites of involvement by hematologic malignancies. Case 3. External auditory canal tumor: a rare chloroma in acute promyelocytic leukemia with a complete response to arsenic trioxide. Author(s): Au WY, Chan GC, Chim CS, Shek TW, Ooi GC, Ho WK, Kwong YL. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2001 October 1; 19(19): 3993-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11579122&dopt=Abstract
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Upregulation of glutathione-related genes and enzyme activities in cultured human cells by sublethal concentrations of inorganic arsenic. Author(s): Schuliga M, Chouchane S, Snow ET. Source: Toxicological Sciences : an Official Journal of the Society of Toxicology. 2002 December; 70(2): 183-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12441363&dopt=Abstract
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Uptake of arsenic by New Zealand watercress (Lepidium sativum). Author(s): Robinson B, Duwig C, Bolan N, Kannathasan M, Saravanan A. Source: The Science of the Total Environment. 2003 January 1; 301(1-3): 67-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12493186&dopt=Abstract
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Urinary arsenic speciation in subjects with or without restriction from seafood dietary intake. Author(s): Hsueh YM, Hsu MK, Chiou HY, Yang MH, Huang CC, Chen CJ. Source: Toxicology Letters. 2002 July 7; 133(1): 83-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076513&dopt=Abstract
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Urinary protein excretion in humans exposed to arsenic and cadmium. Author(s): Buchet JP, Heilier JF, Bernard A, Lison D, Jin T, Wu X, Kong Q, Nordberg G. Source: International Archives of Occupational and Environmental Health. 2003 March; 76(2): 111-20. Epub 2002 December 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733083&dopt=Abstract
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Use of arsenic trioxide (As2O3) in the treatment of patients with acute promyelocytic leukemia: the M. D. Anderson experience. Author(s): Lazo G, Kantarjian H, Estey E, Thomas D, O'Brien S, Cortes J. Source: Cancer. 2003 May 1; 97(9): 2218-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712474&dopt=Abstract
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Use of the fluorescent micronucleus assay to detect the genotoxic effects of radiation and arsenic exposure in exfoliated human epithelial cells. Author(s): Moore LE, Warner ML, Smith AH, Kalman D, Smith MT. Source: Environmental and Molecular Mutagenesis. 1996; 27(3): 176-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8625953&dopt=Abstract
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Validated determination of total arsenic species of toxicological interest (arsenite, arsenate and their metabolites) by atomic absorption spectrometry after separation from dietary arsenic by liquid extraction: toxicological applications. Author(s): Benramdane L, Accominotti M, Vallon JJ. Source: The Analyst. 1998 August; 123(8): 1711-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10071385&dopt=Abstract
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Variability in human metabolism of arsenic. Author(s): Loffredo CA, Aposhian HV, Cebrian ME, Yamauchi H, Silbergeld EK. Source: Environmental Research. 2003 June; 92(2): 85-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854687&dopt=Abstract
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Variation in arsenic-induced sister chromatid exchange in human lymphocytes and lymphoblastoid cell lines. Author(s): Rasmussen RE, Menzel DB. Source: Mutation Research. 1997 June; 386(3): 299-306. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9219567&dopt=Abstract
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Vegetables collected in the cultivated Andean area of northern Chile: total and inorganic arsenic contents in raw vegetables. Author(s): Munoz O, Diaz OP, Leyton I, Nunez N, Devesa V, Suner MA, Velez D, Montoro R. Source: Journal of Agricultural and Food Chemistry. 2002 January 30; 50(3): 642-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11804542&dopt=Abstract
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Whole-bowel irrigation as an adjunct in the treatment of radiopaque arsenic. Author(s): Lee DC, Roberts JR, Kelly JJ, Fishman SM. Source: The American Journal of Emergency Medicine. 1995 March; 13(2): 244-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7893320&dopt=Abstract
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Widespread arsenic contamination of soils in residential areas and public spaces: an emerging regulatory or medical crisis? Author(s): Belluck DA, Benjamin SL, Baveye P, Sampson J, Johnson B. Source: International Journal of Toxicology. 2003 March-April; 22(2): 109-28. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745992&dopt=Abstract
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CHAPTER 2. NUTRITION AND ARSENIC Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and arsenic.
Finding Nutrition Studies on Arsenic 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 “arsenic” (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 “arsenic” (or a synonym): •
Chronic fatigue syndrome (CFS) associated with Staphylococcus spp. bacteremia, responsive to thiacetarsamide sodium in 7 dogs. Author(s): (Clinica Veterinaria Airone de Nus, Aoste (Italie)) Source: Tarello, W. Revue-de-Medecine-Veterinaire (France). (November 2002). volume 152 (11) p. 785-792. 177Page dogs zoonoses bacterioses staphylococcus animal diseases diagnosis drug therapy arsenic 0035-1555
Additional physician-oriented references include: •
A review of arsenic hazards to plants and animals with emphasis on fishery and wildlife resources. Source: Eisler, R. Arsenic in the environment /. New York : Wiley, c1994. 1994. volume 27 page 185-259. ISBN: 0471579297 (pt 1 : alk paper)
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Accumulation and distribution of dietary arsenic in lake whitefish (Coregonus clupeaformis). Author(s): Department of Zoology, University of Manitoba, Winnipeg, MB, Canada R3T2N2. Source: Pedlar, R M Klaverkamp, J F Aquat-Toxicol. 2002 May; 57(3): 153-66 0166-445X
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Advances in the management of acute promyelocytic leukemia and other hematologic malignancies with arsenic trioxide. Author(s): Department of Hematologic Oncology, Roswell Park Cancer Institute, Buffalo, New York, USA. Source: Slack, J L Waxman, S Tricot, G Tallman, M S Bloomfield, C D Oncologist. 2002; 7 Suppl 1: 1-13 1083-7159
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Arsenic contamination in Bangladesh groundwater: a major environmental and social disaster. Author(s): School of Ecology and Environment, Deakin University, PO Box 423, Warrnambool, Victoria 3280, Australia. Source: Alam, M G Allinson, G Stagnitti, F Tanaka, A Westbrooke, M Int-J-EnvironHealth-Res. 2002 September; 12(3): 235-53 0960-3123
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Arsenic in drinking water and skin cancers: cell-type specificity (Taiwan, ROC). Author(s): Graduate Institute of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
[email protected] Source: Guo, H R Yu, H S Hu, H Monson, R R Cancer-Causes-Control. 2001 December; 12(10): 909-16 0957-5243
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Arsenic induces tumor necrosis factor alpha release and tumor necrosis factor receptor 1 signaling in T helper cell apoptosis. Author(s): Department of Dermatology and Biochemistry, Kaohsiung Medical University, Kaohsiung, Taiwan.
[email protected] Source: Yu, H S Liao, W T Chang, K L Yu, C L Chen, G S J-Invest-Dermatol. 2002 October; 119(4): 812-9 0022-202X
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Arsenic keratosis and pigmentation accompanied by multiple Bowen's disease and genitourinary cancer in a psoriasis patient. Author(s): Department of Dermatology, Seoul National University College of Medicine, Korea.
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Source: Park, J Y Rim, J H Choe, Y B Youn, J I J-Dermatol. 2002 July; 29(7): 446-51 03852407 •
Arsenic methylation is a process of detoxification through accelerated excretion. Author(s): Medical Institute of General Hygiene and Environmental Health, University of Goettingen, Windausweg 2, D-37073 Goettingen, Germany.
[email protected] Source: Gebel, T W Int-J-Hyg-Environ-Health. 2002 October; 205(6): 505-8 1438-4639
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Arsenic trioxide arrests cells early in mitosis leading to apoptosis. Author(s): Brander Cancer Research Institute, New York Medical College, Hawthorne, New York 10532, USA. Source: Halicka, H D Smolewski, P Darzynkiewicz, Z Dai, W Traganos, F Cell-Cycle. 2002 May-June; 1(3): 201-9 1538-4101
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Arsenic trioxide as effective therapy for relapsed acute promyelocytic leukemia. Author(s):
[email protected] Source: Mayorga, J Richardson Hardin, C Dicke, K A Clin-J-Oncol-Nurs. 2002 NovDecember; 6(6): 341-6 1092-1095
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Arsenic trioxide induces apoptosis through a reactive oxygen species-dependent pathway and loss of mitochondrial membrane potential in HeLa cells. Author(s): Laboratory of Cell Biology, Korea Cancer Center Hospital, Seoul 139-706, Korea. Source: Woo, S H Park, I C Park, M J Lee, H C Lee, S J Chun, Y J Lee, S H Hong, S I Rhee, C H Int-J-Oncol. 2002 July; 21(1): 57-63 1019-6439
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Arsenic trioxide, a therapeutic agent for APL. Author(s): The First Hospital affiliated to Harbin Medical University, 23 You Zheng Road, Nangang District, Harbin, 150001, PR China. Source: Zhang, T D Chen, G Q Wang, Z G Wang, Z Y Chen, S J Chen, Z Oncogene. 2001 October 29; 20(49): 7146-53 0950-9232
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Arsenic trioxide: mechanisms of action. Author(s): Lady Davis Institute, McGill University, Montreal, Quebec, Canada. Source: Davison, K Mann, K K Miller, W H Jr Semin-Hematol. 2002 April; 39(2 Suppl 1): 3-7 0037-1963
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Arsenic trioxide-induced apoptosis in U937 cells involve generation of reactive oxygen species and inhibition of Akt. Author(s): Department of Immunology, School of Medicine, Keimyung University, 194 Dong San-Dong Jung-Gu, Taegu 700-712, South Korea. Source: Choi, Y J Park, J W Suh, S I Mun, K C Bae, J H Song, D K Kim, S P Kwon, T K Int-J-Oncol. 2002 September; 21(3): 603-10 1019-6439
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Arsenical resistance in the IncHI2 plasmids. Author(s): Department of Applied Biology and Chemistry, Institute of Technology Carlow, Kilkenny Road, Carlow, Ireland.
[email protected] Source: Ryan, D Colleran, E Plasmid. 2002 May; 47(3): 234-40 0147-619X
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Arsenic-related health problems among hospital patients in southern Bangladesh. Author(s): Center for Community Health, The University of Southern Mississippi, Hattiesburg 39406-5122, USA.
[email protected] Source: Mitra, A K Bose, B K Kabir, H Das, B K Hussain, M J-Health-Popul-Nutr. 2002 September; 20(3): 198-204 1606-0997
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Assessment of cancer risk and environmental levels of arsenic in New Hampshire. Author(s): Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, 7927 Rubin 462M-3, One Medical Center Drive, Lebanon, NH 03756001, USA.
[email protected] Source: Karagas, M R Stukel, T A Tosteson, T D Int-J-Hyg-Environ-Health. 2002 March; 205(1-2): 85-94 1438-4639
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Assessment of environmental arsenic levels in Prievidza district. Author(s): Department of Environmental Science and Technology, Imperial College of Science, Technology and Medicine, London SW7 2BP, UK. Source: Keegan, T Hong, Bing Thornton, I Farago, M Jakubis, P Jakubis, M Pesch, B Ranft, U Nieuwenhuijsen, M J J-Expo-Anal-Environ-Epidemiol. 2002 May; 12(3): 179-85 1053-4245
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Biochemistry of arsenic detoxification. Author(s): Department of Biochemistry and Molecular Biology, Wayne State University, School of Medicine, 48201, Detroit, MI, USA.
[email protected] Source: Rosen, B P FEBS-Lett. 2002 October 2; 529(1): 86-92 0014-5793
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Chromosomally encoded arsenical resistance of the moderately thermophilic acidophile Acidithiobacillus caldus. Author(s): Department of Microbiology, Umea University, Sweden. Source: Dopson, M Lindstrom, E B Hallberg, K B Extremophiles. 2001 August; 5(4): 24755 1431-0651
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Cytotoxicity of arsenic trioxide to transitional carcinoma cells. Author(s): Department of Urology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, Republic of China. Source: Pu, Yeong Shiau Hour, Tzyh Chyuan Chen, June Huang, Chao Yuan Guan, Jing Yi Lu, Shiu Hui Urology. 2002 August; 60(2): 346-50 1527-9995
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Daily dietary total arsenic intake in Belgium using duplicate portion sampling and elemental content of various foodstuffs. Source: Robberecht, H. Cauwenbergh, R. van. Bosscher, D. Cornelis, R. Deelstra, H. Eurfood-res-technol. Berlin : Springer, c1999-. January 2002. volume 214 (1) page 27-32. 1438-2377
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Determination of arsenic in water--quality assurance and calculation of metrological characteristics. Author(s): State Institute of Public Health, Cesta k nemocnici 1, SK-975 56 Banska Bystrica, Slovak Republic.
[email protected] Source: Borosova, D Mocak, J Beinrohr, E Bobrowski, A Cent-Eur-J-Public-Health. 2001 November; 9(4): 196-8 1210-7778
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Dose-dependent biotransformation of arsenite in rats--not S-adenosylmethionine depletion impairs arsenic methylation at high dose. Author(s): Department of Pharmacology and Pharmacotherapy, University of Pecs, Medical School, Szigeti ut 12, H-7643 Pecs, Hungary. Source: Csanaky, I Nemeti, B Gregus, Z Toxicology. 2003 February 1; 183(1-3): 77-91 0300-483X
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Effects on levels of glutathione and some related enzymes in tissues after an acute arsenic exposure in rats and their relationship to dietary protein deficiency. Author(s): University Grants Commission, New Delhi 110002, India.
[email protected] Source: Maiti, S Chatterjee, A K Arch-Toxicol. 2001 November; 75(9): 531-7 0340-5761
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Established practice in the treatment of patients with acute promyleocytic leukemia and the introduction of arsenic trioxide as a novel therapy. Author(s): Department of Hematology, Hopital Saint Louis, Paris, France. Source: Dombret, H Fenaux, P Soignet, S L Tallman, M S Semin-Hematol. 2002 April; 39(2 Suppl 1): 8-13 0037-1963
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Estimation of human exposure to and uptake of arsenic found in drinking water. Source: Xu, H. Grimvall, A. Allard, B. Arsenic in the environment /. New York : Wiley, c1994. 1994. volume 27 page 173-183. ISBN: 0471579297 (pt 1 : alk paper)
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Experimental study on apoptosis of HL-60 cell induced by arsenic trioxide. Author(s): Department of Hematology, Xiyuan Hospital, China Academy of Traditional Chinese Medicine, Bejing (10091). Source: Wang, Z Xu, Y Liao, J Zhongguo-Zhong-Xi-Yi-Jie-He-Za-Zhi. 2000 July; 20(7): 536-8 1003-5370
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Feasibility and correlates of arsenic trioxide combined with ascorbic acid-mediated depletion of intracellular glutathione for the treatment of relapsed/refractory multiple myeloma. Author(s): Sylvester Comprehensive Cancer Center, University of Miami, Florida, USA. Source: Bahlis, N J McCafferty Grad, J Jordan McMurry, I Neil, J Reis, I Kharfan Dabaja, M Eckman, J Goodman, M Fernandez, H F Boise, L H Lee, K P Clin-Cancer-Res. 2002 December; 8(12): 3658-68 1078-0432
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Fluoride, vanadium, nickel, arsenic, and silicon in total parenteral nutrition. Source: Nielsen, F.H. Bull-N-Y-Acad-Med. New York, N.Y. : The Academy. March 1984. volume 60 (2) page 177-195. 0028-7091
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Functional analysis of a chromosomal arsenic resistance operon in Pseudomonas fluorescens strain MSP3. Author(s): Department of Experimental Radiation Oncology, University of Texas-MD Anderson Cancer Center, Houston 77030, USA.
[email protected] Source: Prithivirajsingh, S Mishra, S K Mahadevan, A Mol-Biol-Repage 2001; 28(2): 63-72 0301-4851
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Heavy metal intoxications in horses [Pasture contamination with lead, zinc, cadmium, copper, arsenic, selenium, mercury]. Source: Seawright, A.A. Hrdlicka, J. Ng, J.C. Colloq-INRA. Paris : Institut National de la Recherche Agronomique. 1982. (8) page 465-468. 0293-1915
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How acute promyelocytic leukaemia revived arsenic. Author(s): CNRS UPR 9051, Laboratoire associe du comite de Paris de la ligue contre le cancer, affilie a l'universite de Paris VII, Hopital St Louis, 1 avenue C. Vellefaux, 75475 Paris cedex 10, France. Source: Zhu, J Chen, Z Lallemand Breitenbach, V de The, H Nat-Rev-Cancer. 2002 September; 2(9): 705-13 1474-175X
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Immunosuppression by arsenic: a comparison of cathepsin L inhibition and apoptosis. Author(s): Department of Microbiology and Immunology, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298, USA.
[email protected] Source: Harrison, M T McCoy, K L Int-Immunopharmacol. 2001 April; 1(4): 647-56 15675769
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Immunotoxicological investigation of subacute combined exposure by permethrin and the heavy metals arsenic(III) and mercury(II) in rats. Author(s): Department of Public Health, Faculty of Medicine, University of Szeged, H6720 Szeged, Dom ter 10, Hungary.
[email protected] Source: Institoris, L Siroki, O Undeger, U Basaran, N Desi, I Int-Immunopharmacol. 2001 May; 1(5): 925-33 1567-5769
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Indirect spectrophotometric determination of small amounts of selenium(IV) and arsenic(V) by simple extraction using flotation columns. Author(s): Microanalytical Laboratory, Applied Organic Chemistry, National Research Center, Dokki, Cairo, Egypt. Source: Mostafa, G A Ghazy, S E Anal-Sci. 2001 October; 17(10): 1189-93 0910-6340
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Male reproductive effect of arsenic in mice. Author(s): Industrial Toxicology Research Centre, Lucknow, India. Source: Pant, N KuMarch, R Murthy, R C Srivastava, S P Biometals. 2001 June; 14(2): 113-7 0966-0844
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Markers of low level arsenic exposure for evaluating human cancer risks in a US population. Author(s): Department of Community and Family Medicine, Dartmouth Medical School, Lebanon, NH 03756, USA. Source: Karagas, M R Le, C X Morris, S Blum, J Lu, X Spate, V Carey, M Stannard, V Klaue, B Tosteson, T D Int-J-Occup-Med-Environ-Health. 2001; 14(2): 171-5 1232-1087
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Mechanisms of arsenic biotransformation. Author(s): Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 777 Stockholm, Sweden.
[email protected] Source: Vahter, M Toxicology. 2002 December 27; 181-182: 211-7 0300-483X
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Methylation of arsenic in vitro by cell extracts from bentgrass (Agrostis tenuis): effect of acute exposure of plants to arsenate. Source: Wu, J.H. Zhang, R. Lilley, R.M. Funct-plant-biol. Collingwood, VIC, Australia : CSIRO Publishing, c2002-. 2002. volume 29 (1) page 73-80. 1445-4408
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Microbial methylation of metalloids: arsenic, antimony, and bismuth. Author(s): Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA.
[email protected] Source: Bentley, Ronald Chasteen, Thomas G Microbiol-Mol-Biol-Revolume 2002 June; 66(2): 250-71 1092-2172
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Microbial transformation of elements: the case of arsenic and selenium. Author(s): Department of Biological Sciences, Duquesne University, Pittsburgh, PA 15282, USA.
[email protected] Source: Stolz, J F Basu, P Oremland, R S Int-Microbiol. 2002 December; 5(4): 201-7 11396709
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Multidrug-resistance mdr1a/1b double knockout mice are more sensitive than wild type mice to acute arsenic toxicity, with higher arsenic accumulation in tissues. Author(s): Inorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis, Mail Drop F0-09, NCI at NIEHS, 111, Alexander Drive, Research Triangle Park, NC 27709, USA.
[email protected] Source: Liu, Jie Liu, Yaping Powell, Douglas A Waalkes, Michael P Klaassen, Curtis D Toxicology. 2002 January 15; 170(1-2): 55-62 0300-483X
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Oral administration of dimethylarsinic acid, a main metabolite of inorganic arsenic, in mice promotes skin tumorigenesis initiated by dimethylbenz(a)anthracene with or without ultraviolet B as a promoter. Author(s): College of Pharmacy, Nihon University, Funabashi, Chiba, Japan.
[email protected] Source: Yamanaka, K Mizol, M Kato, K Hasegawa, A Nakano, M Okada, S Biol-PharmBull. 2001 May; 24(5): 510-4 0918-6158
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Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission. Author(s): CNRS UPR 9051, Laboratoire associe #11 Comite de Paris de la Ligue Francaise contre le Cancer, Affilie a l'Universite de Paris VII. Hopital St. Louis, 1, Av. C. Vellefaux 75475 Paris Cedex 10, France. Source: Zhu, J Lallemand Breitenbach, V de The, H Oncogene. 2001 October 29; 20(49): 7257-65 0950-9232
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Peripheral vascular diseases resulting from chronic arsenical poisoning. Author(s): Department of Dermatology, Kaohsiung Medical University, Taiwan. Source: Yu, Hsin Su Lee, Chih Hung Chen, Gwo Shing J-Dermatol. 2002 March; 29(3): 123-30 0385-2407
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Physical injury risks associated with drinking water arsenic treatment. Author(s): Lovelace Clinic Foundation, Albuquerque, NM 87108, USA.
[email protected] Source: Frost, F J Chwirka, J Craun, G F Thomson, B Stomps, J Risk-Anal. 2002 April; 22(2): 235-43 0272-4332
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Potential exposure to arsenic and other highly toxic chemicals when handling museum artifacts. Author(s): US Department of Labor, Occupational Safety and Health Administration, Calumet City Area Office, IL 60409, USA. Source: Smith, B Coulehan, B Appl-Occup-Environ-Hyg. 2002 November; 17(11): 741-3 1047-322X
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Respiratory effects and arsenic contaminated well water in Bangladesh. Author(s): Arsenic Cell, NGO Forum for Drinking Water Supply & Sanitation, Dhaka, Bangladesh.
[email protected] Source: Milton, A H Rahman, M Int-J-Environ-Health-Res. 2002 June; 12(2): 175-9 09603123
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Selected mechanisms of genotoxic effects of inorganic arsenic compounds. Author(s): Department of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, Lodz, Poland.
[email protected] Source: Gradecka, D Palus, J Wasowicz, W Int-J-Occup-Med-Environ-Health. 2001; 14(4): 317-28 1232-1087
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Silicon, aluminium, arsenic and lithium: essentiality and human health implications. Author(s): Instituto de Nutricion y Bromotologia (CSIC), Ciudad Universitaria, Madrid, Spain. Source: Perez Granados, A M Vaquero, M P J-Nutr-Health-Aging. 2002; 6(2): 154-62 1279-7707
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Solidification/stabilisation of arsenic bearing fly ash from the metallurgical industry. Immobilisation mechanism of arsenic. Author(s): Department of Chemical Engineering, University of Leuven, Heverlee, Belgium.
[email protected]
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Source: Vandecasteele, C Dutre, V Geysen, D Wauters, G Waste-Manag. 2002; 22(2): 1436 0956-053X •
Some aspects of arsenic toxicity and carcinogenicity in living organism with special regard to its influence on cardiovascular system, blood and bone marrow. Author(s): Department of Internal and Occupational Diseases, Wroclaw University of Medicine, Poland.
[email protected] Source: Szymanska Chabowska, A Antonowicz Juchniewicz, J Andrzejak, R Int-J-OccupMed-Environ-Health. 2002; 15(2): 101-16 1232-1087
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Speciation of arsenic in plants by HPLC-HG-AFS: extraction optimisation on CRM materials and application to cultivated samples. Author(s): Department of Chemistry, Mulawarman University, Samarinda, Indonesia. Source: Bohari, Y Lobos, G Pinochet, H Pannier, F Astruc, A Potin Gautier, M J-EnvironMonit. 2002 August; 4(4): 596-602 1464-0325
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Targeting the mitochondria: an exciting new approach to myeloma therapy. Commentary re: N. J. Bahlis et al., Feasibility and correlates of arsenic trioxide combined with ascorbic acid-mediated depletion of intracellular glutathione for the treatment of relapsed/refractory multiple myeloma. Clin. Cancer Res., 8: 3658-3668, 2002. Author(s): H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA. Source: Dalton, W S Clin-Cancer-Res. 2002 December; 8(12): 3643-5 1078-0432
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Testing the limits of biological tolerance to arsenic in a fungus isolated from the River Tinto. Author(s): Centro Nacional de Biotecnologia, UAM-CSIC, Cantoblanco, Madrid 28049, Spain. Source: Canovas, D Duran, C Rodriguez, N Amils, R de Lorenzo, V Environ-Microbiol. 2003 February; 5(2): 133-8 1462-2912
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The effect of diet containing arsenic (III) oxide on the traits of eggs. Author(s): Ljubljana Univ. (Slovenia). Biotechnical Fac., Zootechnical Dept. Source: Holcman, A. Malovrh, S. Knez, V. Zbornik-Biotehniske-fakultete-Univerze-vLjubljani (Slovenia). Kmetijstvo (Zootehnika). (2001). volume 78(2) page The effect of diet. layer chickens eggs egg characters chemical composition diet arsenic 1408-3434
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The effects of UVB and arsenic and their interaction on beta2-adrenergic receptors in cultured keratinocytes. Author(s): Department of Cosmetic Science, Chia-Nan College of Pharmacy and Science, Tainan, Taiwan. Source: Chang, H R Kao, Y H Yu, C L Yu, H S Arch-Dermatol-Res. 2001 August; 293(8): 427-9 0340-3696
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The inherent cellular level of reactive oxygen species: one of the mechanisms determining apoptotic susceptibility of leukemic cells to arsenic trioxide. Author(s): Department of Cell Biology, Shanghai Second Medical University, Shanghai 200025, People's Republic of China. Source: Yi, J Gao, F Shi, G Li, H Wang, Z Shi, X Tang, X Apoptosis. 2002 June; 7(3): 20915 1360-8185
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The marine polychaete Arenicola marina: its unusual arsenic compound pattern and its uptake of arsenate from seawater. Author(s): Biology Institute, University of Southern Denmark, DK-5230 Odense M, Denmark.
[email protected]
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Source: Geiszinger, Anita E Goessler, Walter Francesconi, Kevin A Mar-Environ-Res. 2002 February; 53(1): 37-50 0141-1136 •
The paradox of arsenic: molecular mechanisms of cell transformation and chemotherapeutic effects. Author(s): The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA. Source: Bode, A M Dong, Z Crit-Rev-Oncol-Hematol. 2002 April; 42(1): 5-24 1040-8428
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Toxicological effects of dietary arsenic exposure in lake whitefish (Coregonus clupeaformis). Author(s): Department of Zoology, University of Manitoba, Winnipeg, MB, Canada R3T 2N2. Source: Pedlar, R M Ptashynski, M D Evans, R Klaverkamp, J F Aquat-Toxicol. 2002 May; 57(3): 167-89 0166-445X
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Treatment of acute promyelocytic leukemia with arsenic trioxide: clinical and basic studies. Author(s): Shanghai Institute of Hematology, Rui Jin Hospital affiliated to Shanghai Second Medical University, People's Republic of China. Source: Zhao, W L Chen, S J Shen, Y Xu, L Cai, X Chen, G Q Shen, Z X Chen, Z Wang, Z Y Leuk-Lymphoma. 2001 Nov-December; 42(6): 1265-73 1042-8194
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United States multicenter study of arsenic trioxide in relapsed acute promyelocytic leukemia. Author(s): Leukemia and Developmental Chemotherapy Services, Department of Medicine, Memorial Sloan-Kettering Cancer Center and Joan and Sanford Weill Medical College of Cornell University, New York, NY 10021, USA.
[email protected] Source: Soignet, S L Frankel, S R Douer, D Tallman, M S Kantarjian, H Calleja, E Stone, R M Kalaycio, M Scheinberg, D A Steinherz, P Sievers, E L Coutre, S Dahlberg, S Ellison, R Warrell, R P Jr J-Clin-Oncol. 2001 September 15; 19(18): 3852-60 0732-183X
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Unusual sites of involvement by hematologic malignancies. Case 3. External auditory canal tumor: a rare chloroma in acute promyelocytic leukemia with a complete response to arsenic trioxide. Author(s): Queen Mary Hospital, Hong Kong. Source: Au, W Y Chan, G C Chim, C S Shek, T W Ooi, G C Ho, W K Kwong, Y L J-ClinOncol. 2001 October 1; 19(19): 3993-5 0732-183X
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 arsenic; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Vitamin K Alternative names: Menadione, Menaphthone, Menaquinone, Phylloquinone Source: Integrative Medicine Communications; www.drkoop.com
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Minerals Chromium Source: Integrative Medicine Communications; www.drkoop.com Copper Source: Integrative Medicine Communications; www.drkoop.com
Nutrition
Iodine Source: Integrative Medicine Communications; www.drkoop.com Iron Alternative names: Ferrous Sulfate Source: Integrative Medicine Communications; www.drkoop.com Manganese Source: Integrative Medicine Communications; www.drkoop.com Retinol Source: Integrative Medicine Communications; www.drkoop.com Vitamin a (retinol) Source: Integrative Medicine Communications; www.drkoop.com Zinc Source: Integrative Medicine Communications; www.drkoop.com •
Food and Diet Ferrous Sulfate Source: Integrative Medicine Communications; www.drkoop.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND ARSENIC Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to arsenic. 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 arsenic 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 “arsenic” (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 arsenic: •
A dugwell program to provide arsenic-safe water in West Bengal, India: preliminary results. Author(s): Smith MM, Hore T, Chakraborty P, Chakraborty DK, Savarimuthu X, Smith AH. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 289-99. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635833&dopt=Abstract
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A study of method robustness for arsenic speciation in drinking water samples by anion exchange HPLC-ICP-MS. Author(s): Day JA, Montes-Bayon M, Vonderheide AP, Caruso JA. Source: Analytical and Bioanalytical Chemistry. 2002 August; 373(7): 664-8. Epub 2002 July 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12185580&dopt=Abstract
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Acute arsenic exposure treated with oral D-penicillamine. Author(s): Watson WA, Veltri JC, Metcalf TJ. Source: Vet Hum Toxicol. 1981 June; 23(3): 164-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7245601&dopt=Abstract
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Acute arsenic intoxication. Author(s): Campbell JP, Alvarez JA. Source: American Family Physician. 1989 December; 40(6): 93-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2686377&dopt=Abstract
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Adsorption and removal of oxo-anions of arsenic and selenium on the zirconium(IV) loaded polymer resin functionalized with diethylenetriamine-N,N,N',N'-polyacetic acid. Author(s): Suzuki TM, Tanaka DA, Tanco MA, Kanesato M, Yokoyama T. Source: Journal of Environmental Monitoring : Jem. 2000 December; 2(6): 550-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11296739&dopt=Abstract
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Ameliorating effect of microdoses of a potentized homeopathic drug, Arsenicum Album, on arsenic-induced toxicity in mice. Author(s): Mallick P, Chakrabarti(Mallick) J, Guha B, Khuda-Bukhsh AR. Source: Bmc Complementary and Alternative Medicine [electronic Resource]. 2003 October 22 [epub Ahead of Print] http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14570596&dopt=Abstract
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Amelioration of selenium toxicity by arsenicals and cysteine. Author(s): Lowry KR, Baker DH. Source: Journal of Animal Science. 1989 April; 67(4): 959-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2715121&dopt=Abstract
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Antagonistic interactions of an arsenic-containing mixture in a multiple organ carcinogenicity bioassay. Author(s): Pott WA, Benjamin SA, Yang RS. Source: Cancer Letters. 1998 November 27; 133(2): 185-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10072168&dopt=Abstract
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Arsenic and Ayurveda. Author(s): Prakash VB. Source: Leukemia & Lymphoma. 1994 December; 16(1-2): 189-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7696927&dopt=Abstract
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Arsenic and Ayurveda. Author(s): Treleaven J, Meller S, Farmer P, Birchall D, Goldman J, Piller G.
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Source: Leukemia & Lymphoma. 1993 July; 10(4-5): 343-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7693104&dopt=Abstract •
Arsenic and mercury in traditional Chinese herbal balls. Author(s): Espinoza EO, Mann MJ, Bleasdell B. Source: The New England Journal of Medicine. 1995 September 21; 333(12): 803-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7643901&dopt=Abstract
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Arsenic and mercury intoxication due to Indian ethnic remedies. Author(s): Kew J, Morris C, Aihie A, Fysh R, Jones S, Brooks D. Source: Bmj (Clinical Research Ed.). 1993 February 20; 306(6876): 506-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8383555&dopt=Abstract
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Arsenic characterisation in industrial soils by chemical extractions. Author(s): Gleyzes C, Tellier S, Sabrier R, Astruc M. Source: Environmental Technology. 2001 January; 22(1): 27-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11286053&dopt=Abstract
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Arsenic content of homeopathic medicines. Author(s): Kerr HD, Saryan LA. Source: Journal of Toxicology. Clinical Toxicology. 1986; 24(5): 451-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3783808&dopt=Abstract
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Arsenic induced neuropathy. Author(s): Mahajan SK, Aggarwal HK, Wig N, Maitra S, Chugh SN. Source: J Assoc Physicians India. 1992 April; 40(4): 268-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1333468&dopt=Abstract
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Arsenic keratosis and pigmentation accompanied by multiple Bowen's disease and genitourinary cancer in a psoriasis patient. Author(s): Park JY, Rim JH, Choe YB, Youn JI. Source: The Journal of Dermatology. 2002 July; 29(7): 446-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12184646&dopt=Abstract
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Arsenic poisoning caused by Indian ethnic remedies. Author(s): Muzi G, Dell'omo M, Madeo G, Abbritti G, Caroli S. Source: The Journal of Pediatrics. 2001 July; 139(1): 169. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11445819&dopt=Abstract
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Arsenic poisoning from anti-asthmatic herbal preparations. Author(s): Tay CH, Seah CS.
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Source: The Medical Journal of Australia. 1975 September 13; 2(11): 424-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1186550&dopt=Abstract •
Arsenic trioxide induces apoptosis of HPV16 DNA-immortalized human cervical epithelial cells and selectively inhibits viral gene expression. Author(s): Zheng J, Deng YP, Lin C, Fu M, Xiao PG, Wu M. Source: International Journal of Cancer. Journal International Du Cancer. 1999 July 19; 82(2): 286-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10389765&dopt=Abstract
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Arsenic trioxide induces apoptosis of myeloid leukemia cells by activation of caspases. Author(s): Huang XJ, Wiernik PH, Klein RS, Gallagher RE. Source: Medical Oncology (Northwood, London, England). 1999 April; 16(1): 58-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10382944&dopt=Abstract
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Arsenic trioxide induces apoptosis of oesophageal carcinoma in vitro. Author(s): Shen ZY, Tan LJ, Cai WJ, Shen J, Chen C, Tang XM, Zheng MH. Source: International Journal of Molecular Medicine. 1999 July; 4(1): 33-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10373634&dopt=Abstract
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Arsenic trioxide produces polymerization of microtubules and mitotic arrest before apoptosis in human tumor cell lines. Author(s): Ling YH, Jiang JD, Holland JF, Perez-Soler R. Source: Molecular Pharmacology. 2002 September; 62(3): 529-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181429&dopt=Abstract
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Arsenic trioxide therapy for relapsed acute promyelocytic leukemia: an useful salvage therapy. Author(s): Huan SY, Yang CH, Chen YC. Source: Leukemia & Lymphoma. 2000 July; 38(3-4): 283-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10830735&dopt=Abstract
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Arsenic trioxide-mediated cytotoxicity and apoptosis in prostate and ovarian carcinoma cell lines. Author(s): Uslu R, Sanli UA, Sezgin C, Karabulut B, Terzioglu E, Omay SB, Goker E. Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2000 December; 6(12): 4957-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11156257&dopt=Abstract
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Arsenic-induced changes in certain neurotransmitter levels and their recoveries following chelation in rat whole brain. Author(s): Tripathi N, Kannan GM, Pant BP, Jaiswal DK, Malhotra PR, Flora SJ.
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Source: Toxicology Letters. 1997 August 22; 92(3): 201-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9334831&dopt=Abstract •
Arsenicosis in India. Author(s): Narang AP. Source: Journal of Toxicology. Clinical Toxicology. 1987; 25(4): 287-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3669114&dopt=Abstract
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Bladder cancer mortality associated with arsenic in drinking water in Argentina. Author(s): Hopenhayn-Rich C, Biggs ML, Fuchs A, Bergoglio R, Tello EE, Nicolli H, Smith AH. Source: Epidemiology (Cambridge, Mass.). 1996 March; 7(2): 117-24. Erratum In: Epidemiology 1997 May; 8(3): 334. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8834549&dopt=Abstract
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Characterization of gene expression changes associated with MNNG, arsenic, or metal mixture treatment in human keratinocytes: application of cDNA microarray technology. Author(s): Bae DS, Hanneman WH, Yang RS, Campain JA. Source: Environmental Health Perspectives. 2002 December; 110 Suppl 6: 931-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634122&dopt=Abstract
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Chronic arsenic toxicity in Bangladesh and West Bengal, India--a review and commentary. Author(s): Rahman MM, Chowdhury UK, Mukherjee SC, Mondal BK, Paul K, Lodh D, Biswas BK, Chanda CR, Basu GK, Saha KC, Roy S, Das R, Palit SK, Quamruzzaman Q, Chakraborti D. Source: Journal of Toxicology. Clinical Toxicology. 2001; 39(7): 683-700. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11778666&dopt=Abstract
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Chronic arsenic toxicity: clinical features, epidemiology, and treatment: experience in West Bengal. Author(s): Guha Mazumder DN. Source: Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering. 2003 January; 38(1): 141-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12635824&dopt=Abstract
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Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India. Author(s): Datta DV, Mitra SK, Chhuttani PN, Chakravarti RN. Source: Gut. 1979 May; 20(5): 378-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=468068&dopt=Abstract
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Clinical aspects of chronic arsenic toxicity. Author(s): Mazumder DN. Source: J Assoc Physicians India. 2001 June; 49: 650-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11584943&dopt=Abstract
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Contaminated herbal tea as a potential source of chronic arsenic poisoning. Author(s): Parsons JS. Source: N C Med J. 1981 January; 42(1): 38-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6937737&dopt=Abstract
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Cutaneous manifestations of arsenic poisoning due to certain Chinese herbal medicine. Author(s): Tay CH. Source: The Australasian Journal of Dermatology. 1974 December; 15(3): 121-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4451534&dopt=Abstract
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Cutaneous manifestations of chronic arsenicism: review of seventeen cases. Author(s): Wong SS, Tan KC, Goh CL. Source: Journal of the American Academy of Dermatology. 1998 February; 38(2 Pt 1): 179-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9486671&dopt=Abstract
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Determination of arsenic and mercury in sunflower oil by electrothermal atomic absorption. Author(s): Karadjova I, Venelinov T. Source: Food Additives and Contaminants. 2002 October; 19(10): 948-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12443556&dopt=Abstract
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Determination of arsenic in homeopathic drugs by bromide volatilization-inductively coupled plasma-atomic emission spectrometry. Author(s): Lopez-Molinero A, Villareal A, Velilla C, Andia D, Castillo JR. Source: J Aoac Int. 2002 January-February; 85(1): 31-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11878616&dopt=Abstract
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Determination of arsenic in traditional Chinese medicine by microwave digestion with flow injection-inductively coupled plasma mass spectrometry (FI-ICP-MS). Author(s): Ong ES, Yong YL, Woo SO. Source: J Aoac Int. 1999 July-August; 82(4): 963-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10444833&dopt=Abstract
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Determination of inorganic and organic anionic arsenic species in water by ion chromatography coupled to hydride generation-inductively coupled plasma atomic
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emission spectrometry. Author(s): Gettar RT, Garavaglia RN, Gautier EA, Batistoni DA. Source: J Chromatogr A. 2000 July 7; 884(1-2): 211-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10917440&dopt=Abstract •
Dietary garlic extract in modifying clastogenic effects of inorganic arsenic in mice: two-generation studies. Author(s): RoyChoudhury A, Das T, Sharma A, Talukder G. Source: Mutation Research. 1996 April 4; 359(3): 165-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8618548&dopt=Abstract
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Dietary selenium and arsenic additions and their effects on tissue and egg selenium. Author(s): Arnold RL, Olson OE, Carlson CW. Source: Poultry Science. 1973 May; 52(3): 847-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4796303&dopt=Abstract
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Distribution of gamma-tubulin in multipolar spindles and multinucleated cells induced by dimethylarsinic acid, a methylated derivative of inorganic arsenics, in Chinese hamster V79 cells. Author(s): Ochi T, Nakajima F, Nasui M. Source: Toxicology. 1999 August 31; 136(2-3): 79-88. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10514001&dopt=Abstract
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D-penicillamine therapy of acute arsenic poisoning. Author(s): Peterson RG, Rumack BH. Source: The Journal of Pediatrics. 1977 October; 91(4): 661-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=908992&dopt=Abstract
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Drug approval summaries: arsenic trioxide, tamoxifen citrate, anastrazole, paclitaxel, bexarotene. Author(s): Cohen MH, Hirschfeld S, Flamm Honig S, Ibrahim A, Johnson JR, O'Leary JJ, White RM, Williams GA, Pazdur R. Source: The Oncologist. 2001; 6(1): 4-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11161223&dopt=Abstract
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Effect of arsenic trioxide on human hepatocellular carcinoma HepG2 cells: inhibition of proliferation and induction of apoptosis. Author(s): Siu KP, Chan JY, Fung KP. Source: Life Sciences. 2002 June 7; 71(3): 275-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12034346&dopt=Abstract
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Effects of homeopathic arsenic on tobacco plant resistance to tobacco mosaic virus. Theoretical suggestions about system variability, based on a large experimental data
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set. Author(s): Betti L, Lazzarato L, Trebbi G, Brizzi M, Calzoni GL, Borghini F, Nani D. Source: Homeopathy. 2003 October; 92(4): 195-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14587686&dopt=Abstract •
Efficacy of a potentized homeopathic drug (Arsenicum-Aalbum-30) in reducing cytotoxic effects produced by arsenic trioxide in mice: IV. Pathological changes, protein profiles, and content of DNA and RNA. Author(s): Kundu SN, Mitra K, Khuda Bukhsh AR. Source: Complementary Therapies in Medicine. 2000 September; 8(3): 157-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11068345&dopt=Abstract
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Efficacy of a potentized homoeopathic drug (Arsenicum Album-30) in reducing genotoxic effects produced by arsenic trioxide in mice: comparative studies of pre-, post- and combined pre- and post-oral administration and comparative efficacy of two microdoses. Author(s): Datta S, Mallick P, Bukhsh AR. Source: Complementary Therapies in Medicine. 1999 June; 7(2): 62-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10444909&dopt=Abstract
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Efficacy of a potentized homoeopathic drug (Arsenicum Album-30) in reducing genotoxic effects produced by arsenic trioxide in mice: II. Comparative efficacy of an antibiotic, actinomycin D alone and in combination with either of two microdoses. Author(s): Datta S, Mallick P, Bukhsh AR. Source: Complementary Therapies in Medicine. 1999 September; 7(3): 156-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10581825&dopt=Abstract
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Efficacy of a potentized homoeopathic drug (Arsenicum Album-30) in reducing toxic effects produced by arsenic trioxide in mice: II. On alterations in body weight, tissue weight and total protein. Author(s): Mitra K, Kundu SN, Khuda Bukhsh AR. Source: Complementary Therapies in Medicine. 1999 March; 7(1): 24-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10361568&dopt=Abstract
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Efficacy of a potentized homoeopathic drug (Arsenicum-album-30) in reducing cytotoxic effects produced by arsenic trioxide in mice: III. Enzymatic changes and recovery of tissue damage in liver. Author(s): Kundu SN, Mitra K, Bukhsh AR. Source: Complementary Therapies in Medicine. 2000 June; 8(2): 76-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10859599&dopt=Abstract
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Elimination of interferences in the determination of arsenic and antimony by hydride generation using molecular emission cavity analysis (MECA). Author(s): Belcher R, Bogdanski SL, Henden E, Townshend A.
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Source: The Analyst. 1975 July; 100(1192): 522-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=806237&dopt=Abstract •
Environmental variables in a holistic evaluation of land contaminated by historic mine wastes: a study of multi-element mine wastes in West Devon, England using arsenic as an element of potential concern to human health. Author(s): Hamilton EI. Source: The Science of the Total Environment. 2000 April 17; 249(1-3): 171-221. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10813455&dopt=Abstract
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Experimental study on apoptosis of HL-60 cell induced by arsenic trioxide. Author(s): Wang Z, Xu Y, Liao J. Source: Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 July; 20(7): 536-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12043582&dopt=Abstract
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Extraction of antimony and arsenic from fresh and freeze-dried plant samples as determined by HG-AAS. Author(s): Krachler M, Emons H. Source: Fresenius' Journal of Analytical Chemistry. 2000 December; 368(7): 702-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11227551&dopt=Abstract
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Fatal cardiac arrhythmia in a patient with interstitial myocarditis related to chronic arsenic poisoning. Author(s): Hall JC, Harruff R. Source: Southern Medical Journal. 1989 December; 82(12): 1557-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2595426&dopt=Abstract
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Gee, honey, why does the iced tea have a garlic taste? Arsenic intoxication. Author(s): Mack RB. Source: N C Med J. 1983 November; 44(11): 753-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6580553&dopt=Abstract
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Gene expression patterns as potential molecular biomarkers for malignant transformation in human keratinocytes treated with MNNG, arsenic, or a metal mixture. Author(s): Bae DS, Handa RJ, Yang RS, Campain JA. Source: Toxicological Sciences : an Official Journal of the Society of Toxicology. 2003 July; 74(1): 32-42. Epub 2003 May 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12773770&dopt=Abstract
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Heavy metals and arsenic uptake by wild vegetation in the Guadiamar river area after the toxic spill of the Aznalcollar mine. Author(s): Del Rio M, Font R, Almela C, Velez D, Montoro R, De Haro Bailon A.
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Source: Journal of Biotechnology. 2002 September 11; 98(1): 125-37. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12126811&dopt=Abstract •
Herbal medicine as a cause of combined lead and arsenic poisoning. Author(s): Mitchell-Heggs CA, Conway M, Cassar J. Source: Human & Experimental Toxicology. 1990 May; 9(3): 195-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2165417&dopt=Abstract
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High arsenic groundwater: mobilization, metabolism and mitigation--an overview in the Bengal Delta Plain. Author(s): Bhattacharyya R, Chatterjee D, Nath B, Jana J, Jacks G, Vahter M. Source: Molecular and Cellular Biochemistry. 2003 November; 253(1-2): 347-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14619986&dopt=Abstract
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History of the development of arsenic derivatives in cancer therapy. Author(s): Waxman S, Anderson KC. Source: The Oncologist. 2001; 6 Suppl 2: 3-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11331434&dopt=Abstract
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Immunotoxicological investigation of subacute combined exposure by permethrin and the heavy metals arsenic(III) and mercury(II) in rats. Author(s): Institoris L, Siroki O, Undeger U, Basaran N, Desi I. Source: International Immunopharmacology. 2001 May; 1(5): 925-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11379047&dopt=Abstract
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In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins. Author(s): Chen GQ, Zhu J, Shi XG, Ni JH, Zhong HJ, Si GY, Jin XL, Tang W, Li XS, Xong SM, Shen ZX, Sun GL, Ma J, Zhang P, Zhang TD, Gazin C, Naoe T, Chen SJ, Wang ZY, Chen Z. Source: Blood. 1996 August 1; 88(3): 1052-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8704214&dopt=Abstract
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Indirect spectrophotometric determination of small amounts of selenium(IV) and arsenic(V) by simple extraction using flotation columns. Author(s): Mostafa GA, Ghazy SE. Source: Anal Sci. 2001 October; 17(10): 1189-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11990594&dopt=Abstract
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Induction of apoptosis and inhibition of human gastric cancer MGC-803 cell growth by arsenic trioxide. Author(s): Zhang TC, Cao EH, Li JF, Ma W, Qin JF. Source: European Journal of Cancer (Oxford, England : 1990). 1999 August; 35(8): 125863. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10615238&dopt=Abstract
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Inhibition of clastogenic effects of arsenic through continued oral administration of garlic extract in mice in vivo. Author(s): Choudhury AR, Das T, Sharma A, Talukder G. Source: Mutation Research. 1997 August 14; 392(3): 237-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=9294023&dopt=Abstract
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Involvement of microtubules and mitochondria in the antagonism of arsenic trioxide on paclitaxel-induced apoptosis. Author(s): Carre M, Carles G, Andre N, Douillard S, Ciccolini J, Briand C, Braguer D. Source: Biochemical Pharmacology. 2002 May 15; 63(10): 1831-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12034367&dopt=Abstract
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Microbial methylation of metalloids: arsenic, antimony, and bismuth. Author(s): Bentley R, Chasteen TG. Source: Microbiology and Molecular Biology Reviews : Mmbr. 2002 June; 66(2): 250-71. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12040126&dopt=Abstract
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Mitochondria-targeting drugs arsenic trioxide and lonidamine bypass the resistance of TPA-differentiated leukemic cells to apoptosis. Author(s): Sordet O, Rebe C, Leroy I, Bruey JM, Garrido C, Miguet C, Lizard G, Plenchette S, Corcos L, Solary E. Source: Blood. 2001 June 15; 97(12): 3931-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11389037&dopt=Abstract
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Modulation of arsenic induced cytotoxicity by tea. Author(s): Sinha D, Roy M, Dey S, Siddiqi M, Bhattacharya RK. Source: Asian Pac J Cancer Prev. 2003 July-September; 4(3): 233-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507244&dopt=Abstract
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Mono- and dimethylation of arsenic in rat liver cytosol in vitro. Author(s): Styblo M, Delnomdedieu M, Thomas DJ. Source: Chemico-Biological Interactions. 1996 January 5; 99(1-3): 147-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8620564&dopt=Abstract
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Papular palmoplantar hyperkeratosis following chronic medical exposure to arsenic: human papillomavirus as a co-factor in the pathogenesis of arsenical keratosis? Author(s): Gerdsen R, Stockfleth E, Uerlich M, Fartasch M, Steen KH, Bieber T. Source: Acta Dermato-Venereologica. 2000 July-August; 80(4): 292-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11028865&dopt=Abstract
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Phytoremediation of arsenic and lead in contaminated soil using Chinese brake ferns (Pteris vittata) and Indian mustard (Brassica juncea). Author(s): Salido AL, Hasty KL, Lim JM, Butcher DJ. Source: International Journal of Phytoremediation. 2003; 5(2): 89-103. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12929493&dopt=Abstract
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Poison control: Dexedrine, metallic mercury, arsenic and arnica intoxications. Author(s): JACOBZINER H, RAYBIN HW. Source: Archives De Pediatrie : Organe Officiel De La Societe Francaise De Pediatrie. 1961 January; 78: 19-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13789077&dopt=Abstract
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Preserving the distribution of inorganic arsenic species in groundwater and acid mine drainage samples. Author(s): Bednar AJ, Garbarino JR, Ranville JF, Wildeman TR. Source: Environmental Science & Technology. 2002 May 15; 36(10): 2213-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12038832&dopt=Abstract
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Prevention of cytotoxic effects of arsenic by short-term dietary supplementation with selenium in mice in vivo. Author(s): Biswas S, Talukder G, Sharma A. Source: Mutation Research. 1999 April 26; 441(1): 155-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10224332&dopt=Abstract
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Protection against cytotoxic effects of arsenic by dietary supplementation with crude extract of Emblica officinalis fruit. Author(s): Biswas S, Talukder G, Sharma A. Source: Phytotherapy Research : Ptr. 1999 September; 13(6): 513-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10479764&dopt=Abstract
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Randomized placebo-controlled trial of 2,3-dimercapto-1-propanesulfonate (DMPS) in therapy of chronic arsenicosis due to drinking arsenic-contaminated water. Author(s): Guha Mazumder DN, De BK, Santra A, Ghosh N, Das S, Lahiri S, Das T. Source: Journal of Toxicology. Clinical Toxicology. 2001; 39(7): 665-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11778664&dopt=Abstract
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Removal of copper, chromium, and arsenic from CCA-C treated wood by EDTA extraction. Author(s): Kartal SN. Source: Waste Management (New York, N.Y.). 2003; 23(6): 537-46. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12909094&dopt=Abstract
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Results of hemodialysis & hemoperfusion in the treatment of acute arsenic ingestion. Author(s): Smith SB, Wombolt DG, Venkatesan R. Source: Clin Exp Dial Apheresis. 1981; 5(4): 399-404. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7341026&dopt=Abstract
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Severe neurotoxicity following arsenic therapy for acute promyelocytic leukemia: potentiation by thiamine deficiency. Author(s): Yip SF, Yeung YM, Tsui EY. Source: Blood. 2002 May 1; 99(9): 3481-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12001905&dopt=Abstract
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Simultaneous exposure to lead, arsenic and mercury from Indian ethnic remedies. Author(s): Sheerin NS, Monk PN, Aslam M, Thurston H. Source: Br J Clin Pract. 1994 November-December; 48(6): 332-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=7848800&dopt=Abstract
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Speciation analysis of arsenic in traditional Chinese medicines by hydride generation-atomic fluorescence spectrometry. Author(s): Yang LL, Gao LR, Zhang DQ. Source: Anal Sci. 2003 June; 19(6): 897-902. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834231&dopt=Abstract
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Speciation and preservation of inorganic arsenic in drinking water sources using EDTA with IC separation and ICP-MS detection. Author(s): Gallagher PA, Schwegel CA, Wei X, Creed JT. Source: Journal of Environmental Monitoring : Jem. 2001 August; 3(4): 371-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11558469&dopt=Abstract
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Speciation of inorganic arsenic and selenium in leachates from landfills in relation to water quality assessment. Author(s): Yusof AM, Salleh S, Wood AK. Source: Biological Trace Element Research. 1999 Winter; 71-72: 139-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10676488&dopt=Abstract
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Statistical analysis of the effect of high dilutions of arsenic in a large dataset from a wheat germination model. Author(s): Brizzi M, Nani D, Peruzzi M, Betti L.
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Source: Br Homeopath J. 2000 April; 89(2): 63-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10826444&dopt=Abstract •
Subacute arsenic neuropathy: clinical and electrophysiological observations. Author(s): Murphy MJ, Lyon LW, Taylor JW. Source: Journal of Neurology, Neurosurgery, and Psychiatry. 1981 October; 44(10): 896900. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=6273506&dopt=Abstract
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Survival following massive arsenic ingestion. Author(s): Fesmire FM, Schauben JL, Roberge RJ. Source: The American Journal of Emergency Medicine. 1988 November; 6(6): 602-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=3178956&dopt=Abstract
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Tetraarsenic oxide, a novel orally administrable angiogenesis inhibitor. Author(s): Park MJ, Park IC, Bae IJ, Seo KM, Lee SH, Hong SI, Eun CK, Zhang W, Rhee CH. Source: International Journal of Oncology. 2003 June; 22(6): 1271-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738993&dopt=Abstract
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The chelating treatment is not useful in human's intoxication with acute herbicidal organic arsenic. Author(s): Chou CJ, Tsai MS, Tsai JL, Lee HH, Lin TJ. Source: Human & Experimental Toxicology. 2002 December; 21(12): 631-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540032&dopt=Abstract
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The danger to livestock of arsenical preparations intended for the treatment of foot rot. Author(s): Stubbings DP, Littlejohn AI, Hunt GE. Source: The Veterinary Record. 1973 August 4; 93(5): 118-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=4763772&dopt=Abstract
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The dose response of arsenic in induced hair of the rat and its relation to the content in various organs following acute exposure. Author(s): Kollmer WE. Source: J Trace Elem Electrolytes Health Dis. 1990 June; 4(2): 79-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2136229&dopt=Abstract
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The spectrum of cutaneous and internal malignancies in chronic arsenic toxicity. Author(s): Wong ST, Chan HL, Teo SK.
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Therapeutic mule: the use of arsenic in the nineteenth century materia medica. Author(s): Haller JS. Source: Pharm Hist. 1975; 17(3): 87-100. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11610136&dopt=Abstract
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Toxic metals and antioxidants: Part II. The role of antioxidants in arsenic and cadmium toxicity. Author(s): Patrick L. Source: Alternative Medicine Review : a Journal of Clinical Therapeutic. 2003 April; 8(2): 106-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12777158&dopt=Abstract
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Toxicological interactions among arsenic, cadmium, chromium, and lead in human keratinocytes. Author(s): Bae DS, Gennings C, Carter WH Jr, Yang RS, Campain JA. Source: Toxicological Sciences : an Official Journal of the Society of Toxicology. 2001 September; 63(1): 132-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11509753&dopt=Abstract
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Ultrastructural cytochemical analysis of intranuclear arsenic inclusions. Author(s): Sorensen EM. Source: Journal of Toxicology and Environmental Health. 1987; 22(3): 273-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=2445999&dopt=Abstract
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Validation of an arsenic sequential extraction method for evaluating mobility in sediments. Author(s): Keon NE, Swartz CH, Brabander DJ, Harvey C, Hemond HF. Source: Environmental Science & Technology. 2001 July 1; 35(13): 2778-84. Erratum In: Environ Sci Technol 2001 August 15; 35(16): 3396. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11452609&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com®: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMD®Health: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to arsenic; 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 Abdominal Wall Inflammation Source: Integrative Medicine Communications; www.drkoop.com Alcoholism Source: Integrative Medicine Communications; www.drkoop.com Anxiety Source: Integrative Medicine Communications; www.drkoop.com Asthma Source: Integrative Medicine Communications; www.drkoop.com Attention Deficit Hyperactivity Disorder Source: Integrative Medicine Communications; www.drkoop.com Breast Cancer Source: Healthnotes, Inc.; www.healthnotes.com Breast Cancer Source: Integrative Medicine Communications; www.drkoop.com Candidiasis Source: Integrative Medicine Communications; www.drkoop.com Diarrhea Source: Integrative Medicine Communications; www.drkoop.com Food Poisoning Source: Integrative Medicine Communications; www.drkoop.com
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Frostbite Source: Integrative Medicine Communications; www.drkoop.com Gastroesophageal Reflux Disease Source: Integrative Medicine Communications; www.drkoop.com Heartburn Source: Integrative Medicine Communications; www.drkoop.com Hypochondriasis Source: Integrative Medicine Communications; www.drkoop.com Hypothyroidism Source: Healthnotes, Inc.; www.healthnotes.com Lung Cancer Source: Healthnotes, Inc.; www.healthnotes.com Lung Cancer Source: Integrative Medicine Communications; www.drkoop.com Lupus Source: Integrative Medicine Communications; www.drkoop.com Lyme Disease Source: Integrative Medicine Communications; www.drkoop.com Peptic Ulcer Source: Integrative Medicine Communications; www.drkoop.com Peritonitis Source: Integrative Medicine Communications; www.drkoop.com Sarcoidosis Source: Integrative Medicine Communications; www.drkoop.com Sinus Headache Source: Integrative Medicine Communications; www.drkoop.com Sinus Infection Source: Integrative Medicine Communications; www.drkoop.com Sinusitis Source: Integrative Medicine Communications; www.drkoop.com Stress Source: Integrative Medicine Communications; www.drkoop.com Systemic Lupus Erythematosus Source: Integrative Medicine Communications; www.drkoop.com
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Vaginal Inflammation Source: Integrative Medicine Communications; www.drkoop.com Vaginitis Source: Integrative Medicine Communications; www.drkoop.com Yeast Infection Source: Integrative Medicine Communications; www.drkoop.com •
Alternative Therapy Chelation Therapy Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,679,00.html
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Chinese Medicine Xionghuang Alternative names: Realgar; Realgar Source: Chinese Materia Medica
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Homeopathy Arsenicum Album Source: Healthnotes, Inc.; www.healthnotes.com
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Herbs and Supplements EDTA Source: Integrative Medicine Communications; www.drkoop.com Ethylenediaminetetraacetic Acid (EDTA) Source: Integrative Medicine Communications; www.drkoop.com Menadione Source: Integrative Medicine Communications; www.drkoop.com Menaphthone Source: Integrative Medicine Communications; www.drkoop.com Menaquinone Source: Integrative Medicine Communications; www.drkoop.com Phylloquinone Source: Integrative Medicine Communications; www.drkoop.com
Alternative Medicine 137
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 ARSENIC Overview In this chapter, we will give you a bibliography on recent dissertations relating to arsenic. 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 “arsenic” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on arsenic, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Arsenic 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 arsenic. 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: •
Arsenic/Gallium Arsenide Quantum-dot Nanostructures: Strain Distribution and Electronic Structure by Stoleru, Valeria Gabriela; Phd from University of Virginia, 2002, 231 pages http://wwwlib.umi.com/dissertations/fullcit/3057465
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A Fluorine-19 Broad Line Nuclear Magnetic Resonance Study of Tungsten Hexafluoride, Indium Septafluoride. Arsenic Pentafluoride, Sulfur Tetrafluoride. Arsenic Pentafluoride by Barr, Matthew Ronald; Advdeg from The University of British Columbia (canada), 1968 http://wwwlib.umi.com/dissertations/fullcit/NK02352
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A Study of Fermi Surfaces of Rhenium Trioxide and Mercury(2.86) Arsenic Hexafluoride by Saadatmand-razavi, Fereidoon; Phd from Mcmaster University (canada), 1979 http://wwwlib.umi.com/dissertations/fullcit/NK42850
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An Investigation of the Microwave Rotational Spectra of Methylselenocyanate and Methylthicoyanate. the Preparation of Substituted Acetylenic Dicobalthexacarbonyl Complexes Containing Phosphorus and Arsenic Donor Ligands by Hall, David N; Phd from Concordia University (canada), 1976 http://wwwlib.umi.com/dissertations/fullcit/NK28438
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Arsenic Exposure, Artificial Tanning and Melanoma in Iowa by Beane Freeman, Laura Elizabeth; Phd from The University of Iowa, 2003, 214 pages http://wwwlib.umi.com/dissertations/fullcit/3087609
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Arsenic Mobility in Water Treatment Sludge and Its Stabilization Mechanisms by Jing, Chuanyong; Phd from Stevens Institute of Technology, 2002, 102 pages http://wwwlib.umi.com/dissertations/fullcit/3050170
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Arsenic Removal from Drinking Water by Newcombe, Remembrance Louisa; Phd from University of Idaho, 2003, 244 pages http://wwwlib.umi.com/dissertations/fullcit/3089434
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Arsenic Speciation and Redox Chemistry in Natural Waters by Bednar, Anthony Joseph; Phd from Colorado School of Mines, 2002 http://wwwlib.umi.com/dissertations/fullcit/f696609
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Arsenic Speciation Studies on Some Marine Invertebrates of British Columbia by Dodd, Matthew; Phd from The University of British Columbia (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL47191
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Arsenic-doping of Silicon by Molecular Beam Epitaxy by Liu, Xian; , Phd from Stanford University, 2003, 90 pages http://wwwlib.umi.com/dissertations/fullcit/3090638
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Arsenic's Anticancer Activities and Its Effects on Global Gene Expression by Chou, Wen-chien; Phd from The Johns Hopkins University, 2003, 254 pages http://wwwlib.umi.com/dissertations/fullcit/3080641
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Bioaccumulation and Metabolism of Arsenic by Rainbow Trout, Salmo Gairdneri by Oladimeji, Adebayo Amusa; Phd from University of Ottawa (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK48600
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Characterization of Arsenic Transport in Northeastern Honey Lake Basin, Lassen County, California by Gamlin, Jeffrey David; Ms from University of Nevada, Reno, 2002, 96 pages http://wwwlib.umi.com/dissertations/fullcit/1411368
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Characterization of Deep-level Defects in Indium-gallium-arsenic-nitride by Kaplar, Robert James; Phd from The Ohio State University, 2002, 155 pages http://wwwlib.umi.com/dissertations/fullcit/3039484
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Controls on Arsenic Mobility in Contaminated Wetland and Riverbed Sediments by Keon, Nicole Elise; Phd from Massachusetts Institute of Technology, 2002 http://wwwlib.umi.com/dissertations/fullcit/f690769
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Determination of Beta-mercaptopyruvic Acid in Cysteine Transamination Mixture by Titration with Omicron-hydroxymercuribenzoic Acid Using Dithiofluorescein As an Indicator. Catalytic Determination of Iodine in Serum at Nanogram Levels Using the Arsenic(iii by Ke, P. J; Phd from University of Windsor (canada), 1972 http://wwwlib.umi.com/dissertations/fullcit/NK14748
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Effects of Anions on Arsenic Adsorption by Iron Hydroxides by Bang, Sunbaek; Phd from Stevens Institute of Technology, 2003, 82 pages http://wwwlib.umi.com/dissertations/fullcit/3088806
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Evaluation of the Effectiveness of Quicklime-based Stabilization/solidification (s/s) in Arsenic (as) Contaminated Soils by Moon, Deok Hyun; Phd from Stevens Institute of Technology, 2003, 131 pages http://wwwlib.umi.com/dissertations/fullcit/3088824
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Excitation Functions and Isomeric Yield Ratios of (p,xn) Reactions Induced in Arsenic-75 and Indium-115 by 20-85 Mev Protons by Brodovitch, Jean-claude; Phd from Mcgill University (canada), 1973 http://wwwlib.umi.com/dissertations/fullcit/NK18162
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Fabrication and Characterization of Rf-magnetron Sputtered Gallium Arsenide, Arsenic Selenium Telluride, and Silicon Thin Films by Ouyang, Li-hsin; Dsc from Washington University, 2002, 170 pages http://wwwlib.umi.com/dissertations/fullcit/3054028
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First-principles Calculation of Self-diffusion, Arsenic Diffusion, and Surface Segregation in Silicon by Centoni, Scott A.; Phd from Stanford University, 2003, 116 pages http://wwwlib.umi.com/dissertations/fullcit/3085167
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Fluorocarbon Derivatives of Arsenic, Sulfur and Nitrogen by Dhaliwal, Pritam Singh; Advdeg from The University of British Columbia (canada), 1966 http://wwwlib.umi.com/dissertations/fullcit/NK00749
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Increasing Arsenic Tolerance in Plants: Unexpected Roles for Phosphate and Phya by Lee, David Alexander; Phd from University of California, San Diego, 2002, 146 pages http://wwwlib.umi.com/dissertations/fullcit/3071018
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Indium Gallium Arsenic Nitride Antimonide: a Novel Material for Long-wavelength Semiconductor Lasers by Yang, Xiaoping; Phd from Columbia University, 2002, 95 pages http://wwwlib.umi.com/dissertations/fullcit/3037778
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Interactions between Metals, Microbes and Plants: Bioremediation of Arsenic and Lead Contaminated Soils (pinus Sylvestris) by Turpeinen, Riina; Phd from Helsingin Yliopisto (finland), 2002, 106 pages http://wwwlib.umi.com/dissertations/fullcit/f652769
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Investigating Susceptibility in Arsenic-exposed Populations by Chung, Joyce Sunny; Phd from University of California, Berkeley, 2002, 193 pages http://wwwlib.umi.com/dissertations/fullcit/3082149
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Long Wavelength Gallium Indium Nitrogen Arsenide and Gallium-indium-nitrogenarsenic-antimony Lasers on Gallium Arsenide by Ha, Wonill; Phd from Stanford University, 2003, 150 pages http://wwwlib.umi.com/dissertations/fullcit/3085295
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Long Wavelength Luminescence from Gallium-indium-nitrogen-arsenic-antimony on Gallium Arsenide by Gambin, Vincent F.; Phd from Stanford University, 2003, 81 pages http://wwwlib.umi.com/dissertations/fullcit/3085288
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Magnetic Properties of Arsenic and Magnetic Properties of Transition Metal Diarsenides by Bennett, S. L; Advdeg from Queen's University at Kingston (canada), 1966 http://wwwlib.umi.com/dissertations/fullcit/NK00198
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Magneto-optical Kerr Effect and Magnetic Circular Dichroism in Ferromagnetic Indium-manganese-arsenic/gallium-antimony Heterostructures by Wang, Jigang; Ms from Rice University, 2002, 81 pages http://wwwlib.umi.com/dissertations/fullcit/1408716
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Modeling and Simulation of Arsenic Activation and Diffusion in Silicon by Fastenko, Pavel; Phd from University of Washington, 2002, 113 pages http://wwwlib.umi.com/dissertations/fullcit/3041020
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Modeling Arsenic(v) Removal in Iron Oxide Impregnated Activated Carbon Columns by Vaughan, Ronald Lee, Jr.; Phd from University of Missouri - Columbia, 2002, 78 pages http://wwwlib.umi.com/dissertations/fullcit/3060150
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Modelling the Fate and Transport of Arsenic and Other Inorganic Chemicals in Lakes by Diamond, Miriam L; Phd from University of Toronto (canada), 1990 http://wwwlib.umi.com/dissertations/fullcit/NL57027
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Monitoring Reductions in Arsenic Concentrations during Groundwater Recharge and Recovery Operations by Guadamuz, Mario Adolfo; Ms from University of Nevada, Reno, 2002, 152 pages http://wwwlib.umi.com/dissertations/fullcit/1411376
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Multi-metal Equilibrium Sorption and Transport Modeling for Copper, Chromium, and Arsenic in an Iron Oxide-coated Sand, Synthetic Groundwater System by Osathaphan, Khemarath; Phd from Oregon State University, 2002, 214 pages http://wwwlib.umi.com/dissertations/fullcit/3044345
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Optical Characterization of Indium Gallium Arsenic Nitride/gallium Arsenide Semiconductor Heterostructures and Their Potential for Photodetector Applications by Heroux, Jean Benoit; Phd from Columbia University, 2002, 108 pages http://wwwlib.umi.com/dissertations/fullcit/3037714
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-oriented (indium,gallium)arsenic/(aluminum,gallium)arsenic Quantum Well Structures and Their Optical and Strain-induced Piezoelectric and Pyroelectric Properties by Cho, Soohaeng; Phd from University of Colorado at Boulder, 2002, 180 pages http://wwwlib.umi.com/dissertations/fullcit/3057746
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Part 1: Structure, Stability and Reactivity of Small Biologically-active Organosulfur Compounds. Part 2: Generation of Reactive Oxygen Species in the Enzymatic Reduction of Chromium(vi) and Arsenic(v) and Its Implications in Metal-induced Carcinogenesis by Olojo, Oluwarotimi Odunayo; Phd from West Virginia University, 2002, 236 pages http://wwwlib.umi.com/dissertations/fullcit/3076378
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Phosphorus(iii) and Arsenic(iii) Thionylimides and Sulfurdiimides Synthesis, Structure and Coordination Chemistry by Lensink, Cornelis; Phd from University of Calgary (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL42416
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Porous Alumina Packed-bed Reactors: a Treatment Technology for Arsenic Removal by Trotz, Maya Ayanna; Phd from Stanford University, 2002, 180 pages http://wwwlib.umi.com/dissertations/fullcit/3067966
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Pressure Chloride Leaching of a Complex Uranium/radium/nickel/arsenic Ore: Statistical Modelling and Solution Chemistry by Kondos, Petros Dimitri; Phd from Mcgill University (canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL52468
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Reaction Dynamics and Chemical Speciation of Phosphorus and Arsenic (iii and V) at the Metal Oxide-water Interface and in Soils by Arai, Yuji; Phd from University of Delaware, 2002, 324 pages http://wwwlib.umi.com/dissertations/fullcit/3046603
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Reactions of Some Unsaturated Fluorocarbon Derivatives with Organo Compounds of Arsenic, Silicon, Germanium and Tin by Styan, G. E; Advdeg from The University of British Columbia (canada), 1965 http://wwwlib.umi.com/dissertations/fullcit/NK00190
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Semiconductor Optical Amplifiers Made of Ridge Waveguide Bulk Indium Gallium Arsenic Phosphide/indium Phosphide: Experimental Characterisation and Numerical Modelling of Gain, Phase, and Noise by Occhi, Lorenzo; Drsctech from Eidgenoessische Technische Hochschule Zuerich (switzerland), 2002, 202 pages http://wwwlib.umi.com/dissertations/fullcit/f640993
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Socio-hydrologic Approaches for Managing Groundwater Contamination Problems: Strategies for the Arsenic Problem in Bangladesh by Yu, Winston H.; Phd from Harvard University, 2003, 305 pages http://wwwlib.umi.com/dissertations/fullcit/3076920
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Stability of Arsenic and Selenium Immobilized by In-situ Microbial Reduction by Simonton, David Scott; Phd from The University of New Mexico, 2002, 140 pages http://wwwlib.umi.com/dissertations/fullcit/3058951
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Studies of Tolerance Induction in Rainbow Trout by Pre-exposure to Copper, Arsenic or Cyanide by Dixon, Douglas George; Phd from University of Guelph (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK48708
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Study of Local Structural Order in Glassy Arsenic Selenide Using Nuclear Quadrupole Resonance by Ahn, Eungho; Phd from The University of Utah, 2003, 74 pages http://wwwlib.umi.com/dissertations/fullcit/3073870
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Superprotonic Phase Transitions in Solid Acids: Parameters Affecting the Presence and Stability of Superprotonic Transitions in the Mh(n)xo(4) Family of Compounds (x = Sulfur, Selenium, Phosphorus, Arsenic; M = Lithium, Sodium, Potassium,ammonium, Rubidi by Chisholm, Calum Ronald Inneas; Phd from California Institute of Technology, 2003, 272 pages http://wwwlib.umi.com/dissertations/fullcit/3081243
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Synthesis and Characterisation of Bisaminopnictines (pnictines = Phosphorus, Arsenic and Antimony) by Walsh, Denise M.; Phd from Dalhousie University (canada), 2002, 132 pages http://wwwlib.umi.com/dissertations/fullcit/NQ67656
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The Decay of Arsenic, 76, 78 and 80 by Mcmillan, Donald Kenneth; Advdeg from Simon Fraser University (canada), 1971 http://wwwlib.umi.com/dissertations/fullcit/NK07906
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The Development of a Biochemical Probe for Sulfurospirillum Barnesii Strain Ses-3 Grown on Arsenic by Tiwari, Sagarika; Ms from Duquesne University, 2002, 81 pages http://wwwlib.umi.com/dissertations/fullcit/1409929
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The Direct Determination of Arsenic and Antimony in Sea Water by Anodic Stripping Voltammetry by Whang, Chen-wen; Phd from Queen's University at Kingston (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK65842
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The Effects of Arsenic on the Ubiquitin Dependent Proteolytic Pathway by Kirkpatrick, Donald Scott; Phd from The University of Arizona, 2003, 264 pages http://wwwlib.umi.com/dissertations/fullcit/3089976
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The Influence of Folate Deficiency on the Genotoxicity of Arsenic by Mcdorman, Elena Whitley; Phd from The University of North Carolina at Chapel Hill, 2002, 162 pages http://wwwlib.umi.com/dissertations/fullcit/3070881
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 ARSENIC Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning arsenic.
Recent Trials on Arsenic The following is a list of recent trials dedicated to arsenic.8 Further information on a trial is available at the Web site indicated. •
Arsenic Trioxide and Dexamethasone in Treating Patients With Recurrent or Refractory Stage II or Stage III Multiple Myeloma Condition(s): refractory plasma cell neoplasm; stage II multiple myeloma; stage III multiple myeloma Study Status: This study is currently recruiting patients. Sponsor(s): Cell Therapeutics; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combining arsenic trioxide and dexamethasone in treating patients who have recurrent or refractory stage II or stage III multiple myeloma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00017069
8 These
are listed at www.ClinicalTrials.gov.
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Arsenic Trioxide and Imatinib Mesylate in Treating Patients With Chronic Myelogenous Leukemia Condition(s): chronic phase chronic myelogenous leukemia; Philadelphia chromosome positive chronic myelogenous leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Imatinib mesylate may stop the growth of cancer cells by blocking the enzymes necessary for cancer cell growth. Combining chemotherapy with imatinib mesylate may kill more cancer cells. PURPOSE: Phase I/II trial to study the effectiveness of combining arsenic trioxide with imatinib mesylate in treating patients who have chronic phase chronic myelogenous leukemia. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00053248
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Arsenic Trioxide in Treating Men With Germ Cell Cancer Condition(s): recurrent testicular cancer; extragonadal germ cell tumor Study Status: This study is currently recruiting patients. Sponsor(s): Southwest Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating men who have germ cell cancer that has not responded to previous treatment. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00036842
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Arsenic Trioxide in Treating Patients With Advanced Cancer of the Esophagus or Gastroesophageal Junction Condition(s): Adenocarcinoma of the Esophagus; stage III esophageal cancer; stage IV esophageal cancer Study Status: This study is currently recruiting patients. Sponsor(s): M.D. Anderson Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy such as arsenic trioxide use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have metastatic or unresectable cancer of the esophagus or gastroesophageal junction. Phase(s): Phase II Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00061958 •
Arsenic Trioxide in Treating Patients With Advanced Neuroblastoma or Other Childhood Solid Tumors Condition(s): childhood cancer Study Status: This study is currently recruiting patients. Sponsor(s): Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating children who have advanced neuroblastoma or other solid tumors. Phase(s): Phase II; MEDLINEplus consumer health information Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00024258
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Arsenic Trioxide in Treating Patients With Liver Cancer Condition(s): advanced adult primary liver cancer; localized unresectable adult primary liver cancer; recurrent adult primary liver cancer; adult primary hepatocellular carcinoma Study Status: This study is currently recruiting patients. Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase I trial to study the effectiveness of arsenic trioxide in treating patients who have hepatocellular (liver) cancer. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049270
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Arsenic Trioxide in Treating Patients With Myelodysplastic Syndromes Condition(s): atypical chronic myeloid leukemia; Chronic Myelomonocytic Leukemia; myelodysplastic and myeloproliferative disease; Myelodysplastic Syndromes Study Status: This study is currently recruiting patients. Sponsor(s): Cell Therapeutics; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have myelodysplastic syndromes. Phase(s): Phase II Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00020969 •
Arsenic Trioxide in Treating Patients With Pancreatic Cancer That Has Not Responded to Gemcitabine Condition(s): recurrent pancreatic cancer; stage II pancreatic cancer; stage III pancreatic cancer; stage IVA pancreatic cancer; stage IVB pancreatic cancer; adenocarcinoma of the pancreas Study Status: This study is currently recruiting patients. Sponsor(s): University of Chicago Cancer Research Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have locally advanced or metastatic pancreatic cancer that has not responded to gemcitabine. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00053222
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Arsenic Trioxide in Treating Patients With Refractory or Recurrent Acute Promyelocytic Leukemia Condition(s): recurrent childhood acute myeloid leukemia; recurrent adult acute myeloid leukemia; adult acute promyelocytic leukemia (M3); childhood acute promyelocytic leukemia (M3) Study Status: This study is currently recruiting patients. Sponsor(s): Washington University Siteman Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase I/II trial to study the effectiveness of arsenic trioxide in treating patients with refractory or recurrent acute promyelocytic leukemia. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00008697
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Arsenic Trioxide in Treating Patients With Relapsed or Refractory Lymphoma or Leukemia Condition(s): Waldenstrom's Macroglobulinemia; adult non-Hodgkin's lymphoma; Chronic Lymphocytic Leukemia; Hairy Cell Leukemia; Prolymphocytic Leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Mount Sinai Medical Center; National Cancer Institute (NCI)
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Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have relapsed or refractory lymphoma or leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005786 •
Arsenic Trioxide in Treating Patients With Stage IV Prostate Cancer That Has Not Responded to Previous Hormone Therapy Condition(s): stage IV prostate cancer; recurrent prostate cancer Study Status: This study is currently recruiting patients. Sponsor(s): Albert Einstein Cancer Research Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have stage IV prostate cancer that has not responded to hormone therapy. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004149
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Arsenic Trioxide Plus Vitamin C in Treating Patients With Recurrent or Refractory Multiple Myeloma Condition(s): refractory plasma cell neoplasm Study Status: This study is currently recruiting patients. Sponsor(s): Sylvester Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Vitamin C may increase the effectiveness of arsenic trioxide by making cancer cells more sensitive to the drug. PURPOSE: Phase I/II trial to determine the effectiveness of arsenic trioxide plus vitamin C in treating patients who have recurrent or refractory multiple myeloma. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006021
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Arsenic Trioxide to Treat Children with Leukemia or Lymphoma Condition(s): Acute Promyelocytic Leukemia; Leukemia; Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute (NCI)
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Purpose - Excerpt: Arsenic trioxide (As(2)O(3)) is an inorganic trivalent arsenical. Preclinical studies demonstrate a dose-dependent induction of apoptosis and partial differentiation in myeloid leukemia cell lines, and induction of apoptosis and cell cycle arrest in lymphoid neoplasms. The effects of As(2)O(3) are independent of the promyelocytic leukemia (PML) gene product and the specific fusion protein with the Retinoic Acid Receptor alpha (PML-RAR(alpha)) in acute promyelocytic leukemia (APL). Since 1971, As(2)O(3) has been used in the Northeastern region of China to treat more than one thousand adults with cancer. In clinical trials of adults with relapsed all trans retinoic acid (ATRA) resistant APL, durable clinical remission with minimal side effects was achieved in 70% of the patients. Pharmacokinetic analysis showed that daily intravenous administration of As(2)O(3) did not result in plasma accumulation of arsenic; tissue (hair and nail) arsenic content increased five to seven fold over pretreatment content but was still within reference range of normal individuals. A phase I trial and pharmacokinetic study of As(2)O(3) will be conducted in children. The spectrum of toxicity and the maximum tolerated dose will be defined in pediatric patients with refractory leukemia and lymphoma. Additionally, biological studies of cell cycle control parameters will be examined to further elucidate the effect of arsenicals in leukemia, lymphoma and in particular acute promyelocytic leukemia. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004548 •
Bladder Cancer Case Control Study of Arsenic in Water Condition(s): Bladder Cancer Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Environmental Health Sciences (NIEHS) Purpose - Excerpt: This study is examining the relationship between ingested arsenic and bladder cancer in two areas of California where a large percentage of the population was exposed to drinking water containing arsenic at low to moderate levels. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00011518
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Tretinoin, Cytarabine, and Daunorubicin With or Without Arsenic Trioxide Followed by Tretinoin With or Without Mercaptopurine and Methotrexate in Treating Patients With Acute Promyelocytic Leukemia Condition(s): untreated adult acute myeloid leukemia; untreated childhood acute myeloid leukemia and other myeloid malignancies; adult acute promyelocytic leukemia (M3); childhood acute promyelocytic leukemia (M3) Study Status: This study is currently recruiting patients. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI); Eastern Cooperative Oncology Group; National Cancer Institute of Canada; Southwest Oncology Group; Children's Oncology Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Tretinoin may help
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leukemia cells develop into normal white blood cells. It is not yet known which regimen is more effective for acute promyelocytic leukemia. PURPOSE: Randomized phase III trial to determine the effectiveness of tretinoin, cytarabine, and daunorubicin with or without arsenic trioxide followed by tretinoin with or without mercaptopurine and methotrexate in treating patients who have acute promyelocytic leukemia that has not been treated previously. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003934 •
Arsenic Trioxide in Treating Patients With Recurrent or Refractory Acute Lymphoblastic Leukemia or Chronic Myelogenous Leukemia Condition(s): recurrent adult acute lymphoblastic leukemia; relapsing chronic myelogenous leukemia; blastic phase chronic myelogenous leukemia; Philadelphia chromosome positive chronic myelogenous leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): H. Lee Moffitt Cancer Center and Research Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have recurrent or refractory acute lymphoblastic leukemia or chronic myelogenous leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006092
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Arsenic Trioxide in Treating Patients With Relapsed or Refractory Acute Lymphoblastic Leukemia Condition(s): L3 adult acute lymphoblastic leukemia; L1 adult acute lymphoblastic leukemia; recurrent adult acute lymphoblastic leukemia; L2 adult acute lymphoblastic leukemia Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Eastern Cooperative Oncology Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have relapsed or refractory acute lymphoblastic leukemia. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006008
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Arsenic Trioxide in Treating Patients With Stage IVB or Recurrent Cervical Cancer Condition(s): recurrent cervical cancer; cervical squamous cell carcinoma; cervical adenocarcinoma; stage IVB cervical cancer Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI); Memorial Sloan-Kettering Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of arsenic trioxide in treating patients who have stage IVB or recurrent cervical cancer. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005999
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Arsenic Trioxide Plus Radiation Therapy in Treating Patients With Newly Diagnosed Malignant Glioma Condition(s): adult glioblastoma multiforme Study Status: This study is suspended. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage tumor cells. Combining chemotherapy with radiation therapy may kill more tumor cells. PURPOSE: Phase I trial to study the effectiveness of combining arsenic trioxide with radiation therapy in treating patients who have newly diagnosed malignant glioma. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00045565
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 “arsenic” (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
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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 ARSENIC 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 “arsenic” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on arsenic, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Arsenic By performing a patent search focusing on arsenic, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We
9Adapted from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on arsenic: •
Anti-cancer therapy agent of arsenic hexoxide (As4O6) of a natural chemical substance and its pharmaceutical composition Inventor(s): Bae; Ill-Ju (24-5, 393-86, Daebang-dong, Tongjak-ku, Seoul, KR), Doo; Myoung-Sool (Pohang, KR), Eun; Choong-Ki (Pusan, KR), Kang; Tae-Bong (Pohang, KR), Kim; Jong-Bae (Pohang, KR), Kwak; Jin-Hwan (Pohang, KR), Lee; Kwan-Hee (Pohang, KR), Park; Choon-Ho (Pohang, KR), Song; Byung-Doo (Pohang, KR), Song; Seung-Kyu (Pohang, KR), Suh; Byung-Sun (Pohang, KR), Yoon; Taek-Joon (Koyang, KR) Assignee(s): Bae; Ill-Ju (Seoul, KR) Patent Number: 6,589,567 Date filed: September 14, 2001 Abstract: This invention is about the identification of the HD-2, a natural chemical substance that was separated and purified from a natural product, Sinsuk, as arsenic hexoxide (As.sub.4 O.sub.6) and about its therapeutic efficacy as an anti-cancer drug and pharmaceutical composition.Arsenic hexoxide (As.sub.4 O.sub.6), a natural chemical substance obtained from Sinsuk after eliminating the toxic property, has a potent anti-cancer efficacy by its direct cytotoxicity on tumor cells and suppresses the formation of new blood vessels of tumor masses, which results in complete cure of malignant cancers. Excerpt(s): The present invention relates to the identification of HD-2, a natural chemical substance that was separated and purified from a natural product, Sinsuk, as arsenic hexoxide (As.sub.4 O.sub.6) and about its therapeutic efficacy as an anti-cancer drug and pharmaceutical composition, and more particularly, to the purification processes of a natural chemical substance (arsenic hexoxide, As.sub.4 O.sub.6) from Sinsuk while eliminating the toxicity and the novel anti-cancer effect of As.sub.4 O.sub.6 and its pharmaceutical composition by their direct cytotoxicity and suppression of new angiogenesis at and around tumor sites. In general, various drugs are presently available for anti-cancer chemotherapy. Alkylating agents, such as cisplatin and cyclophosphamide, manifest their anti-cancer effect by forming covalent bonds with nitrogen atoms of DNA nucleotides because of its highly electrophilic property of the active site. Antimetabolites, such as 5-fluorouracil, act by inhibiting enzymes involved in biosynthesis of nucleic acids or by being inserted into DNA or RNA structures by itself. Some antibiotics, such as adriamycin, act potently on DNA to inhibit the normal function, which results in suppression of tumor growth. But all of these anti-cancer agents affect not only pathological tumor cells, but also normal healthy cells, especially bone marrow cells or intestinal epithelia with high turnover rate, which cause serious complications and toxicity, such as myelosuppression, alopecia, renal failure, nausea and vomiting, neurotoxicity, etc. On the other hand, arsenic has been known as a potent, environmental carcinogen, affecting skin and lung often. Arsenic is reported to bind to sulfohydryl structure of enzymes to inactivate target enzymes, to inhibit phosphorylation and dephosphorylation reactions, which are vital for regulation of enzyme activities, and to cause abnormalities in chromosomes. Therefore arsenic has been studied mostly from toxicological aspect, related to these reports up to now. Web site: http://www.delphion.com/details?pn=US06589567__
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Catalyst for producing acrylonitrile Inventor(s): Chen; Xin (Shanghai, CN), Guan; Xingya (Shanghai, CN), Wu; Lianghua (Shanghai, CN) Assignee(s): China Petro-Chemical Corporation (Beijing, CN), Research Institute of Petroleum Processing (Beijing, CN) Patent Number: 6,596,897 Date filed: June 30, 2000 Abstract: A fluidized-bed catalyst for producing acrylonitrile by the ammoxidation of propylene, which comprises a silica carrier and a composite having the following formula:A.sub.a C.sub.c D.sub.d Na.sub.f Fe.sub.g Bi.sub.h M.sub.i Mo.sub.12 O.sub.xwherein A selected from the group consisting of potassium, rubidium, cesium, samarium, thallium and mixtures thereof; C is selected from the group consisting of phosphorus, arsenic, boron, antimony, chromium and mixtures thereof; D is selected from nickel, cobalt or mixtures thereof; M is selected from tungsten, vanadium or mixtures thereof. The catalyst of the present invention particularly suits the use under higher pressure and higher duties, and still maintains very high single-pass yield of acrylonitrile and a high ammonia conversion. This catalyst particularly suits the requirement for existing acrylonitrile plants to raise capacity. For new plants it can also reduce the investment on the catalyst and the pollution. Excerpt(s): The present invention relates to a fluidized-bed catalyst for producing acrylonitrile by the ammoxidation of propylene. The production of acrylonitrile by the ammoxidation has been developed for more than 30 years and a balance has been approached between the capacity of the acrylonitrile plants and the demand for acrylonitrile. Now the major development tendency of the production of acrylonitrile has been transformed from the construction of new devices to the reformation of existing plants in order to reduce the consumption of the feed stock and raise the capacity. By reformation of existing plants, change to effective catalysts and elimination of the bottleneck in the production process, it is possible to raise the capacity of acrylonitrile by 50-80%, while the investment required is only 20-30% of that of a newly constructed device. The economic benefit is enormous. Two problems will arise in the reformation of the plant: (1) the reaction pressure in the fluidized reactor will rise; (2) the catalyst loading can not be too heavy. Therefore, the substitution catalyst should have a higher duty for propylene and the capability to endure higher reaction pressures. Web site: http://www.delphion.com/details?pn=US06596897__
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CMOS integrated circuit devices and substrates having unstrained silicon active layers Inventor(s): Bae; Geum-jong (Kyungki-do, KR), Choe; Tae-hee (Seoul, KR), Kim; Sang-su (Kyungki-do, KR), Lee; Kyung-wook (Kyungki-do, KR), Lee; Nae-in (Seoul, KR), Rhee; Hwa-sung (Seoul, KR) Assignee(s): Samsung Electronics Co., Ltd. (KR) Patent Number: 6,633,066 Date filed: November 13, 2000 Abstract: CMOS integrated circuit devices include an electrically insulating layer and an unstrained silicon active layer on the electrically insulating layer. An insulated gate
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electrode is also provided on a surface of the unstrained silicon active layer. A Si.sub.1-x Ge.sub.x layer is also disposed between the electrically insulating layer and the unstrained silicon active layer. The Si.sub.1-x Ge.sub.x layer forms a first junction with the unstrained silicon active layer and has a graded concentration of Ge therein that decreases monotonically in a first direction extending from a peak level towards the surface of the unstrained silicon active layer. The peal Ge concentration level is greater than x=0.15 and the concentration of Ge in the Si.sub.1-x Ge.sub.x layer varies from the peak level to a level less than about x=0.1 at the first junction. The concentration of Ge at the first junction may be abrupt. More preferably, the concentration of Ge in the Si.sub.1-x Ge.sub.x layer varies from the peak level where 0.2<x<0.4 to a level where x=0 at the first junction. The Si.sub.1-x Ge.sub.x layer also has a retrograded arsenic doping profile therein relative to the surface. Excerpt(s): This application is related to Korean Application No. 00-00670, filed Jan. 7, 2000, the disclosure of which is hereby incorporated herein by reference. The present invention relates to semiconductor devices and fabrication methods, and more particularly, to MOS-based semiconductor devices and substrates and methods of forming same. Partially-depleted silicon-on-insulator (PDSOI) MOSFETs offer high speed and low power performance, but typically remain susceptible to parasitic floating body effects (FBE) which can seriously degrade device performance. Various techniques have been proposed for reducing FBE in SOI MOSFETs. One such technique includes using a narrow bandgap SiGe layer adjacent a source of an SOI NMOS field effect transistor. As will be understood by those skilled in the art, the use of a SiGe layer reduces the potential barrier for holes passing from the body region to the source region. Therefore, holes generated in the body region by impact ionization can more readily flow into the source region through the path of the pSi(body)/n+SiGe(source)/n+Si(source). This and other related techniques are disclosed in articles by J. Sim et al. entitled "Elimination of Parasitic Bipolar-induced Breakdown Effects in Ultra-Thin SOI MOSFETs Using Narrow-Bandgap-Source (NBS) Structure," IEEE Trans. Elec. Dev., Vol. 42, No. 8, pp. 1495-1502, August (1995) and M. Yoshimi et al. entitled "Suppression of the Floating-Body Effect in SOI MOSFETs by the Bandgap Engineering Method Using a Si.sub.1-x Ge.sub.x Source Structure," IEEE Trans. Elec. Dev., Vol. 44, No. 3, pp. 423-429, March (1997). U.S. Pat. No. 5,698,869 to Yoshimi et al. entitled "Insulated-Gate Transistor Having Narrow-Bandgap-Source" also discloses the use of a narrow bandgap material within a source region of a MOSFET. Web site: http://www.delphion.com/details?pn=US06633066__ •
Continuous emissions monitor of multiple metal species in harsh environments Inventor(s): Efthimion; Phillip C. (Bedminster, NJ) Assignee(s): Efthimion Emerging Industries, LLC (Bedminster, NJ) Patent Number: 6,577,390 Date filed: January 17, 2002 Abstract: A continuous emissions monitor for the measurement of vapor phase and particulate-based metals in gas streams such as those at coal-fired utility plants, incinerators and manufacturing facilities, in which a pulsed plasma source (10), utilizing a resonant reentrant microwave cavity (12) which is powered by a microwave generator (34), operates at sub atmospheric pressures (<50 Torr.) by using a pump (48) in order to eliminate quenching of the light emission processes by other species in the gas stream and reduce the background emission and where the pulsed operation of the source
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reduces background light emission from oxides of nitrogen produced in plasma sources operating with nitrogen and oxygen gases thus enhancing the contrast and signal-tobackground; resulting in the instrument having a minimum detection level of 0.01 micrograms/m-3 for mercury, as well as, other metal elements such as arsenic and selenium, and requiring less than 10 Watts of microwave power. Excerpt(s): This invention relates to a device to measure mercury and other metals in flue gas from municipal waste incinerators, electric power utility plants, and manufacturing plants at concentrations as low as 10 parts per trillion (0.1 micrograms/m.sup.-3). The 1990 Clean Air Act Amendments and other legislation have raised the concerns over low trace concentrations of metals, especially mercury, in flue gas from electrical generation plants, municipal waste incinerators, and heavy industry. Monitoring will be used to determine the extent of the environmental impact and offers the possibility of empirically minimizing it. In particular, mercury has been found in significant quantities in the lakes and streams of the mid-west of the United States. The source of this mercury has been found to be from the air emissions from large stationary combustion systems. Technology to monitor the levels of mercury may be required by regulations and by technology to control emission levels. The mercury levels at incinerators will be in the range of 0.1-10 parts per billion. However, the levels at electric power utility plants are only 0.03-1.0 parts per billion. For an instrument to measure the lower levels of mercury, for example, it must have a minimum sensitivity on the order of 10 parts per trillion. Furthermore, the instrument must make measurements on flue gas that contains many different molecular gas species that can compromise the measurement of the trace metals, especially mercury. One approach to measuring metals in gas streams uses plasma emission spectroscopy. U.S. Pat. Nos. 5,479,254 and 5,671,045 describe a device using high-powered (300 Watts) and high-pressure microwave plasma emission spectroscopy to measure metals in gas streams. The plasma source is continuous in operation. The device uses a shorted-waveguide as the plasma source and it is inserted in the gas stream. A microwave tuner is used to couple the high-powered microwaves to the shorted-waveguide. A high-resolution spectrometer (0.01 nm) is used to make the measurements. In U.S. Pat. No. 5,671,045 the device is modified for operation in harsh gas and high-temperature environment. There are no provisions for reducing competing emission from flue gas components nor enhancing the metals emission. The high-pressure operation requires the high microwave power to sustain the plasma discharge. There is no disclosure of measuring mercury. There are examples of measuring magnesium, chromium, and iron in a high temperature furnace as well as the laboratory. Web site: http://www.delphion.com/details?pn=US06577390__ •
Geothermal steam processing Inventor(s): Kitz; Kevin R. (Metro Manila, PH) Assignee(s): Union Oil Company of California (El Segundo, CA) Patent Number: 6,539,717 Date filed: March 5, 2001 Abstract: As geothermal steam containing contaminants such as boron, arsenic, and mercury is passed through a turbine-condenser system, the contaminants preferentially collect in the initial condensate produced from the steam. Collecting this initiallyproduced condensate and segregating it from the remainder of the steam being condensed ensures that condensate produced from the remainder of the steam is
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contaminants-lean, preferably containing the contaminants in concentrations allowing for discharge of the contaminants-lean condensate to the environment. Excerpt(s): Geothermal brine and steam reservoirs exist in many areas of the world and are a valuable energy resource. Some steam reservoirs yield a superheated steam which, after treatment to remove contaminants, can be used to power a turbine connected to an electrical generator. More usually, the reservoir yields a geothermal brine which must be flashed to produce steam to power the turbine. After powering the turbine, the exhausted steam is condensed in either a direct contact condenser or a surface condenser (e.g., a shell-and-tube-condenser) to produce steam condensate. The steam condensate is then, in the vast majority of cases, used as liquid water make-up to a cooling tower which provides the working fluid (i.e., the cooling medium) for condensing steam in the condenser. Cooling in the cooling tower is accomplished by evaporation, which produces, as a side effect, the concentration of salts, minerals, and chemicals in the nonevaporated water. If a direct contact condenser is used, as is the case with most geothermal power plants, the cycles of concentration in the cooling tower are normally not controlled. If a surface condenser is used, such as a tube-and-shell condenser, the cooling tower is usually operated to control the concentration of salts by maintaining the cycles of concentration within predetermined limits. This is accomplished by controlling the cooling tower blow down, i.e., controlling the rate at which liquid water is discharged from the cooling tower system. Depending upon the location of the geothermal power plant, the percentage of total condensate produced in the turbinecondenser system which eventually is evaporated or discharged as cooling tower blowdown is between about 70 and 95%, leaving about 5 to 30% of excess condensate for disposal, e.g., discharge to the environment (i.e., by distribution upon a natural earth surface or by discharge to a water body, such as a lake, creek, river, or ocean). Ideally, where possible, the environmental discharge can also serve a beneficial purpose, e.g., agricultural irrigation. Alternatively, the excess condensate can be used for other beneficial purposes, e.g., industrial water. Alternatively again, the excess condensate can be re-injected into the geothermal resource formation, and in many cases this is desired to maintain the resource pressure and volume. However, in other cases, it is not desired, but becomes a necessity because the condensate contains one or more components in excess of applicable environmental discharge regulations. The cost of complying with such regulations--i.e., the cost to construct one or more re-injection wells and the associated surface facilities--is quite high, on the order of $4 million. Web site: http://www.delphion.com/details?pn=US06539717__ •
High performance bipolar transistor Inventor(s): Asbeck; Peter (San Diego, CA), Kempf; Paul (Santa Ana, CA), Schuegraf; Klaus F. (Aliso Viejo, CA), Zampardi; Peter J. (Newbury Park, CA) Assignee(s): Newport Fab, LLC (Newport Beach, CA) Patent Number: 6,506,659 Date filed: March 17, 2001 Abstract: In one disclosed embodiment, a collector is deposited and a base is grown on the collector, for example, by epitaxially depositing either silicon or silicon-germanium. An emitter is fabricated on the base followed by implant doping an extrinsic base region. For example, the extrinsic base region can be implant doped using boron. The extrinsic base region doping diffuses out during subsequent thermal processing steps in chip fabrication, creating an out diffusion region in the device, which can adversely
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affect various operating characteristics, such as parasitic capacitance and linearity. The out diffusion is controlled by counter doping the out diffusion region. For example, the counter doped region can be implant doped using arsenic or phosphorous. Also, for example, the counter doped region can be formed using tilt implanting or, alternatively, by implant doping the counter doped region and forming a spacer on the base prior to implanting the extrinsic base region. Excerpt(s): The present invention relates to the field of fabrication of semiconductor devices. More specifically, the invention relates to the fabrication of silicon-germanium semiconductor devices. In a heterojunction bipolar transistor ("HBT"), a thin silicongermanium layer is grown as the base of a bipolar transistor on a silicon wafer. The silicon-germanium HBT has significant advantages in speed, frequency response, and gain when compared to a conventional silicon bipolar transistor. Speed and frequency response can be compared by the cutoff frequency which, simply stated, is the frequency where the gain of a transistor is drastically reduced. Cutoff frequencies in excess of 100 GHz have been achieved for the HBT, which are comparable to the more expensive GaAs. Previously, silicon-only devices have not been competitive for use where very high speed and frequency response are required. The higher gain, speeds, and frequency response of the HBT have been achieved as a result of certain advantages of silicon-germanium not available with pure silicon, for example, narrower band gap, and reduced resistivity. In addition, silicon-germanium may be epitaxially grown on silicon wafers using conventional silicon processing and tools, and allows one to engineer device properties such as the band gap, energy band structure, and mobilities. For example, it is known in the art that grading the concentration of germanium in the silicon-germanium base builds into the HBT device an electric field, which accelerates the carriers across the base, thereby increasing the speed of the HBT device compared to a silicon-only device. One method for fabricating silicon and silicon-germanium devices is by chemical vapor deposition ("CVD"). A reduced pressure chemical vapor deposition technique, or RPCVD, used to fabricate the HBT device allows for a controlled grading of germanium concentration across the base layer. Web site: http://www.delphion.com/details?pn=US06506659__ •
Laser diodes and manufacturing methods Inventor(s): Goto; Shigeo (Tokorozawa, JP), Kikawa; Takeshi (Kodaira, JP) Assignee(s): Hitachi, Ltd. (Tokyo, JP) Patent Number: 6,576,503 Date filed: July 12, 2001 Abstract: A laser diode having an optical cavity which is formed on top of a semiconductor substrate and has semiconductor crystals and an oxide layer that is substantially free from arsenic oxide. The oxide layer may be formed by using the matrix of the optical cavity as a matrix or a layer formed by the hydrogenation or oxygenation of the matrix of the cavity on at least one side of the optical cavity. The laser diode has a long operational life and high reliability without facet degradation. Excerpt(s): This application claims priority to Japanese Patent Application No. P2000307385. The present invention relates to laser diodes, and more particularly, relates to laser diodes having an oscillation wavelength of at least 600 nm and manufacturing techniques therefor. High-output and high-reliability laser diodes for use in an excitation source for an optical amplifier are used frequently in devices for writing an
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optical or optomagnetic disk and in optical communication systems. These laser diodes are typically required to operate stably in a fundamental mode for an extended period of time. A insulation coating film may be formed on the surface of a semiconductor as the radiation facet of a laser diode. This process may improve the external differential quantum efficiency by obtaining appropriate reflectance and may prevent a reduction in the peak output caused by an increase in threshold carrier density. Web site: http://www.delphion.com/details?pn=US06576503__ •
Lead- and arsenic-free borosilicate glass having improved melting characteristic Inventor(s): Marlor; Richard C. (Beverly, MA) Assignee(s): Osram Sylvania Inc. (Danvers, MA) Patent Number: 6,589,896 Date filed: June 6, 2002 Abstract: A lead- and arsenic-free borosilicate glass having an improved melting characteristic is described. The melting rate of the glass was improved dramatically by making the composition substantially free of MgO and CaO and adding 1.0 to 4.0 weight percent BaO. The improved melting characteristic yielded up to a ninety-nine percent reduction in the number of unmelted batch stones. Excerpt(s): This invention is related to borosilicate glasses and in particular to lead- and arsenic-free borosilicate glasses. In another aspect, this invention is related to glass envelopes for electric lamps. In recent years, the glass industry has been moving toward the elimination of lead and arsenic from borosilicate glass compositions. For example, commonly-owned U.S. Pat. No. 6,284,686, which is incorporated herein by reference, describes a useful lead- and arsenic-free borosilicate glass composition for use in electric lamps (OSRAM SYLVANIA Type SG773). Other lead- and arsenic-free borosilicate glasses used to manufacture electric lamps include types 8486 and 8487 manufactured by Schott Glas. While the elimination of lead and arsenic is beneficial to the environment, their elimination can result in an increase in the number of glass defects, particularly knots, stones, and cord. It is believed that the majority of the defects which occur in lead- and arsenic-free borosilicate glasses are caused by incomplete melting and a reduced convective mixing of the batch components, e.g., knots and stones are the remnants of incomplete melting and surface scum. Therefore, it would be desirable to improve the melting characteristics of lead- and arsenic-free borosilicate glasses to reduce the number of glass defects. Web site: http://www.delphion.com/details?pn=US06589896__
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Method and apparatus for wavelength calibration Inventor(s): Kleinschmidt; Jurgen (Weissanfels, DE), Lokai; Peter (Bovenden, DE), Stamm; Uwe (Gottingen, DE), Vogler; Klaus (Gottingen, DE) Assignee(s): Lambda Physik AG (Goettingen, DE) Patent Number: 6,608,848 Date filed: May 4, 2001 Abstract: A wavelength calibration system determines an absolute wavelength of a narrowed spectral emission band of an excimer or molecular laser system. The system
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includes a module including an element which optically interacts with a component of an output beam of the laser within the tunable range of the laser system around the narrowed band. An inter-level resonance is detected by monitoring changes in voltage within the module, or photo-absorption is detected by photodetecting equipment. The absolute wavelength of the narrowed band is precisely determinable when the optical transitions occur and are detected. When the system specifically includes an ArFexcimer laser chamber, the module is preferably a galvatron containing an element that photo-absorbs around 193 nm and the element is preferably a gas or vapor selected from the group consisting of arsenic, carbon, oxygen, iron, gaseous hydrocarbons, halogenized hydrocarbons, carbon-contaminated inert gases, germanium and platinum vapor. When the system specifically includes F.sub.2 -laser chamber, the module is preferably a galvatron containing an element that photo-absorbs around 157 nm and the element is preferably a gas or vapor selected from the group consisting of selenium, bromine and silicon. The module is alternatively a purge chamber configurable for purging with a photo-absorbing gas. Excerpt(s): The present invention relates to a wavelength calibration module and technique, and particularly to an absolute wavelength calibration module which optically absorbs at known wavelengths and detects such optical absorption when a narrowed emission band of an excimer or molecular laser is incident on the module. Excimer lasers emitting pulsed UV-radiation are becoming increasingly important instruments in specialized material processing. The KrF-excimer laser emitting around 248 nm and the ArF-excimer laser emitting around 193 nm are rapidly becoming the light sources of choice for photolithographic processing of integrated circuit devices (IC's). The F.sub.2 -laser is also being developed for such usage and emits light around 157 nm. It is important for their respective applications to the field of submicron silicon processing that each of the above excimer laser systems become capable of emitting a narrow spectral band around a very precisely determined and finely adjustable absolute wavelength. Techniques for reducing bandwidths by special resonator designs to less than 100 pm, and in some cases to less than 1 pm, are well known. Techniques are also available for tuning and controlling central wavelengths of emission. However, most of these techniques do not accurately determine absolute wavelengths and only serve to relatively tune and control wavelengths. Moreover, even relative wavelength changes cannot be as precisely determined as is desired, using these techniques. Web site: http://www.delphion.com/details?pn=US06608848__ •
Method and structure for a single-sided non-self-aligned transistor Inventor(s): Jenne; Fredrick B. (Los Gatos, CA), Pai; Sheng Yueh (Saratoga, CA), Sethi; Rakesh B. (Campbell, CA) Assignee(s): Cypress Semiconductor Corporation (San Jose, CA) Patent Number: 6,586,806 Date filed: September 3, 1997 Abstract: A transistor includes a non-self-aligned gate-terminal junction in a substrate having a relatively thick oxide layer disposed between a gate region and a terminal region and a relatively thin oxide layer disposed between the gate structure and the substrate. The terminal region may be the drain region of the transistor and it may include a buried N+ region within the substrate. The transistor may be formed in a pwell. Further, the transistor may also include a self-aligned gate-terminal junction between the gate structure and a source region. In a further embodiment, a transistor
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fabrication method includes forming an active area in a substrate and implanting an Ntype impurity into a first terminal region of the active area. An oxide layer is differentially grown over the active area so that the oxide layer has a first thickness over the first terminal region and a second thickness over the remaining portion of the active area. The first thickness is substantially thicker than the second thickness and, in some embodiments, may be up to twice as thick as the second thickness. A gate structure is formed within the active area, overlapping the oxide layer over the first terminal region. A second terminal region within the active area is then formed adjacent to the gate structure. The first terminal region may be a drain region and the N-type impurity may be Arsenic or Phosphorous or a combination of Arsenic and Phosphorous. Excerpt(s): The present invention relates to fabrication of transistor devices and, in particular, to such devices which have high breakdown voltages. Programmable devices, e.g., memory devices, programmable devices, etc., are commonly fabricated using CMOS processing techniques. Often, these techniques include the formation of drain and source regions of a storage element (i.e., a transistor) using a previously created polysilicon gate structure as a mask. When a gate structure is used in this fashion, the resulting drain and source regions of the transistor are said to be selfaligned. That is, the boundaries of the source and drain regions will be aligned to the edge of the polysilicon gate structure which was used as a mask. In addition to storage elements, i.e., memory cells, however, a programmable device often includes other circuitry such as address decoding circuitry and/or programming circuitry (e.g., in the case of EEPROMs, CPLDs, FPGAs and the like). Some of these peripheral circuits, e.g., those controlling the programming and/or erasing of the storage elements, require transistors capable of withstanding high voltages far in excess of the signal voltages which are otherwise used in the programmable device. For example, a CMOS memory device such as an EEPROM may typically use voltages of 3.3 volts or 5 volts for internal or external signals but may use voltages of 18-20 volts for programming and/or erasing operations. Transistors in the programmable device may be required to block these high voltages at some times and pass them at others. In essence then, these transistors operate as high voltage switches. During such operations the transistors must provide low leakage currents so as not to present increased power consumption for the programmable device as a whole and further to avoid latch up. Web site: http://www.delphion.com/details?pn=US06586806__ •
Method for controlling the oxidation of implanted silicon Inventor(s): Bamnolker; Hanna (San Jose, CA), Ramkumar; Krishnaswamy (San Jose, CA) Assignee(s): Cypress Semiconductor Corp. (San Jose, CA) Patent Number: 6,555,484 Date filed: June 19, 1997 Abstract: Two different regions of a semiconductor substrate are implanted with dopants/ions. The implantation may occur though a sacrificial oxide layer disposed over the substrate. Following implantation in one or both regions, the substrate may be annealed and the sacrificial oxide layer removed. An oxide layer is then grown over the implanted regions of the substrate. For some embodiments, the substrate may be implanted with arsenic and/or with phosphorus. Further, the anneal may be performed for approximately 30 to 120 minutes at a temperature between approximately 900.degree. C. and 950.degree. C.
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Excerpt(s): The present invention relates to the growth of oxides on semiconductors and, in particular, relates to the differential growth of oxide layers over implanted areas of a silicon based substrate. In the manufacture of semiconductor devices, thin layers of gate oxide are grown over active areas. It has long been known that slow oxide growth rates should be used to reproducibly grow quality thin oxide films of proper thicknesses over semiconductor dies. However, with the advent of new technologies there has been a need grow gate oxide layers of different thicknesses on different sections of a given semiconductor die. For example, in the manufacture of programmable devices some areas of a semiconductor die on a wafer may require gate oxide thicknesses of between 70.ANG. and 80.ANG. In other areas on the same semiconductor die, however, gate oxide thicknesses of 150.ANG. to 180.ANG. may be required. Historically, it has been difficult to control the proper oxide thicknesses within the separate regions of a given semiconductor die or wafer using conventional oxide growth methods. In other applications, again in the manufacture of programmable devices, thin oxide layers are to be grown over areas of silicon that have been heavily doped. Oxidation rates for such areas are typically very much higher than for areas of undoped silicon. For example, areas of silicon that have been doped with phosphorus will exhibit an affinity for oxygen and so such areas of a semiconductor die will tend to oxidize much more quickly than undoped areas. Indeed, oxide growth rates over heavily doped areas of a semiconductor die have been observed that are five times faster than growth rates in undoped areas of the same semiconductor die. Web site: http://www.delphion.com/details?pn=US06555484__ •
Method for enhancing the solubility of dopants in silicon Inventor(s): De La Rubia; Tomas Diaz (Danville, CA), Lenosky; Thomas J. (Santa Clara, CA), Sadigh; Babak (Oakland, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,627,522 Date filed: September 4, 2001 Abstract: A method for enhancing the equilibrium solid solubility of dopants in silicon, germanium and silicon-germanium alloys. The method involves subjecting siliconbased substrate to biaxial or compression strain. It has been determined that boron solubility was largely enhanced (more than 100%) by a compressive bi-axial strain, based on a size-mismatch theory since the boron atoms are smaller than the silicon atoms. It has been found that the large enhancement or mixing properties of dopants in silicon and germanium substrates is primarily governed by their, and to second order by their size-mismatch with the substrate. Further, it has been determined that the dopant solubility enhancement with strain is most effective when the charge and the sizemismatch of the impurity favor the same type of strain. Thus, the solid solubility of small p-type (e.g., boron) as well as large n-type (e.g., arsenic) dopants can be raised most dramatically by appropriate bi-axial (compressive) strain, and that solubility of a large p-type dopant (e.g, indium) in silicon will be raised due to size-mismatch with silicon, which favors tensile strain, while its negative charge prefers compressive strain, and thus the two effects counteract each other. Excerpt(s): The present invention relates to improving the solubility of dopants in silicon (Si), germanium (Ge), and silicon-germanium alloys (Si.sub.x Gel.sub.1-x) and particularly to enhancing solubility of dopants by subjecting the silicon based substrate to an appropriate strain, and more particularly to a method of enhancing solubility of
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dopants in silicon wherein the type of strain (compressive or tensile) is governed by the dopant's charge and its size-mismatch with the Si-based substrate. Ion implantation allows for exceptional control and reproducibility in the introduction of dopants into the near-surface region of semiconductors. As a result, it has been the universal method of choice for doping MOS transistors in silicon-based integrated circuits since the beginning of the semiconductor revolution. However, an undesirable effect of ionimplantation is that it introduces significant damage into the silicon wafer in the form of point defects and their dusters, Fahey et al. Rev. Mod. Phys. 61, 289 (1989). For a device to be operational these defects must be removed and the dopants electrically activated through high-temperature annealing. The annealing procedure leads to unwanted dopant diffusion, as well as nucleation and growth of dopant clusters and precipitates which results in incomplete activation. Experience has shown that the solubility of boron in silicon under non-equilibrium thermodynamic conditions that prevail during the annealing procedure, i.e., in the presence of excess silicon self-interstitial atoms, is lower than its equilibrium thermodynamic value. The latter thus determines an upper bound for the concentration of substitutional B atoms in silicon. As technology continues to evolve toward smaller and faster transistors, this limit may soon be reached unless new ideas and/or technologies are brought forward that can reduce dopant diffusion during processing while at the same time increasing their electrical activity, see Packan, Science 285,2079 (1999). Web site: http://www.delphion.com/details?pn=US06627522__ •
Method for establishing dopant profile to suppress silicidation retardation effect in CMOS process Inventor(s): Yu; Bin (Fremont, CA) Assignee(s): Advanced Micro Devices, Inc. (Sunnyvale, CA) Patent Number: 6,503,817 Date filed: September 23, 1999 Abstract: A method for suppressing silicidation retardation effects caused by high dopant concentrations, in particular high Arsenic concentrations, at the surface of a semiconductor substrate. The method includes implanting a preamorphization substance into the substrate to define the boundary of the source/drain, then implanting the dopant at high energy to establish a dopant concentration peak that is distanced from the surface of the substrate. The dopant is activated by rapid thermal annealing, with the relatively deep dopant concentration peak facilitating subsequent improved formation of silicide on the surface of the substrate. Excerpt(s): The present invention relates generally to semiconductor fabrication, and more particularly to methods for fabricating improved large scale integration CMOS semiconductor devices. Semiconductor chips are used in many applications, including as processor chips for computers, and as integrated circuits and as flash memory for hand held computing devices, wireless telephones, and digital cameras. Regardless of the application, it is desirable that a semiconductor chip hold as many circuits or memory cells as possible per unit area. In this way, the size, weight, and energy consumption of devices that use semiconductor chips advantageously is minimized, while nevertheless improving the memory capacity and computing power of the devices. A common circuit component of semiconductor chips is the transistor. In ULSI semiconductor chips, a transistor is established by forming a polysilicon gate on a silicon substrate and separated therefrom by a gate insulator. Source and drain regions
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are then formed in the substrate beneath the gate by implanting appropriate dopant materials into the areas of the substrate that are to become the source and drain regions. This generally-described structure cooperates to function as a transistor. Web site: http://www.delphion.com/details?pn=US06503817__ •
Method for fabricating nonvolatile semiconductor memory device Inventor(s): Nitta; Toshinari (Kyoto, JP) Assignee(s): Matsushita Electric Industrial Co., Ltd. (Osaka, JP) Patent Number: 6,582,998 Date filed: April 16, 2001 Abstract: Ions of arsenic are selectively implanted at a high concentration into a substrate through a first passivation film of silicon dioxide to obtain a shallow junction, thereby forming a source region with a low resistivity and a first drain region. Then, after the first passivation film is removed, a second passivation film of silicon dioxide is deposited over the substrate as well as over a stacked cell electrode by a CVD process performed at a relatively low temperature. Thereafter, the substrate is annealed in a nitrogen ambient at such a temperature as activating the dopant introduced. In this manner, the dopant in source region and first drain region is activated. Excerpt(s): The present invention relates to a method for fabricating a nonvolatile semiconductor memory device including a tunnel insulating film, and more particularly relates to a nonvolatile semiconductor memory device that can eliminate crystal defects from parts of a source or drain region under an end of a floating gate electrode. A known nonvolatile semiconductor memory device and a method of fabricating the device will be described, with reference to the drawings. In this process, arsenic ions, which easily do damage on the silicon dioxide film 108, are implanted into the source region 109. In addition, the edge of the source region 109 reaches the region under the end of the tunnel oxide film 103. Furthermore, the large-angle-tilt ion implantation is performed to form the threshold voltage setting region 110. As a result, both ends of the tunnel oxide film 103 in the gate length direction are damaged by the implantation and have its quality degraded. In order to repair the damage, the tunnel oxide film 103 is thickened at both ends in the gate length direction. Web site: http://www.delphion.com/details?pn=US06582998__
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Method for increasing the trench capacitance Inventor(s): Morhard; Klaus-Dieter (Dresden, DE), Penner; Klaus (Ottendorf-Okrilla, DE), Sperl; Irene (Dresden, DE) Assignee(s): Infineon Technologies AG (Munich, DE) Patent Number: 6,544,856 Date filed: June 13, 2001 Abstract: A method for increasing a trench capacitance in deep trench capacitors is described, in which, in a standard method, after the etching of the arsenic glass, a wetchemical etching is additionally performed. An n+-doped substrate results from the driving-out of the arsenic glass being widened in the trench, by about 20 nm, selectively
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both with respect to the lightly doped substrate and with respect to the oxide layer and with respect to the nitride layer. Excerpt(s): The invention relates to a method for increasing a trench capacitance in deep trench capacitors used as memory elements in semiconductor components. The trench has a bottle-shaped widened portion reaching into the depth of the wafer, an oxide layer is situated on a silicon substrate and a nitride layer is situated on the oxide layer. A hard mask is formed in them by a preceding photolithographic steps, the openings in the hard mask determine the position of the trench to be formed. The silicon subsequently is etched down to a first depth in order to form the trench, and afterward a conformal deposition of arsenic glass in the trench is performed. Then the steps of filling the trench with a photoresist, etching the photoresist down to a second, smaller depth, etching the arsenic glass selectively with respect to the photoresist, incinerating the residual photoresist in the trench, driving out the arsenic from the arsenic glass into the surrounding substrate, thereby producing an n+-doped substrate, and also etching the arsenic glass and depositing the node dielectric in the trench and depositing the n.sup.+ -type poly-silicon are carried out. Memory elements are usually embodied as capacitors that make it possible to realize particularly small feature sizes. However, such capacitors must satisfy various requirements. These include not only an adequate capacitance but also, in particular, the capability of long-term storage of the information, i.e. the retention time is intended to be as long as possible. It must therefore be ensured that as far as possible no leakage currents, or small leakage currents, flow to adjacent semiconductor structures. Recent publications have disclosed embodying such memory cells as deep trench capacitors. Such capacitors have a relatively low capacitance, which is likewise reduced as the feature size decreases further. However, the lower capacitance aggravates the problems already mentioned, owing to the fact that, in particular, the retention time, i.e. the charge retention time, is shortened. It has been shown in DRAM development, however, that every structural miniaturization (shrink) also leads to impairment of the retention time. The requirements made of the product remain the same, however. The hitherto sole practically employed possibility for solving this problem consists in increasing the trench capacitance. For this purpose, use was made of the possibility of using a thinner node dielectric. However, distinct limits are exhibited in this case, these being limited by the leakage current through the dielectric. Web site: http://www.delphion.com/details?pn=US06544856__ •
Method for integrating a metastable base into a high-performance HBT and related structure Inventor(s): Schuegraf; Klaus F. (Aliso Viejo, CA), U'Ren; Greg D. (Corona del Mar, CA) Assignee(s): Newport Fab, LLC (Newport Beach, CA) Patent Number: 6,586,297 Date filed: June 1, 2002 Abstract: According to one exemplary embodiment, a heterojunction bipolar transistor is fabricated by forming a metastable epitaxial silicon-germaniuim base on a collector. The metastable epitaxial silicon-gernaniuim base, for example, may have a concentration of germanium greater than 20.0 atomic percent of germanium. The heterojunction bipolar transistor, for example, may be an NPN silicon-germanium heterojunction bipolar transistor. According to this exemplary embodiment, the heterojunction bipolar transistor is further fabricated by fabricating an emitter over the metastable epitaxial silicongermanium base. The heterojunction bipolar transistor is further fabricated by
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doping the emitter with a first dopant. The first dopant, for example, may be arsenic. The heterojunction bipolar transistor is further fabricated by heating the metastable epitaxial silicon-germanium base in a spike anneal process so as to maintain the metastable epitaxial silicon-germanium base as a strained crystalline structure after the spike anneal process and so as to diffusion the first dopant to form emitter-base junction. Excerpt(s): The present invention is in the field of fabrication of semiconductor devices. More specifically, the invention is in the field of fabrication of HBT semiconductor devices. In a silicon-germanium ("SiGe") heterojunction bipolar transistor ("HBT"), a thin silicon-germanium layer is grown as the base of a bipolar transistor on a silicon wafer. The SiGe HBT has significant advantages in speed, frequency response, and gain when compared to a conventional silicon bipolar transistor. Cutoff frequencies in excess of 100 GHz, which are comparable to the more expensive gallium-arsenide based devices, have been achieved for the SiGe HBT. The higher gain, speed and frequency response of the SiGe HBT are possible due to certain advantages of silicon-germanium, such as a narrower band gap and reduced resistivity. These advantages make silicon-germanium devices more competitive than silicon-only devices in areas of technology where high speed and high frequency response are required. Web site: http://www.delphion.com/details?pn=US06586297__ •
Method for producing aldehydes and/or alcohols or amines Inventor(s): Paciello; Rocco (Bad Durkheim, DE), Ulonska; Armin (Mutterstadt, DE), Zehner; Peter (Ludwigshafen, DE) Assignee(s): BASF Aktiengesellschaft (Ludwigshafen, DE) Patent Number: 6,642,420 Date filed: February 7, 2001 Abstract: A process for the preparation of aldehydes and/or alcohols or amines by reacting olefins in the liquid phase with carbon monoxide and hydrogen, a part of these gases being dispersed in the form of gas bubbles in the reaction liquid and another part being dissolved in the reaction liquid, in the presence or absence of a primary or secondary amine and in the presence of a cobalt carbonyl, rhodium carbonyl, palladium carbonyl or ruthenium carbonyl complex dissolved homogeneously in the reaction liquid and having a phosphorus-, arsenic-, antimony- or nitrogen-containing ligand, at elevated temperatures and at 1 to 100 bar, wherein the reaction is carried out in a vertically arranged, tubular reactor comprising a reactor body and at least one circulation line, a part of the reaction liquid is fed continuously via the circulation line to at least one nozzle which is mounted in the upper part of the reactor body and is coordinated with a guide member, open at the top and bottom and bounded by parallel walls, in the interior of the reactor and with a baffle present below the lower opening of the guide member, and a downward-directed liquid stream containing dispersed gas bubbles is produced by means of this nozzle in this guide member and, after leaving the guide member, is deflected into a stream flowing upward in the space between the wall of the guide member and the wall of the reactor body and is sucked into the guide member at the upper end of the guide member by the jet of the nozzle coordinated with the guide member. Excerpt(s): The present invention relates to a process for the preparation of aldehydes and/or alcohols or, if required, amines by reacting olefins with carbon monoxide and
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hydrogen in the presence or absence of ammonia or a primary or secondary amine and in the presence of a catalyst which is homogeneously soluble in the reaction medium and contains at least one element selected from cobalt, rhodium or ruthenium in the presence or absence of a phosphorus-, arsenic-, antimony- or nitrogen-containing ligand at elevated temperatures and at superatmospheric pressure with the use of a jet loop reactor. About 7 million metric tonnes of various products are produced annually worldwide by the hydroformylation of olefins. These are aldehydes, alcohols or amines. Aldehydes are produced essentially by the hydroformylation of olefins with cobalt carbonyl compounds or rhodium carbonyl or ruthenium carbonyl complexes which are homogeneously soluble in the reaction medium, as a rule rhodium carbonyl complexes whose reactivity and selectivity have been modified with a phosphorus-, arsenic-, antimony- or nitrogen-containing ligand. in the presence of a catalyst from subgroup VIII of the Periodic Table of Elements. Furthermore, the hydroformylation under hydrogenating conditions, in which the aldehyde formed in the hydroformylation step is hydrogenated in situ in the hydroformylation reactor by the hydroformylation catalyst to give the corresponding alcohol, and the hydroformylation under aminating conditions, can be assigned to the area of hydroformylation reactions. Although it is also possible to use heterogeneous hydroformylation catalysts, the use of complexes of these elements which are homogeneously soluble in the hydroformylation medium has become established in the industrial application of the hydroformylation reaction. Usually, cobalt carbonyl, rhodium carbonyl, palladium carbonyl or ruthenium carbonyl compounds are used, these compounds being preferred with respect to their reactivity and chemoselectivity as a result of complexing with phosphorus-, arsenic-, antimony- or nitrogen-containing ligands. Web site: http://www.delphion.com/details?pn=US06642420__ •
Method for simultaneous removal of arsenic and fluoride from aqueous solutions Inventor(s): Dick; Paul H. (San Jose, CA), Golden; Josh H. (Santa Cruz, CA), Jung; Jay (Sunnyvale, CA), Krulik; Gerald A. (San Clemente, CA), Sverdlov; Gennadiy (Castro Valley, CA) Assignee(s): Ionics, Incorporated (Watertown, MA) Patent Number: 6,613,230 Date filed: June 27, 2001 Abstract: A method of removing arsenic and fluoride from aqueous solutions in the same process is provided. Specifically, the pH of the aqueous solution is adjusted to a pH in the range of about 5 to 8. A combination of calcium salts, and ferric or aluminum salts are added to form insoluble arsenic and fluoride bearing solids. The solids are then removed from the aqueous solution. Excerpt(s): The present invention relates generally to a system and method for removal of arsenic and fluoride from aqueous solutions, such as drinking water or wastewaters. More specifically, the present invention provides an enhanced system and method of simultaneously removing arsenic and fluoride from aqueous solutions using pretreatment with certain salts and maintaining the solution at certain pH ranges to assist removal of the arsenic and fluoride. Arsenic bearing aqueous solutions, such as wastewaters, are obtained from a variety of industries including agriculture, mining, semiconductor, and petroleum. Other sources of arsenic bearing surface and groundwaters include natural erosion processes and water obtained from wells. Recent studies on the carcinogenic properties of arsenic (As) have raised concern about the
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concentration of As in wastewater and drinking water in the US and worldwide. It has been recognized that many potable water sources are contaminated with unacceptable levels of arsenic and may represent a serious health risk. Arsenic in drinking water is designated as a priority contaminant in the United States under the 1986 Safe Drinking Water Act and amendments thereto. Since 1974, the maximum contaminant level (MCL) for arsenic imposed by the United States Environmental Protection Agency (EPA) is 50 parts per billion (ppb) or (.mu.g/L). As a result of more recent findings pertaining to health risks associated with populations exposed to high concentrations of arsenic in drinking water, the EPA recommends lowering the MCL are arsenic from 50 ppb to 2 ppb. It is expected that in the United States alone, more than 12,000 public water utilities would fail to meet the more stringent proposed arsenic standard. One estimate places the cost of compliance with the proposed MCL standard of 2 ppb to be in excess of $5 billion dollars a year. Web site: http://www.delphion.com/details?pn=US06613230__ •
Method for the removal of sulfide interference in common tests for arsenic Inventor(s): Kroll; Dan J. (Ft. Collins, CO) Assignee(s): Hach Company (Loveland, CO) Patent Number: 6,576,143 Date filed: February 2, 2001 Abstract: A method for removing sulfide from a liquid sample such as water in a test for arsenic. The method involves adding a strong oxidizing agent to the sample to oxidize the sulfide to sulfate, and then adding an organic amine to the sample to react with any remaining oxidizing agent. Excerpt(s): This invention relates to arsenic testing in all matrixes in which sulfide interference is likely to be encountered including groundwater, surface water, drinking water, industrial and municipal wastewater. More particularly, this invention relates to removing interferences caused by the presence of sulfides in the water when testing for arsenic. In the Gutzeit test the liberated arsine gas is then reacted with a detector paper that has been impregnated with mercuric bromide (HgBr). The arsine reacts with the mercuric bromide to form mixed arsenic mercury halogenides and create a yellow to tan to brown color change. In the most common photometric method for the detection of arsenic (silver diethyldithiocarbamate method), the generation of arsine is also used to remove interferences. In this method the silver diethyldithiocarbamate is dissolved in pyridine. The generated arsine gas is then bubbled through this solution. Arsine reacts with the silver salt, forming a soluble red complex suitable for photometric measurement. Web site: http://www.delphion.com/details?pn=US06576143__
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Method molding a glass composition into an optical element with reduced pull-out Inventor(s): Hashimoto; Kazuaki (Tokyo, JP), Hirota; Shin-Ichiro (Tokyo, JP), Oogami; Yu (Tokyo, JP) Assignee(s): Hoya Corporation (Tokyo, JP) Patent Number: 6,588,231 Date filed: November 12, 1999 Abstract: A mold has a moling surface of a material containing silicon carbide and/or silicon nitride as a main component and a carbon thin film formed on the molding surface to prevent fusion sticking. A glass substance which has a sag point not higher than 565.degree. C. and a predetermined composition free from arsenic oxide is introduced into the mold. The glass substance is press-formed in a heated and softened condition into a glass optical element of high precision. Excerpt(s): This invention relates to a method of producing a glass optical element with a high precision and to a glass substance processed by the method into the glass optical element. A wide variety of development and research have been made about the technique of press-forming or press-molding a glass substance within a mold to produce a glass optical element of high precision. For example, one attempt has been directed to a mold which has a molding surface of silicon carbide, silicon nitride, and the like. Herein, silicon carbide and silicon nitride are excellent in hardness and strength against a high temperature. Such a molding surface of silicon carbide and/or silicon nitride may be deposited by a chemical vapor deposition (CVD) method. In this event, the molding surface has an excellent compactness without occurrence of surface defects, such as pores, and can be polished into a mirror surface. However, the molding surface of such materials is liable to be oxidized to form a silicon oxide surface layer of several tens of angstroms thick. In this case, it has been pointed out that fusion sticking often takes place between the molding surface and the glass substance during a press-forming step when the glass substance is composed of borosilicate glass or silicate glass containing a large amount of modification components, such as alkali or alkaline earth positive ions. Moreover, stress is concentrated in a following cooling step here and there on the molding surface, which causes cracks to occur on the molding surface. This results in a phenomenon such that the molding surface of the mold is scooped or removed in spots. This phenomenon will hereinafter be simply called a "pullout" or a "pullout" phenomenon. Web site: http://www.delphion.com/details?pn=US06588231__
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Method of fabricating a distributed Bragg reflector by controlling material composition using molecular beam epitaxy Inventor(s): Almuneau; Guilhem (Aesch Bei Birmensdorf, CH), Hall; Eric M. (Santa Barbara, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,583,033 Date filed: August 21, 2001 Abstract: A distributed Bragg reflector for a vertical cavity surface emitting laser has a semiconductor material system including the elements aluminum, gallium, arsenic, and antimony. Accurate control of the composition of the semiconductor material system
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must be maintained to result in a distributed Bragg reflector suitable for use in a VCSEL. A method of fabricating the distributed Bragg reflector includes calibrating the incorporation of at least one of the elements into the material system as different semiconductor materials are grown on a substrate. Excerpt(s): The invention relates in general to a vertical cavity surface emitting laser (VCSEL). More particularly, the invention relates to growth methods and structures for distributed Bragg reflectors (DBRs) utilized in VCSELs. Semiconductor lasers are widely used in optical applications, in part because semiconductor fabrication techniques are relatively inexpensive and yield reliable, consistent results. Also, they are easily packaged into current microelectronics. A relatively new class of semiconductor lasers, vertical cavity surface emitting lasers (VCSELs), has been developed through the evolution of this technology. Unlike conventional edge emitting lasers that emit light in a direction parallel to the semiconductor substrates where the lasers are formed, VCSELs have optical cavities perpendicular to the substrate, and thus emit optical radiation in a direction perpendicular to the substrate. In addition to various performance and application-adaptable improvements created thereby, VCSELs simply require reduced complexity in their fabrication and testing, as compared to conventional edge emitting semiconductor lasers. Vertical cavity surface emitting lasers (VCSELs) have been proven to be solutions for low-cost transmitters for high-speed data communications at 980 nm and 850 nm and have shown great potential for cost-effective telecommunication systems at longer wavelengths as well, such as 1.55.mu.m and 1.3.mu.m. These long wavelength VCSELs will satisfy increasing demand for high speed data transmission over tens of kilometers. 10-Gigabit Ethernet is one example, which requires inexpensive transmitters with a data rate of 10 G bit per second (Gbps) and up to 40 km reach over single-mode fiber. Web site: http://www.delphion.com/details?pn=US06583033__ •
Method of fabricating field effect transistor Inventor(s): Tenkou; Li (Kanagawa, JP) Assignee(s): Oki Electric Industry CO, Ltd. (Tokyo, JP) Patent Number: 6,562,685 Date filed: October 12, 2000 Abstract: There is provided a method of fabricating a MOSFET having a source region and a drain region, having a LDD region, respectively, in respective regions directly beneath the edges of the gate electrode even without forming the sidewalls of the gate electrode. A silicide layer 18 is formed on the surface of a polysilicon layer 16 through selective growth of material used for a gate silicide {FIG. 1(A)}, and thereby a gate electrode made up of the polysilicon layer 16 and the silicide layer 18 is formed. Subsequently, a first implantation of ions in low concentration is performed whereby arsenic ions As.sup.+ or phosphorus ions P.sup.+, in low concentration, are implanted into the surface of a silicon substrate 10 from a direction at a slant to the surface thereof such that a dopant is implanted into respective regions directly beneath the edges of the polysilicon layer 16, within a region set to form a source and a drain, respectively, on respective sides of the gate electrode {FIG. 1(B)}. A second implantation of ions in high concentration is performed whereby arsenic ions As.sup.+, in high concentration, are implanted into a source region 20a and a drain region 22a, in shallow junction state, formed on respective sides of the gate electrode, from the direction vertical to the surface of the silicon substrate 10 {FIG. 1(C)}.
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Excerpt(s): The present invention relates to a method of fabricating a field effect transistor (referred to hereinafter as a MOSFET), and in particular, to a method of fabricating a MOSFET having a source region as well as a drain region of a LDD (light doped drain) structure. In order to maintain pressure resistance without deteriorating device performance, it has been in practice to form the source region and the drain region into the LDD (light doped drain) structure. The LDD structure is a structure having a lightly doped region in comparison with the source region and the drain region, in a region directly beneath the gate electrode, within the source region and the drain region, respectively, and can be formed by implanting ions in two stages when forming the source region and the drain region. That is, as a result of implantation of ions in low concentration, a source region 40a and a drain region 42a, which are in shallow junction state, are formed. Web site: http://www.delphion.com/details?pn=US06562685__ •
Method of forming semiconductor device with LDD structure Inventor(s): Chaudhry; Samir (Orlando, FL), Chetlur; Sundar S. (Orlando, FL), Vaidya; Hem M. (Orlando, FL) Assignee(s): Agere Systems Inc. (Allentown, PA) Patent Number: 6,576,521 Date filed: April 7, 1998 Abstract: A NMOSFET semiconductor device is formed having an LDD structure by simultaneous co-implantation of arsenic and phosphorous to form an N- layer. The coimplantation is performed subsequent to the formation of the gate structure and a thin (100.ANG.-300.ANG.) gate spacer but prior to the implantation of a highly doped N+ source/drain. Excerpt(s): This invention relates to semiconductor integrated circuit fabrication and, more particularly, to an improved process for fabricating MOS devices having lightly doped drain (LDD) and source regions. Semiconductor integrated circuits are comprised of a plurality of devices which invariably include transistors. Transistors are of two general types, namely bipolar and field effect transistors (FET'S). Semiconductor processing techniques as described above as well as variations of the structure described above are well known in the art and can be found in many references. By way of example, reference may be had to Silicon Processing For the VLSI Era, Lattice Press 1990; U.S. Pat. No. 5,573,965 to Chen et al, U.S. Pat. No. 5,679,589 to Lee et al, U.S. Pat. No. 5,721,443 to Zhiqiang, U.S. Pat. No. 5,719,424 to Ahmad et al and U.S. Pat. No. 5,723,352 to Shih et al, all of which are incorporated herein by reference. Web site: http://www.delphion.com/details?pn=US06576521__
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Method of photolithography using super-resolution near-field structure Inventor(s): Guo; Wen-Rei (Chiayi Hsien, TW), Tseng; Tzu-Feng (Hsinchu Hsien, TW), Wu; Kuei-Yen (Hsinchu, TW) Assignee(s): Ritek Corporation (Hsinchu, JP) Patent Number: 6,506,543 Date filed: October 20, 2000
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Abstract: A method of photolithography using super-resolution near-field structure. A super-resolution near-field structure is formed on a semiconductor chip comprising a substrate and a photoresist layer thereon. An incident light beam penetrates through the super-resolution near-field structure to expose the photoresist layer. While penetrating through the super-resolution near field structure, the intensity of the incident light beam is increased, and the aperture of the light beam is reduced. As a result, the line width of the pattern formed on the photoresist layer is narrowed. The super-resolution near-field structure has a first dielectric layer, a second dielectric layer and an active layer sandwiched between the first and the second dielectric layers. The active layer is formed of one of gallium (Ga), germanium (Ge), arsenic (As), selenium (Se), indium (In), tin (Sn), antimony (Sb), tellurium (Te), and silver (Ag). Or alternatively, the active layer can be formed of one of the materials of gallium oxide, germanium oxide, arsenic oxide, selenium oxide, indium oxide, tin oxide, antimony oxide, tellurium oxide and silver oxide. Excerpt(s): This application claims the priority benefit of Taiwan application serial no. 89114791, filed Jul. 24, 2000. The invention relates in general to a method of photolithography using super-resolution near-field structure. More particularly, this invention relates to a method of photolithography using super-resolution near-field structure to form a pattern with a smaller line width on a photoresist layer. Photolithography process is one of the most crucial steps in semiconductor fabrication process. Through photolithography, the layout of the integrated circuit can be transferred into the semiconductor chip. Typically, a pattern is designed on a photomask. Via exposure and etching processes, the pattern is transferred from the photomask to the photoresist layer with a certain proportion. Web site: http://www.delphion.com/details?pn=US06506543__ •
Method of preparing inorganic pentafluorides Inventor(s): Rieland; Matthias (Hannover, DE), Rudolph; Werner (Hannover, DE), Schulz; Alf (Wedemark, DE), Seffer; Dirk (Neustadt, DE) Assignee(s): Solvay Fluor und Derivate GmbH (Hannover, DE) Patent Number: 6,645,451 Date filed: June 16, 1997 Abstract: The preparation of phosphorus pentafluoride and arsenic pentafluoride by reacting corresponding trihalides with elemental chlorine, bromine or iodine and also with hydrogen fluoride. Excerpt(s): The invention relates to the preparation of phosphorus and arsenic pentafluoride. Phosphorus pentafluoride can be reacted with lithium fluoride to form lithium hexafluorophosphate. Arsenic pentafluoride can also be used for the same purpose, and in the form of lithium hexafluoroarsenate can likewise be used as a conducting salt in lithium-ion batteries as disclosed in U.S. Pat. No. 5,427,874. Phosphorus pentafluoride is prepared, for example, from phosphorus pentachloride and hydrogen fluoride. Arsenic pentafluoride is prepared from the metal and elemental fluorine. This method is disadvantageous in energy terms. Furthermore, elemental fluorine is very aggressive. It is an aim of the present invention to provide a method for the preparation of pentafluorides of phosphorus and arsenic which is technically simple to perform. Web site: http://www.delphion.com/details?pn=US06645451__
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Method of providing polysilicon spacer for implantation Inventor(s): Chidambaram; PR (Richardson, TX) Assignee(s): Texas Instruments Incorporated (Dallas, TX) Patent Number: 6,573,165 Date filed: June 28, 2002 Abstract: An improved method of implanting source and drain for CMOS devices is provided by a hard mask and dry etching to form polysilicon gates 20 percent longer than desired, implanting to form the source and drain of the PMOS transistor with dopant that moves faster during annealing such as Boron and then wet etching the polysilicon gates down to the shorter length such as the final length before implanting with the faster dopant such as arsenic. Excerpt(s): This invention relates to CMOS processing and more particularly to using polysilicon as a spacer for implantation. Complementary Metal Oxide semiconductor (CMOS) technology employs both NMOS (n-channel transistor) and PMOS (p-channel transistor) to form logic elements. The structures and fabrication procedures are described in a book entitled "VLSI Technology, second edition edited by S. M. Sze, a McGraw Hill Publication (ISBN 0-07-062735-5). In particular, see section 11.4 beginning on page 483. The fabrication process for CMOS is similar to NMOS. Fabrication is also disclosed in many patents such as, for example, Hutter et al. U.S. Pat. No. 4,472,887. This patent is incorporated herein by reference. The NMOS and PMOS differences occur due to individual doping adjustment for n-channel and p-channel devices. Twin tubs may be formed using lithographic mask process. A composite layer of silicon dioxide SiO2 and Silicon Nitride Si3N4 are defined and silicon is exposed over the n-tub region. Phosphorus is implanted as the n-tub dopant at low energy and enters the exposed silicon; but is masked from the adjacent region by the Silicon Nitride Si3N4. The wafers are then selectively oxidized over the n-tub regions. The nitride is stripped and Boron is implanted for the p-tub. The Boron enters the silicon through the oxide but is masked from the tub by the thicker SiO2 layer. All oxides are then stripped away and the two tubs are driven in by heat. After the tubs are formed, there is the formation of the field oxide and gates. The gate is polysilicon and is formed by a polysilicon deposit on the silicon base of the n-channel and p-channel. Photoresist is placed over the gate regions and etched. It is then necessary to selectively implant the n-channel and p-channel source/drain to form the n+ region for the n-channel and p+ regions for the p-channels. In accordance with one technique the implanting includes implanting Boron nonselectively into all sources and drains. This may then be followed with a selective implant. Phosphorus or Arsenic may be implanted in accordance with one technique into the n-channel source and drain regions at higher dose to overcome the Boron. Web site: http://www.delphion.com/details?pn=US06573165__
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Methods for negative atmospheric pressure removal of arsenic and other metals Inventor(s): Bondiett; Mark (Sandy, UT), Gritton; Kenneth S. (Murray, UT) Assignee(s): Watermark Technologies, LLC (Sandy, UT) Patent Number: 6,562,241 Date filed: November 10, 2000
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Abstract: The methods and apparatus of embodiments of the present invention serve to precipitate dissolved inorganic arsenic from an aqueous solution. The pressurization/negative pressurization protocol promotes precipitation of dissolved inorganic arsenic. After pressurization/negative pressurization method is applied the newly created precipitates may be separated from the solution using known separation methods. Aeration of the solution prior to or during pressurization and addition of chemical oxidants and air injection prior to or during pressurization aid precipitation. The methods of embodiments of the present invention may be applied to batch-process and continuous, in-flow apparatus. Excerpt(s): The present invention relates to methods and apparatus for removing arsenic contaminants from water. More particularly, embodiments of the present invention create conditions that remove arsenic contaminants from anoxic or oxic water using continuous in-stream and batch process methods at atmospheric or aboveatmospheric solution pressures followed by negative pressurization of the solution. Negative solution pressurization within the treatment sequence rapidly and surprisingly increases particulation and reduces aqueous concentrations of arsenic. Domestic water supplies often come from underground aquifers which contain anoxic water that has leached through and otherwise contacted minerals, sediments and rock layers for extended periods of time. These minerals, sediments and rocks often contain high concentrations of minerals, metals and other elements and compounds that are deleterious to human health. As a consequence of this contact, water in these aquifers becomes contaminated with some of the indigenous contaminants rendering the water unsafe for human consumption. Other water sources that may be used for domestic water supplies may also become contaminated with metallic ions and other contaminants through industrial pollution and other processes. These contaminated waters, prior to human consumption, will require remediation treatments. Arsenic is one element that is often found in water sources and is pathological, in terms of human health of specific population segments, at all levels of concentration in drinking water concentrations. Several methods are known for removing arsenic species from water, however each has limitations and or disadvantages, which make embodiments of the present invention preferable in many applications. Web site: http://www.delphion.com/details?pn=US06562241__ •
Molecular, inorganic glasses Inventor(s): Aitken; Bruce G. (Corning, NY) Assignee(s): Corning Incorporated (Corning, NY) Patent Number: 6,503,859 Date filed: June 28, 2001 Abstract: The invention resides in a molecular, inorganic glass and a method of making the glass, the glass being vitreous and resistant to devitrification, that is composed, in substantial part at least, of thermally-stable, zero-dimensional clusters or molecules, composed of four atoms of arsenic and three atoms of sulfur, the glass further containing up to 12 atomic percent of germanium, adjoining clusters being bonded to each other primarily by van der Waals forces, and at least 95% of the glass composition consisting of 42-60% arsenic, 37-48% sulfur plus selenium, the selenium being 0-14%. Excerpt(s): The invention relates to molecular, inorganic glasses composed, in part at least, of thermally-stable, zero-dimensional clusters, each of which is composed of
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arsenic and sulfur atoms and associated with germanium atoms. The physical structure of a glass may be characterized by its dimensionality, that is, by the number of directions in which its components extend. Thus, vitreous selenium, which is believed to consist of intertwined chains of selenium atoms, is said to have a one-dimensional structure. Likewise, glassy AS.sub.2 S.sub.3, which consists of corrugated sheets of As.sub.2 S.sub.3 pyramids that share corners, is described as having a two-dimensional structure. Considered in these structural terms, most oxide glasses are said to be threedimensional. A certain class of crystalline, inorganic compounds, known as molecular solids, have a zero-dimensional structure. This structure consists of molecular clusters in a cage-like form. As such, the clusters are repeated periodically in three dimensions, but are only bonded to each adjacent cluster by van der Waals forces. Examples of crystalline, inorganic compounds that have such a structure are known. They include arsenic sulfide, which consists of eight atom clusters designated As.sub.4 S.sub.4, and phosphorous sulfide, which consists of 14 atom clusters designated as P.sub.4 S.sub.10. Web site: http://www.delphion.com/details?pn=US06503859__ •
Non-arsenic N-type dopant implantation for improved source/drain interfaces with nickel silicides Inventor(s): Besser; Paul R. (Austin, TX), Buynoski; Matthew S. (Palo Also, CA), Xiang; Qi (San Jose, CA) Assignee(s): Advanced Micro Devices, Inc. (Sunnyvale, CA) Patent Number: 6,518,107 Date filed: March 21, 2001 Abstract: Disadvantageous roughness of interfaces between electrically conductive NiSi layers and n-doped Si interfaces arising during conventional salicide processing for forming shallow-depth source and drain junction regions of NMOS transistors and/or CMOS devices is avoided, or at least substantially reduced, by substituting implanted non-As-containing n-type dopant ions, such as P and/or Sb ions, for the conventionally utilized implanted As n-type dopant ions. If desired, shallow-depth source and drain extensions may be formed by implantation of As-containing n-type dopant ions above the region comprising the non-As-containing dopant ions without causing roughness of the NiSi/n-doped Si interface. Excerpt(s): The present invention relates to a method of manufacturing semiconductor devices, e.g., high-density integrated circuit ("IC") semiconductor devices exhibiting reliable, high quality, adherent, low resistance, well-aligned contacts to source, drain, and gate regions of active devices, such as MOS and CMOS transistors formed in or on a semiconductor substrate, by utilizing self-aligned, metal silicide ("salicide") processing methodology. The present invention enjoys particular utility in the manufacture of highdensity integration semiconductor devices, including multi-level devices, having design rules of 0.18.mu.m and below, e.g., 0.15.mu.m and below. The escalating requirements for high density and performance associated with ultra-large scale integration (ULSI) devices necessitate design rules of 0.18.mu.m and below, such as 0.15.mu.m and below, with increased transistor and circuit speeds, high reliability, and increased manufacturing throughput. The reduction in feature sizes, e.g., of source, drain, and gate regions of transistors formed in or on a common semiconductor substrate, challenges the limitations of conventional contact and interconnection technology, including conventional photo-lithographic, etching, and deposition techniques. As a result of the ever-increasing demand for large-scale and ultra small-dimensioned IC
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devices, self-aligned techniques have become the preferred technology for forming such devices in view of their simplicity and capability of high-density integration. As device dimensions decrease in the deep sub-micron range, both vertically and laterally, many problems arise, especially those caused by an increase in the sheet resistance of the contact areas to the source and drain regions and junction leakage as junction layer thickness decreases. To overcome this problem, the use of self-aligned, highly electrically conductive metal silicides, i.e., "salicides" (derived from Self-ALIgnedsiliCIDE), has become commonplace in the manufacture of IC semiconductor devices comprising, e.g., MOS type transistors. Another technique employed in conjunction with metal silicide technology is the use of lightly-doped, shallow-depth source and drain extensions formed just at the edge of the gate region, while more heavily-doped source and drain regions, to which ohmic contact is to be provided, are laterally displaced away from the gate by provision of sidewall spacers on opposing sides of the gate electrode. Web site: http://www.delphion.com/details?pn=US06518107__ •
Preparation of arsenic pentafluoride Inventor(s): McCloskey; Joel (Phildelphia, PA), Smith; W. Novis (Philadelphia, PA) Assignee(s): Lithdyne International (Anaheim, CA) Patent Number: 6,635,231 Date filed: March 6, 2001 Abstract: A process for the preparation of high purity arsenic pentafluoride in high yield. The process uses sulfur trioxide or oleum and an excess of hydrogen fluoride to react arsenic acid or arsenic pentoxide in a reaction medium containing an excess of hydrogen fluoride to yield high purity arsenic pentafluoride as a gas. Excerpt(s): This invention relates to the preparation of anhydrous high purity arsenic pentafluoride in high yield. U.S. Pat. No. 3,875,292 to Wiesboeck et al. discloses the preparation of Arsenic pentafluoride and fluoroarsenic acids by fluorinating an arsenic source selected from arsenic acid and monofluoroarsenic acid. Therefore, there exists a need to provide high purity arsenic pentafluoride in a simple and economical procedure without the need for extensive fractionation or high-pressure equipment and not to have extensive acid gases present that require special disposal. Web site: http://www.delphion.com/details?pn=US06635231__
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Prevention of polymerization in Li/MnO2 organic electrolyte electrochemical systems Inventor(s): Atwater; Terrill B. (North Plainfield, NJ), Branovich; Louis E. (Howell, NJ), Pellegrino; Anthony G. (Middletown, NJ) Assignee(s): The United States of America as represented by the Secretary of the Army (Washington, DC) Patent Number: 6,551,748 Date filed: June 29, 2000 Abstract: This invention provides a number of phosphorous and arsenic reducing agents to eliminate gas formation and polymerization of Li/MnO.sub.2 and other lithium cells caused by the formation of dialcohol. The phosphorous reducing agents
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when added to the Li/MnO.sub.2 and other lithium battery electrolytes cause the phosphorous compound and alcohol to react and produce ether and orthophosphorous acid, which prevents gas formation and the polymerization of Li/MnO.sub.2 cells caused by the formation of dialcohol. The preferred reducing agent is phosphoric acid tri-ester. The arsenic reducing agents when added to the Li/MnO.sub.2 and other lithium battery electrolytes cause the arsenic compound and alcohol to react and produce ether and orthoarsenic acid, which also prevents gas formation and the polymerization of Li/MnO.sub.2 cells caused by the formation of dialcohol. Similar reactions and effects are also achieved with numerous other useful phosphorous and arsenic compounds that react with alcohol to produce ether and related acid compounds. Excerpt(s): The invention described herein may be manufactured, used, imported, sold, and licensed by or for the Government of the United States of America without the payment to me of any royalty thereon. The present invention relates generally to the field of lithium batteries, and more particularly to providing reducing agents that prevent gas formation and electrolyte polymerization in lithium organic manganese dioxide electrochemical cells. Portable batteries with increased energy and power densities are required as the use of portable electronic equipment by the military and civilians continues to rapidly increase. Additionally, these batteries must operate safely in all environments. Presently most military applications use the primary lithium/sulfur dioxide electrochemical system introduced to the field in the early 1980's, which provide significant increases in capacity, rate and low temperature operation capability. Although the lithium/sulfur dioxide system has served its purpose well, today's needs for portable electric power require that such primary batteries contain more energy and more power, as well as matching or surpassing the safety of current batteries. The lithium/manganese dioxide (Li/MnO.sub.2) electrochemical system may become the future primary battery in numerous military and civilian applications. Web site: http://www.delphion.com/details?pn=US06551748__ •
Process for eliminating arsenic in the presence of an absorption mass comprising partially pre-sulfurized lead oxide Inventor(s): Didillon; Blaise (Francheville, FR), Savary; Laurent (Rueil-Malmaison, FR) Assignee(s): Institut Francais du Petrole (Cedex, FR) Patent Number: 6,623,629 Date filed: March 8, 2001 Abstract: The invention concerns a process for eliminating arsenic from a hydrocarbon cut in which said cut is brought into contact with an absorption mass that is at least partially pre-sulfurized and comprises a support and lead oxide. The support, for example alumina, or said mass preferably has a specific surface area in the range 10 to 300 m.sup.2 /g, a total pore volume in the range 0.2 to 1.2 cm.sup.3 /g and a macroporous volume in the range 0.1 to 0.5 cm.sup.3 /g. The lead content of said mass, expressed as lead oxide, is preferably in the range of 5% to 50% by weight. The fraction of the sulfurized mass preferably represents at least 1/20th of the total volume of the absorption mass. Excerpt(s): The subject matter of this invention concerns a process for capturing arsenic using a mass of lead deposited on alumina, wherein the active phase is in the oxide form regarding a portion of the catalytic bed, preferably the major portion of the catalytic bed,
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and in the pre-sulphurised form regarding the other portion. Mercaptans are known to be powerful arsenic capture inhibitors. However, it has been observed that presulphurising a portion of the catalytic bed can result in a very good arsenic capture gradient over the remainder of the bed even when mercaptans are present in the feed, in contrast to that observed in the absence of a pre-sulphurisation step. Processes for cracking heavy petroleum cuts, for example catalytic cracking, visbreaking or cokefaction, produce light cuts that are strongly contaminated with various compounds containing sulphur, nitrogen and oxygen. Arsenic is often detected alongside those impurities. The sulphur-containing compounds are usually hydrogen sulfide and mercaptans. The nitrogen-containing compounds, present in the light cuts, are principally ammonia or light amines. Arsenic is itself also present in the form of compounds with the general formula AsR.sub.3, R being a hydrocarbon radical such as CH.sub.3 or a hydrogen atom. Web site: http://www.delphion.com/details?pn=US06623629__ •
Process for fabricating a deep submicron complementary metal oxide semiconductor device having ultra shallow junctions Inventor(s): Hsien; Li-Jen (Taichung, TW) Assignee(s): United Microelectronics Corp. (Hsinchu, TW) Patent Number: 6,624,014 Date filed: February 27, 2001 Abstract: A process for fabricating a deep submicron complementary metal oxide semiconductor device having ultra shallow junctions. After a gate is formed on the substrate on which an N well region and a P well region are separated from each other by shallow trench isolation, a silicon nitride is formed as a diffusion source layer. Subsequently, a P type ion implantation is performed in the N well region by using boron ions to form a P type diffusion source layer in the N well region. An N type ion implantation is performed in the diffusion source layer of the P well region by using arsenic ions to form a N type diffusion source layer on the P well region. Spacers are formed at the sidewalls of the gate by deposition and etching back. Heavy ion implantation is performed in the N well region and the P well region, respectively. Finally, a rapid thermal process is carried out to form a source/drain region and ultra shallow junctions in the complementary metal oxide semiconductor device. Excerpt(s): The present invention relates to a process for semiconductor devices. More specifically, it relates to a process for fabricating a deep submicron complementary metal oxide semiconductor device having ultra shallow junctions. The design of a lightly doped drain is widely used to reduce the short channel effects generated in NMOS and CMOS devices. It is achieved by further providing a source/drain region near the channel having less dopants than the original MOS source/drain region. By increasing the integration of the integrated circuit, the area of the semiconductor device is decreased and the design dimension is thus reduced. Due to the advances in the semiconductor technology, the integration of integrated circuit devices have been developed to deep submicron. In deep submicron complementary metal oxide semiconductor devices, the doping is carried out with an implanting energy of only thousand eV, called a shallow junction process. An ultra shallow junction is formed for the lightly doped drain to prevent the short channel effect. Web site: http://www.delphion.com/details?pn=US06624014__
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Process for preparation of an EUO-structural-type zeolite, the zeolite that is obtained and its use as catalyst for isomerization of C8-aromatic compounds Inventor(s): Alario; Fabio (Neuilly sur Seine, FR), Kolenda; Frederic (Chaponost, FR), Merlen; Elisabeth (Rueil-Malmaison, FR), Rouleau; Loic (Oullins, FR) Assignee(s): Institut Francais du Petrole (Cedex, FR) Patent Number: 6,616,910 Date filed: May 7, 2001 Abstract: This invention relates to a process for synthesis of an EUO-structural-type zeolite that comprises at least one element X that is selected from among silicon and germanium and at least one element T that is selected from among aluminum, iron, gallium, boron, titanium, vanadium, zirconium, molybdenum, arsenic, antimony, chromium and manganese, whereby said process is carried out in the presence of an organic structuring agent that is derived from dibenzyldimethylammonium (DBDMA) or its precursors and in the presence of nuclei of at least one zeolitic material of the same structure as the zeolite that is to be synthesized. The zeolite that is thus obtained has an X/T ratio of between 5 and 50. It is used in particular as a catalyst, for example in a process for isomerization of aromatic compounds with 8 carbon atoms per molecule. Excerpt(s): This invention relates to a process for preparation of an EUO-structural-type zeolite that contains, after synthesis, in its intracrystalline pores, a nitrogen-containing organic cation with a chemical formula that is defined and synthesized with nuclei to obtain a zeolite that has a well-determined chemical composition of its crystalline framework. The invention also relates to the zeolite that is prepared by this process and the use of said zeolite in a process for isomerization of aromatic compounds with 8 carbon atoms that are also called "C8-aromatic fractions" in the presence of a catalyst with an EUO zeolite base that is prepared according to the process of this invention. The isomerization of xylenes of ethylbenzene or a mixture of xylenes and ethylbenzene requires the presence of an acid function and a metal of group VIII. The main purpose of the isomerization of the C8-aromatic fractions is to produce the paraxylene that is the most desired isomer because of its application particularly in the textile industry. The isomerization reaction of the C8-aromatic compounds leads to parasitic reactions that result from the opening of naphthene rings that may or may not be followed by cracking or else reactions of dismutation and/or transalkylation of the C8 aromatic compounds that generate undesirable aromatic compounds. Catalysts for isomerization of aromatic compounds with 8 carbon atoms were already described. Patents U.S. Pat. Nos. 4,723,051 and 4,665,258 describe, for example, optimized formulations with a mordenite zeolite base and a metal of group VIII, but they result in catalysts with which the parasitic reactions are non-negligible. These catalysts lack selectivity of paraxylene in favor of the above-mentioned parasitic reactions that constitute net losses for the desired isomerization reaction. Web site: http://www.delphion.com/details?pn=US06616910__
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Process for preparing a zeolite with structure type MTT using specific template precursors Inventor(s): Benazzi; Eric (Chatou, FR), Kolenda; Frederic (Francheville le Haut, FR), Rouleau; Loic (Oullins, FR) Assignee(s): Institut Francais du Petrole (FR) Patent Number: 6,548,040 Date filed: September 29, 2000 Abstract: The present invention concerns a process for synthesising a zeolite with structure type MTT comprising at least one element X selected from silicon and germanium and at least one element T selected from aluminium, iron gallium, boron, titanium, vanadium, zirconium, molybdenum, arsenic, antimony, chromium and manganese, comprising reacting an aqueous mixture comprising at least one source of at least one element X, at least one source of at least one element T, and at least one precursor of an organic compound comprising at least one alkylated polymethylene.alpha.-.omega. diammonium derivative, characterized in that at least one precursor is selected from monoamines. The present invention also concerns the use of the zeolite obtained as a catalyst in a process for converting hydrocarbon-containing feeds, as an adsorbent to control pollution and as a molecular sieve for separation. Excerpt(s): The present invention relates to a novel process for preparing zeolites with structure type MTT. More particularly, for example, this process is applicable to synthesising ZSM-23 zeolite. ZSM-23 zeolite generally HAS the following formula in the anhydrous form: 0-20 R.sub.2 O: 0-10 T.sub.2 O.sub.3 : 100XO.sub.2 where R represents a monovalent cation or 1/n of a cation with valency n, T represents at least one element selected from aluminium, iron, gallium, boron, titanium, vanadium, zirconium, molybdenum, arsenic, antimony, chromium and manganese, and X represents silicon and/or germanium. Zeolites with structure type MTT such as ZSM-23 zeolite are generally synthesised by mixing, in an aqueous medium, at least one source of silica and/or germanium and at least one source of at least one element selected from aluminium, iron, gallium, boron, titanium, vanadium, zirconium, molybdenum, arsenic, antimony, chromium and manganese in the presence of at least one organic template such as a quaternary diammonium compound. The mixture is generally maintained at a certain temperature until the zeolite crystallises. Other zeolites have structure type MTT and differ from ZSM-23 zeolite in the mode of preparation, in particular in the organic template used. These are EU-13 zeolite (European patent EP-A-0 108 486), using a quaternary methylated ammonium or phosphonium salt, ISI-4 zeolite (EP-A-0 102 497) using ethylene glycol or a monoethanolamine, SSZ-32 zeolite (U.S. Pat No. 4,483,835) using imidazole derivatives or KZ-1 zeolite using a variety of amines (L. M. Parker et al., Zeolites, 3, 8, 1988). Web site: http://www.delphion.com/details?pn=US06548040__
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Process for producing a coating on a refractory structural member Inventor(s): Kock; Wulf (Alzenau, DE), Kruger; Frank (Wolfersheim, DE), Lupton; David (Gelnhausen, DE), Manhardt; Harald (Bruchkobel, DE), Merker; Jurgen (Kahla, DE) Assignee(s): W. C. Heraeus GmbH & Co. KG (DE) Patent Number: 6,607,787 Date filed: August 7, 2001
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Abstract: A process for producing a coating on a refractory structural member, in which a noble metal alloy is applied as a coating material to the refractory structural member. The noble metal alloy contains, among other constituents, an oxidizable substance, which includes boron and/or phosphorus and/or antimony and/or arsenic. The refractory structural member and the coating are heated at least once in an oxygencontaining atmosphere to a temperature T that is greater than or equal to the liquidus temperature T.sub.L of the noble metal alloy. The oxidizable substance is oxidized during this heating process, and the oxide that has formed is at least partially vaporized. The temperature T is maintained until the proportion of oxidizable substance in the coating is <0.1 atomic percent, and the coated refractory structural member is then cooled. Excerpt(s): The invention concerns a process for producing a coating on a refractory structural member, in which a noble metal alloy is applied as a coating material to the refractory structural member. The noble metal of the noble metal alloy has a melting point greater than 1,400.degree. C. and consists of platinum and/or iridium and/or rhodium and/or ruthenium and/or gold. The noble metal alloy is used in the form of a powder, and the refractory structural member is coated with the powder. The invention also relates the use of a coating produced in this way on refractory structural members in the glass industry. Structural members that are used in the production of glass, especially in the area of glass melting furnaces and feeders, are exposed to high temperatures and corrosive atmospheres. Especially severe corrosive attack occurs, for example, at the three-phase boundary between the molten glass, the gas atmosphere above the molten glass, and the refractory material. This causes the refractory material to erode. Refractory material that has worn away contaminates the molten glass and reduces its quality. To guarantee high quality of the glass and to prolong the useful life of the structural members, it is customary to coat, clad, or line the structural members with a noble metal. In the coating processes described above, it is necessary to include a process stop in which the last layer, which contains the noble metal and which will come into contact with the molten glass and corrosive atmosphere, is subsequently consolidated and its open porosity is closed. This is disadvantageous and cost-intensive. Web site: http://www.delphion.com/details?pn=US06607787__ •
Process for producing a high and low pressure integrated turbine rotor Inventor(s): Fujita; Akitsugu (Nagasaki, JP), Kamada; Masatomo (Yokohama, JP) Assignee(s): Mitsubishi Heavy Industries, Ltd. (Tokyo, JP) Patent Number: 6,569,269 Date filed: November 14, 2000 Abstract: In CrMoV based heat resistant steels and tungsten-containing CrMoV based heat resistant steels, trace impurities, such as phosphorus, sulfur, copper, aluminum, arsenic, tin, and antimony are reduced lower than a specific level. Furthermore, alloy steels having increased creep strengths in a creep test on an unnotched test piece by addition of trace impurities such as cobalt, tantalum, nitrogen, boron, or the like is used. The production process therefor includes heating a turbine rotor member having the specific composition at a temperature between 980.degree. C. and 1100.degree. C. at a part corresponding to the high-pressure part thereof and at a temperature between 850.degree. C. and 980.degree. C. at a part corresponding to the low-pressure part thereof, and cooling the turbine rotor member at a cooling rate higher than an air impact cooling rate at the part corresponding to the high-pressure part thereof, and at a cooling
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rate no lower than an oil quenching rate at the part corresponding to the low-pressure part thereof. The rotor member has a creep rupture time in a creep test on a notched test piece of 10000 hours or longer. Excerpt(s): The present invention relates to turbine rotors and in particular it relates to high pressure and low pressure integrated type turbine rotors used in steam turbines employed in thermal electric power generation. Conventionally, as one type of turbine rotor for steam turbines for thermal electric power generation, high pressure and low pressure integrated turbine rotors utilizing integrated materials from the high pressure part to the low-pressure part have been known. The steam turbine is exposed to hightemperature and high-pressure steam on the side of its steam inlet. As the end portion is being approached, the temperature and pressure of steam decrease, so that the steam turbine is exposed to steam that has a highly expanded volume. Therefore, in the highpressure part, the turbine blades are short in length and the stress applied to the turbine rotor is relatively small, and thus the diameter of the turbine rotor may be small. On the other hand, in the low pressure part, to receive the force exerted by a larger amount of steam, the length of the turbine blades must be large and the diameter of the turbine rotor must be large, resulting in a large stress being applied to the turbine rotor. Therefore, the characteristics required for the high pressure and low pressure integrated type rotors are high temperature strength, in particular excellent creep strength at the high-pressure part, and on the other hand, at the low pressure part, mechanical strength and excellent toughness at ordinary temperature. Conventionally, as examples of heatresistant steels for use in high pressure and low pressure integrated type turbine rotors, CrMoV steels, which belong to low-alloys, and 12Cr steels, which belong to high-Cr steels, have been exclusively used (see Japanese Patent Applications, First Publications (Kokai), Nos. Sho 60-165359 and Sho 62-103345). A process for obtaining a turbine rotor having creep properties and toughness simultaneously has been proposed, in which a CrMoV based steel species is processed into a turbine rotor member and the highpressure and low-pressure parts of a single turbine rotor are separately heat treated under different conditions. For example, Japanese Patent Application, First Publication (Kokai), No. Hei 5-195068 discloses a process for obtaining a high pressure and low pressure integrated type turbine rotor having creep strength at high temperatures and toughness simultaneously, in which the high pressure part of a rotor member is quenched after heating at a temperature higher than the low pressure part and then the whole rotor member is tempered at a predetermined temperature. Japanese Patent Application, First Publication (Kokai) No. Hei 8-176671 discloses a process for obtaining a high pressure and low pressure integrated turbine rotor having excellent creep properties at high temperatures and toughness simultaneously, in which a rotor member is normalizing-treated at 1100 to 1150.degree. C. and pearlite-transformed, further normalizing-treated at 920 to 950.degree. C., the high pressure part and low pressure part are quenched at different temperatures, and then the whole rotor member is tempered. Web site: http://www.delphion.com/details?pn=US06569269__
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Process for the epoxidation of CIS double bonds Inventor(s): Droste; Elisabeth (Goslar, DE), Krebs; Bernt (Muenster, DE), Oenbrink; Georg (Duelmen, DE), Piepenbrink; Markus (Muenster, DE), Schiffer; Thomas (Haltern, DE), Vollmer; Guido (Guetersloh, DE) Assignee(s): Degussa AG (Duesseldorf, DE) Patent Number: 6,610,864 Date filed: November 5, 2001 Abstract: The selective epoxidation of cis double bonds of macrocyclic aliphatic hydrocarbons having 8 to 20 ring carbon atoms occurs by a catalytic process. The macrocyclic aliphatic hydrocarbons may optionally contain one or more side chains and in which at least one further trans double bond is simultaneously present. The used catalyst system consists of a cationic phase-transfer catalyst and an anionic polyoxometallate which is a polytungstate or a polymolybdate. Additionally, it comprises one or more elements selected from germanium, tin, lead, arsenic, antimony, bismuth, selenium, tellurium and polonium, and optionally one or more transition metals from group 4 to 12 of the Periodic Table. Excerpt(s): The present invention relates to a catalytic process for the selective epoxidation of cis double bonds in macrocyclic aliphatic hydrocarbons. Macrocyclic olefins are important building blocks in the synthesis of numerous specialty chemicals. An important representative of such cyclic hydrocarbons is cis,trans,trans-1,5,9cyclododecatriene, which is formed on an industrial scale by the cyclotrimerization of 1,3-butadiene, preferably on a titanium catalyst, and is used as the precursor for cyclododecanone, dodecanedioc acid and laurolactam/nylon 12. Numerous processes for the epoxidation of macrocyclic olefins are known. Organic peracids, such as performic acid, peracetic acid or perpropionic acid, can be employed. EP-A-0 033 763 (Degussa AG) describes the reaction of cyclododecatriene (CDT) with performic acid, which is formed in situ from hydrogen peroxide and formic acid. EP-A-0 032 990 (Henkel KGaA, Degussa AG) describes the reaction of derivatives of cyclododecatriene with performic acid. In the case of acid-sensitive olefins, problems arise from side reactions or subsequent reactions which the epoxides can undergo under the acidic reaction conditions. The acid-catalyzed addition of water onto the epoxide results in a vicinal diol; isomerization at the double bonds also occurs. Web site: http://www.delphion.com/details?pn=US06610864__
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Process for the hydroformylation of olefinically unsaturated compounds in a nonaqueous ionic solvent Inventor(s): Commereuc; Dominique (Meudon, FR), Favre; Frederic (Saint Fons, FR), Olivier-Bourbigou; Helene (Rueil Malmaison, FR) Assignee(s): Institut Francais du Petrole (Rueil Malmaison Cedex, FR) Patent Number: 6,617,474 Date filed: January 24, 2002 Abstract: A process for the hydroformylation of an olefinically unsaturated compound in the liquid phase by reaction, in a reaction section, with carbon monoxide and hydrogen in the presence of a polar phase comprising:a non-aqueous ionic liquid which is at least partly miscible with the reaction products and comprises a salt of general
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formula Q.sup.+ A.sup.-, in which Q.sup.+ represents a quaternary ammonium and/or phosphonium and A.sup.- represents an anion;and a catalyst comprising a compound or a complex of a transition metal of groups 8, 9 and 10, optionally co-ordinated with a ligand containing at least one atom of phosphorus, arsenic, antimony or nitrogen,comprises addition to the medium, after the reaction section, of an organic solvent in a manner such as to improve the separation by demixing of the crude reaction products from the said polar phase, which is recycled to the reaction section. Excerpt(s): The present invention relates to an improved process for the hydroformylation of olefinically unsaturated compounds. The invention also relates to an installation for carrying out the said process. The hydroformylation of olefinic compounds is a reaction of great industrial importance, and the majority of processes utilize homogeneous catalysts dissolved in an organic phase made up of the reagents, the products and, where appropriate, an excess of ligand, with the result that difficulties are encountered in separating off and recovering the catalyst, in particular if this is employed in a relatively large amount, as is the case with catalysts based on cobalt, or if this is a noble metal, as is the case with catalysts based on rhodium. One solution aimed at solving this problem has been mentioned by Bartik et al.: Organometallics (1993) 12 164-170, J. Organometal. Chem. (1994) 480 15-21 and by Beller et al.: J. Molecular Catal. A: Chemical (1999) 143 31-39. It consists of carrying out the hydroformylation in the presence of an aqueous solution comprising a cobalt complex which is rendered watersoluble due to the presence of a phosphine-sulfonate ligand, such as the sodium salt of trisulfonated triphenylphosphine or of a trisulfonated tris-(alkylphenyl)-phosphine. The Patent Application WO-A-97/00132 describes cobalt clusters substituted by trialkoxysilylmethyl groups, which renders them soluble in water. In this manner, the organic phase containing the aldehydes is easily separated from the aqueous phase containing the catalyst. Web site: http://www.delphion.com/details?pn=US06617474__ •
Semiconductor device and method of fabricating thereof Inventor(s): Akaishi; Yumiko (Gunma, JP), Kikuchi; Shuichi (Gunma, JP), Suzuki; Takuya (Saitama, JP) Assignee(s): Sanyo Electric Co., Ltd. (Osaka, JP) Patent Number: 6,599,782 Date filed: November 20, 2000 Abstract: To enhance the withstand voltage of an LD MOS transistor, a method of fabricating a semiconductor device according to the invention is characterized in that a process for forming a drift region is composed of a step for implanting phosphorus ions and arsenic ions different in a diffusion coefficient into the superficial layer of a substrate, a step for forming a selective oxide film (a first gate insulating film) 9A and an element isolation film 9B by selective oxidation and diffusing the phosphorus ions and the arsenic ions and a step for implanting and diffusing boron ions, and in that in the step for forming the selective oxide film 9A and the element isolation film 9B by selective oxidation in a state in which an oxide film and a polycrystalline silicon film are laminated on the substrate, only a drift region formation region is selectively oxidized in a state in which the polycrystalline silicon film is removed. Excerpt(s): The present invention relates to a semiconductor device and method of fabricating thereof, in detail, further relates to the technology of a lateral double-
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diffused (LD) MOS transistor as a high-voltage device utilized for IC for driving a liquid crystal and others. In LD MOS transistor structure, a new diffusion region is formed by diffusing impurities the respective conductive types of which are different into a diffusion region formed on the side of the surface of a semiconductor substrate so as to utilize difference in diffusion in a lateral direction between these diffusion regions for effective channel length, and the corresponding device becomes a device suitable for reducing on-state resistance because a short channel is formed. The N+-type diffusion region 4 functions as a source region, the N+-type diffusion region 5 functions as a drain region and the N-type well region 2 formed from an region under the gate electrode 7 so that it surrounds the drain region functions as a drift region. S and D respectively denote a source electrode and a drain electrode, a reference number 12 denotes a P+type diffusion region for applying electric potential to the P-type body region 3 and 11 denotes a layer insulation film. Web site: http://www.delphion.com/details?pn=US06599782__ •
Semiconductor device and method of manufacture thereof Inventor(s): Yamamoto; Naoki (Kawaguchi, JP) Assignee(s): Hitachi, Ltd. (Tokyo, JP) Patent Number: 6,503,788 Date filed: August 16, 2000 Abstract: In order to realize a dual gate CMOS semiconductor device with little leakage of boron that makes it possible to divisionally doping a p-type impurity and an n-type impurity into a polycrystalline silicon layer with one mask, a gate electrode has a high melting point metal/metallic nitride barrier/polycrystalline silicon structure. The boron is pre-doped in the polycrystalline silicon layer. The phosphorus or arsenic is doped in an n-channel area. Then, the annealing in a hydrogen atmosphere with vapor added therein is performed. As a result, the boron is segregated on the interface of the metallic nitride film and the phosphorus is segregated on the interface of the gate oxide film, for forming an n+ gate. Excerpt(s): The present invention relates to a CMOS (Complementary Metal-oxide Semiconductor) type semiconductor device having as a gate electrode p type and n type conductive polycrystalline silicon and a method of manufacture thereof. The current trend of the semiconductor device has been changed from a CMOS semiconductor device whose gate electrode is composed of only polycrystalline silicon containing an ntype impurity into the so-called dual gate CMOS semiconductor device in which the gate electrode of an n-channel MOS transistor is composed of polycrystalline silicon containing an n-type impurity and the gate electrode of a p-channel MOS transistor is composed of polycrystalline silicon containing a p-type impurity. This dual gate contains a silicon oxide film, a silicon nitride film or resist coated on the surface of the polycrystalline silicon except a target area. A target area (for example, n-type) impurity is implanted in the non-coated area with these films as a mask by means of the ionimplantation technique or the diffusion technique. After removing this mask materials, the surface of the polycrystalline silicon on the area having the above-mentioned impurity is covered with the similar mask materials. The impurity having the opposite conductive type (for example, p type) to the above-mentioned impurity is implanted in the non-covered area by means of the ion-implantation technique. For dividing the polycrystalline area into an n+ and a p+ conductive areas, as mentioned above, a mask material is formed on a specific area in doping a target impurity, which needs two
Patents 189
associative processes of forming a mask. It is thus necessary to perform each process of forming a mask film, doing photolithography, and dry-etching a mask film twice. It means that the dual gate CMOS semiconductor composed as above has more manufacturing steps than the CMOS semiconductor device composed of polycrystalline silicon containing only one conductive impurity. This brings about the lowering of a manufacturing yield and the rise of a manufacturing cost of the semiconductor device and therefore the rise of a product cost. Further, the slip of fitting the mask patterns may be brought about in dividing the n-type and the p-type areas in the photolithography process. Hence, the fitting allowance is required, which has been an obstacle to finning the element and enhancing the concentration of the semiconductor device. Web site: http://www.delphion.com/details?pn=US06503788__ •
Semiconductor device with lightly doped drain layer Inventor(s): Eikyu; Katsumi (Tokyo, JP), Nishida; Yukio (Tokyo, JP) Assignee(s): Mitsubishi Denki Kabushiki Kaisha (Tokyo, JP) Patent Number: 6,576,965 Date filed: October 8, 1999 Abstract: Arsenic is ion-implanted through a thin insulative through film formed on an active region in the vicinity of a gate insulating film towards the inside of a semiconductor substrate at a dose of 3E13 cm.sup.-2 at an energy of 100 keV at a tilt angle, which is made by an ion implantation direction and a normal direction (NL), of 45 degrees with respect to a (100) surface of the semiconductor substrate, with which a channeling phenomenon can be caused. Next, phosphorus is ion-implanted towards the inside of the semiconductor substrate at a dose of 1E13 cm.sup.-2 at an energy of 50 keV at an angle with which no channeling phenomenon can be caused. After that, a sidewall is formed and then arsenic is ion-implanted towards the inside of the semiconductor substrate at a dose of 4E15 cm.sup.-2 at an energy of 50 keV at an angle with which no channeling phenomenon can be caused, to form n.sup.+ layers. Excerpt(s): The present invention relates to a semiconductor device for a semiconductor LSI, and more particularly to a lightly doped drain (hereinafter, referred to as LDD) layer structure and a technique of forming the same. (2) In the double LDD layer structure of the second prior art, a double-layered structure consisting of the outer P layer of relatively low concentration and the inner arsenic layer of relatively high concentration located near a surface forms a step-like impurity concentration distribution, and therefore the LDD layer made of P of relatively low concentration relieves the drain electric field and the LDD layer made of arsenic of relatively high concentration reduces the resistance element, to thereby achieve a driving capability higher than the first prior art. Thus, it is disadvantageous that the second prior art can show only intermediate characteristics between the single LDD layer structure of the first prior art and a single drain structure in an integrated evaluation of its characteristics such as driving capability, withstand voltage and hot-carrier resistance. Web site: http://www.delphion.com/details?pn=US06576965__
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Stabilization of arsenic-contaminated materials Inventor(s): Chowdhury; Ajit K (Madison, WI), Tickanen; Lane D (Madison, WI) Assignee(s): RMT, Inc. (Madison, WI) Patent Number: 6,543,964 Date filed: December 29, 2000 Abstract: A method for stabilizing arsenic in a waste matrix includes the steps of combining with the waste matrix an agent for controlling the oxidation-reduction potential of the matrix, an agent for controlling the pH of the matrix and an agent for adsorbing or coprecipitating the arsenic in the matrix. Excerpt(s): Not-applicable. The present invention relates to methods for treating an arsenic-contaminated waste matrix to stabilize the arsenic and reduce arsenic leaching to contaminant acceptable levels. Arsenic, which is carcinogenic in its inorganic form, is identified in the Resource Conservation Recovery Act (RCRA) as a hazardous metal and is reportedly the third most common regulated inorganic contaminant found at Superfund sites. wood preservative manufacturing wastes. Web site: http://www.delphion.com/details?pn=US06543964__
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Trench transistor with self-aligned source Inventor(s): Mo; Brian Sze-Ki (Stanford, CA) Assignee(s): Fairchild Semiconductor Corporation (South Portland, ME) Patent Number: 6,583,010 Date filed: April 20, 2001 Abstract: A trench field-effect transistor with a self-aligned source. At least a portion of the source implantation dose (604) is implanted underneath the gate (610) of a trench transistor by implanting an a non-orthogonal angle to the sidewall (608) of the trench. In one embodiment, a slow diffuser, such as arsenic, is implanted to minimize the postimplant diffusion. The resulting structure ensures gate-source overlap, and a consistent, small, gate-source capacitance with a lower thermal budget for the resultant device. The narrow depth of the source, in conjunction with its unique L-shape, improves device ruggedness because the source doping does not compensate the heavy body doping as much as with conventional devices. In one embodiment, the substrate is rotated 90 degrees within the implanter to implant both sidewalls of a trench. Excerpt(s): The present invention relates in general to field effect transistors, and in particular to trench metal-oxide semiconductor field-effect transistors ("MOSFETs"), and methods of their manufacture. The gate conductive material may be doped polysilicon or the like, and forms an overlap 22 with the drain and another overlap 24 with the source. The overlaps ensure that the active region turns on when voltage is applied to the gate. In conventional devices, the overlap is achieved by implanting a mobile dopant, such as phosphorous, in the source region, and then driving the dopant into the substrate such that it overlaps the gate. The dopant diffuses laterally as well as vertically, thus consuming space between gates of adjacent cells. Trench transistors are often used in power-handling applications, such as DC--DC conversion, power switching, as in a computer power management circuitry, for example. Trench transistors often operate at 5-100 V, as compared to 2-5 V for a logic-type MOSFET. The gate of a trench transistor is made relatively "wide" to improve the current-handling
Patents 191
capability of the trench transistor, and a heavy body 30 is formed to make the device more rugged and able to operate more effectively during switching. Web site: http://www.delphion.com/details?pn=US06583010__ •
Zinc oxide films containing p-type dopant and process for preparing same Inventor(s): Ryu; Yungryel (Columbia, MO), White; Henry W. (Columbia, MO), Zhu; Shen (Huntsville, AL) Assignee(s): The Curators of the University of Missouri (Columbia, MO) Patent Number: 6,610,141 Date filed: November 15, 2001 Abstract: A p-type oxide film and a process for preparing the film and p-n or n-p junctions is disclosed. In a preferred embodiment, a p-type zinc oxide film contains arsenic and is grown on a gallium arsenide substrate. The p-type oxide film has a net acceptor concentration of at least about 10.sup.15 acceptors/cm.sup.3, a resistivity of no greater than about 1 ohm-cm, and a Hall mobility of between about 0.1 and about 50 cm.sup.2 /Vs. Excerpt(s): This invention is directed to oxide films, such as zinc oxide (ZnO) films, for use in electrically excited devices such as light emitting devices (LEDs), laser diodes (LDs), field effect transistors (FETs), photodetectors, and transducers. More particularly, this invention is directed to oxide films containing a p-type dopant for use in LEDs, LDs, FETs, and photodetectors wherein both n-type and p-type materials are required, for use as a substrate material for lattice matching to other materials in such devices, and for use as a layer for attaching electrical leads. For some time there has been interest in producing wide band gap semiconductors to produce green/blue LEDs, LDs and other electrical devices. Historically, attempts to produce these devices have centered around zinc selenide (ZnSe) or gallium nitride (GaN) based technologies. However, these approaches have not been entirely satisfactory due to the short lifetime of light emission that results from defects, and defect migration, in these devices. Recently, because ZnO has a wide direct band gap of 3.3 eV at room temperature and provides a strong emission source of ultraviolet light, ZnO thin films on suitable supporting substrates have been proposed as new materials for light emitting devices and laser diodes. Undoped, as well as doped ZnO films generally show n-type conduction. Impurities such as aluminum and gallium in ZnO films have been studied by Hiramatsu et al. who report activity as n-type donors (Transparent Conduction Zinc Oxide Thin Films Prepared by XeCl Excimer Laser Ablation, J. Vac. Sci. Technol. A 16(2), Mar/Apr 1998). Although n-type ZnO films have been available for some time, the growth of p-type ZnO films necessary to build many electrical devices requiring p-n junctions has to date been much slower in developing. Web site: http://www.delphion.com/details?pn=US06610141__
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Patent Applications on Arsenic 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 arsenic: •
Absorbent for arsenic species and method of treating arsenic-contaminated waters Inventor(s): Vempati, Rajan K.; (Plano, TX) Correspondence: Charles D. Gunter, Jr.; BRACEWELL & PATTERSON, LLP; Suite 1600; 201 Main Street; Fort Worth; TX; 76102-3105; US Patent Application Number: 20030116504 Date filed: July 24, 2001 Abstract: The present invention is directed to an adsorbent for removing arsenic species from ground water and/or surface water systems. Such adsorbent removes both As(III) and As(V), thereby providing potable water. Also provided is a method and/or device (e.g., filter) for removing arsenic species from contaminated waters utilizing such adsorbent. Excerpt(s): The present invention relates to an adsorbent for arsenic species and a method and/or device for removing arsenite (As(III)) and arsenate (As(V)) from ground water and surface water systems. Particularly, the present invention relates to natural zeolite coated with nanophase Mn--Fe oxides (NZNPF), and a method and/or device for removing As(III) and As(V) from arsenic-contaminated waters using NZNPF. High concentrations of arsenic in drinking water result from either anthropogenic contamination or weathering of naturally occurring subsurface materials. The two most important anthropogenic sources of arsenic are agricultural chemicals and wood preservatives. Furthermore, use of arsenic species in manufacturing of sulfuric acid and leather tanning have resulted in significant contamination. In the geological occurrence, arsenic is found at high levels in primary sulfide minerals, such as arsenopyrite (FeAsS), pyrite (FeS.sub.2), pyrrhotite (Fe.sub.1-xS), orpiment (As.sub.2S.sub.3) and realgar (AsS). In addition, its ionic and valence states allow arsenic to substitute in trace amounts for many elements in silicate rock-forming minerals (Onken and Hossner, 1996). The chemical similarity between arsenate and phosphate lead to anion solid solutions between such minerals arsenate pyromorphite (Pb.sub.5(PO.sub.4).sub.3Cl) and mimetite (Pb.sub.5(AsO.sub.4).sub.3Cl (Klein and Hurlbut, 1985). In surface water systems, arsenic can be dissolved either directly from weathering of geological materials (Baker et al, 1998) or through mixing with high-arsenic geothermal waters (Wilkie and Hering, 1998). In groundwater systems, arsenic can also be derived from the dissolution of As-bearing iron oxides in unconsolidated aquifer materials (Korte, 1991). Aqueous arsenate concentrations are controlled by anion exchange and coprecipitation with Fe and Mn oxyhydroxides and are therefore a function of Eh and pH. Arsenate anion exchange dynamics are analogous to phosphate with competition for exchange sites generally favoring phosphate over arsenate. As(III) exists as a neutral As(OH).sub.3 species and therefore is mobile under most conditions. Hence, As(III) has to be oxidized to As(V) which will result in formation of arsenate. The arsenate ion can then be adsorbed on to amphoteric Fe oxides. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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This has been a common practice outside the United States prior to December 2000.
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Additive for nonaqueous-electrolyte secondary battery Inventor(s): Endo, Shigeki; (Tokorozawa-shi, JP), Ogino, Takao; (Tokorozawa-shi, JP), Otsuki, Masashi; (Musashimurayama-shi, JP) Correspondence: Oliff & Berridge; P O Box 19928; Alexandria; VA; 22320; US Patent Application Number: 20030175597 Date filed: March 31, 2003 Abstract: The present invention provides an additive which is able to make a nonaqueous-electrolyte secondary cell or a non-aqueous electrolyte electric double layer capacitor which is excellent in low-temperature characteristics, while maintaining a necessary cell properties, and a non-aqueous-electrolyte secondary cell or a nonaqueous electrolyte electric double layer capacitor that contains therein the additive. The additive contains at least one of tautomers of phosphazene derivatives represented by formulae (1) and (2): 1wherein R.sup.1, R.sup.2 and R.sup.3 independently represent a monovalent substituent or a halogen element; X represents a substituent containing at least one selected from a group of carbon, silicon, germanium, tin, nitrogen, phosphorus, arsenic, antimony, bismuth, oxygen, sulfur, selenium, tellurium and polonium; and Y.sup.1 and Y.sup.2 independently represent a divalent connecting group, a divalent element or a single bond. Excerpt(s): The present invention relates to a non-aqueous electrolyte secondary cell which is excellent in self-extinguishability or flame retardancy, deterioration resistance, and low-temperature characteristics, while maintaining the same cell properties as those of conventional non-aqueous electrolyte secondary cells. Further, the present invention relates to a non-aqueous electrolyte double layer capacitor which is used for various energy storage devices such as backup power supplies and auxiliary power supplies, and more particularly to a non-aqueous electrolyte electric double layer capacitor which is excellent in self-extinguishability or flame retardancy, deterioration resistance, and low-temperature characteristics. Conventionally, nickel-cadmium cells have been the main cells used as secondary cells for memory-backup or sources for driving AV (Audio Visual) and information devices, particularly personal computers, VTRs (video tape recorders) and the like. Lately, non-aqueous electrolyte secondary cells have been drawing a lot of attention as a replacement for the nickel-cadmium cells because nonaqueous electrolyte secondary cells have advantages of high voltage, high energy concentration, and displaying excellent self-dischargeability. Various developments of the non-aqueous electrolyte secondary cells have been performed and a portion of these developments has been commercialized. For example, more than half of notebook type personal computers, cellular phones and the like are driven by the non-aqueous electrolyte secondary cells. Carbon is often used as a cathode material in the nonaqueous electrolyte secondary cells, and various organic solvents are used as electrolytes in order to mitigate the risk when lithium is produced on the surface of cathode, and to increase outputs of driven voltages. Further, particularly in nonaqueous electrolyte secondary cells for use in cameras, alkali metals (especially, lithium metals or lithium alloys) are used as the cathode materials, and aprotic organic solvents such as ester organic solvents are ordinarily used as the electrolytes. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Arsenic removal catalyst and method for making same Inventor(s): Bhan, Opinder Kishan; (Katy, TX) Correspondence: John J. Cikut; c/o Shell Oil Company; Legal-Intellectual Property; P.O. Box 2463; Houston; TX; 77252-2463; US Patent Application Number: 20030111391 Date filed: December 17, 2001 Abstract: A catalyst for removing arsenic from petroleum feedstocks comprising a porous refractory support impregnated with at least 8 wt. % of a Group VIB metal and an amount of Group VIII metal such that the atomic ratio of Group VIII metal to Group VIB metal is between about 1.5 and 2.5. A method of making such catalyst and a process for removing arsenic metals from a petroleum fraction using said catalyst. Excerpt(s): This invention relates to a catalyst for removal of arsenic from hydrocarbon oils and fractions and a method of making such catalyst. Arsenic is naturally present in petroleum feedstocks. Although the concentration of arsenic is low in most petroleum feeds, some crude oils, especially those found on the West Coast of the United States, contain high levels of arsenic. Some shale oils are also known to have high levels of arsenic. In these and other feedstocks, arsenic is usually found in the form of organometallic complexes and is present in light petroleum fractions such as naphtha and distillates. This arsenic is deposited on hydrotreating catalysts during operations designed to remove sulfur and nitrogen compounds. The deposition of only 0.1 wt. % arsenic on a hydrotreating catalyst can cause significant catalyst deactivation. In some services, as little as 0.5 wt. % arsenic deposited on a catalyst can cause the loss of more than 70% of such catalyst activity. Refiners cope with this problem by regularly replacing conventional hydrotreating catalysts that have been poisoned by arsenic. Heretofore, catalysts having specific activity and selectivity for arsenic removal have not been developed. The present invention provides for a catalyst that is effective at selectively removing arsenic from petroleum feedstocks, particularly from naphtha and light distillates, while simultaneously catalyzing the removal of sulfur and nitrogen. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Arsenic removal from aqueous media using chemically treated zeolite materials Inventor(s): Litz, John E.; (Lakewood, CO), Williams, Charles S.; (Golden, CO) Correspondence: DORSEY & WHITNEY, LLP; INTELLECTUAL PROPERTY DEPARTMENT; 370 SEVENTEENTH STREET; SUITE 4700; DENVER; CO; 80202-5647; US Patent Application Number: 20030132155 Date filed: September 25, 2002 Abstract: Systems and methods are provided for the removal and disposal of arsenic from an aqueous medium. The systems and methods include the removal of arsenic from a source by contact with either a chemically treated natural or synthetic zeolite, for example a ferric-loaded zeolite. The spent zeolite is disposed of at an appropriate arsenic disposal site. A system for monitoring and maintaining an arsenic removal/disposal system by an off-site provider is also disclosed. Excerpt(s): The present non-provisional patent application claims priority to U.S. Provisional Application Serial No. 60/325,265, filed on Sep. 26, 2001, entitled TRACE
Patents 195
ELEMENT REMOVAL FROM AQUEOUS MEDIA USING CHEMICALLY TREATED ZEOLITE MATERIALS, which is incorporated herein by reference. The invention generally relates to the removal of arsenic from aqueous media. More specifically, the invention provides systems and methods for cost effectively removing arsenic from water as it is treated in a water treatment facility, and in particular, to systems and methods for the removal and disposal of arsenic from drinking water by contacting the water with chemically treated zeolite materials before or after the water has been purified in a water treatment facility. Cities and towns throughout the world depend on having clean potable water supplies. The dependence on clean water has increased as the population of the world has increased, especially as industrial use of rivers and lakes have become commonplace. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Arsenic removal media Inventor(s): Shaniuk, Thomas J.; (Strongsville, OH) Correspondence: Engelhard Corporation; 101 Wood Avenue; P.O. Box 770; Iselin; NJ; 08830-0770; US Patent Application Number: 20030089665 Date filed: November 15, 2001 Abstract: A media for removal of arsenic from an aqueous system comprising a mixture of: activated bauxite, aluminum trihydrate and a ferric compound selected from the group consisting of ferric hydroxide, ferric oxyhydroxide, ferric hydroxyoxide and mixtures thereof. The mixture is preferably calcined and is thereafter formed into a powder, granules or extruded particles. Preferably, the mixture prior to calcination also contains a natural or synthetic filler which has the capability of modifing the porosity of the mixture. Removal of arsenic from the aqueous system is readily accomplished by contacting the aqueous system with the media until the arsenic is substantially removed from the aqueous system. If arsenic is present in the aqueous system in the +3 valence state, the aqueous system is preferably oxidized to convert the arsenic to the +5 valence state prior to contact of the aqueous system with the media. Excerpt(s): The invention relates to a novel media for the substantial removal of arsenic from aqueous systems. Arsenic, classified by the EPA as a Class A carcinogen, is the 20th most abundant element in the earth's crust. As a result, arsenic contamination of drinking water sources is common, particularly in the western United States. The removal of arsenic from water by adsorption is generally known in the art. See, for example, J. H. Gulledge and J. T. O'Connor, "Removal of Arsenic (V) from Water by Adsorption on Aluminum and Ferric Hydroxides," Water Technology/Quality Journal AWWA, August, pages 548-552 (1973) and M. A. Anderson, J. F. Ferguson and J. Gavis, "Arsenate Adsorption on Amorphous Aluminum Hydroxide," Journal of Colloid and Interface Science, Vol. 54, No. 3, March (1976). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Biosensor for small molecule analytes Inventor(s): Laing, Lance G.; (Belmont, MA) Correspondence: DARBY & DARBY P.C.; Post Office 5257; NEW YORK; NY; 101505257; US Patent Application Number: 20030096275 Date filed: August 15, 2002 Abstract: A biosensor device for detecting small molecules analytes is provided. The device employs a first class of molecules, e.g., protein that binds to both the analyte and a second class of molecules, e.g., nucleic acid. The binding of the protein to the analyte and nucleic acid can be mutually exclusive, and the presence of analyte in a sample results in a detectable displacement of protein from nucleic acid. Alternatively, binding of the protein to the nucleic acid can depend on the presence of analyte in the sample. In a specific embodiment, either the protein or nucleic acid is immobilized on a solid phase support. An arsenic detection system is exemplified. An ArsR binding sequence from the E. coli ars operon is immobilized on a gold-plated surface. ArsR protein binds to the DNA in the absence of arsenic, and is released in the presence of sodium arsenate or phenylarsine oxide. Protein release results in a change in surface plasmon resonance, and the magnitude or kinetics of the change indicate the concentration of arsenic. Excerpt(s): The present application claims the benefit of priority under 35 U.S.C.sctn. 119(e) of Provisional Application Serial No. 60/313,714, filed Aug. 20, 2001, which is hereby incorporated herein by reference in its entirety. The invention relates to the field of biosensors and, more particularly to a biosensor for detecting the presence of molecules and small compounds, particularly metal ions and metal ion complexes, using a competitive molecular binding assay. The term biosensor refers generally to a class of devices that recognize a desired compound (analyte) in a sample and selectively generate a signal which can be resolved to determine the concentration of the compound within the sample. One desirable characteristic of many biosensors is their ability to distinguish a specific analyte without the need for separation or isolation. For example, biosensors can detect the presence of a particular compound within a blood or water sample directly thereby eliminating the need for lengthy or complex purification steps to recover the analyte of interest. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Catalyst compositions for the selective conversion of alkanes to unsaturated carboxylic acids, methods of making and methods of using thereof Inventor(s): Ellis, Paul E. JR.; (Sugar Land, TX), Hazin, Paulette N.; (Houston, TX) Correspondence: SABIC AMERICAS, INC.; 1600 INDUSTRIAL BLVD.; SUGAR LAND; TX; 77478; US Patent Application Number: 20030135071 Date filed: December 20, 2002 Abstract: A catalyst composition for the selective conversion of an alkane to an unsaturated carboxylic acid having the general formula:MoV.sub.aNb.sub.bAg.sub.cM.sub.dO.sub.xwherein optional element M may be one or more selected from aluminum, copper, lithium, sodium, potassium, rubidium, cesium, gallium, phosphorus, iron, rhenium, cobalt, chromium, manganese, arsenic,
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indium, thallium, bismuth, germanium, tin, cerium or lanthanum; a is 0.05 to 0.99, b is 0.01 to 0.99, c is 0.01 to 0.99, d is 0 to 0.5 and x is determined by the valence requirements of the other components of the catalyst composition. This catalyst is prepared by coprecipitation of compounds of molybdenum, vanadium, niobium, silver and M to form a mixed metal oxide catalyst. This catalyst can be used for the selective conversion of an alkane to an unsaturated carboxylic acid in a one-step process or the ammoxidation of alkanes and olefins. Excerpt(s): This invention relates to a catalyst for producing an unsaturated carboxylic acid from an alkane, a method of making said catalyst and a method of using said catalyst. In particular, this invention relates to a catalyst for producing acrylic acid from propane by a single step vapor phase oxidation reaction. The production of an unsaturated carboxylic acid, such as acrylic acid or methacrylic acid, is conventionally done by catalytically reacting an olefin, such as propylene or isobutylene, with oxygen to form an alkenylaldehyde, such as acrolein or methacrolein, which is subsequently catalytically reacted with oxygen. Alkanes, such as propane, have advantages of cost and of availability over olefins. Furthermore, a one step process would have advantages over the present commercial process. There are instances of producing acrylic acid and other unsaturated carboxylic acids from propane and other alkanes in a one step vapor phase catalytic oxidation reaction. U.S. Pat. No. 5,380,933 discloses a catalyst of oxides of molybdenum, vanadium, tellurium, and elements selected from niobium, tantalum, tungsten, titanium, aluminum, zirconium, chromium, manganese, iron, ruthenium, cobalt, rhodium, nickel, palladium, platinum, antimony, bismuth, boron, indium or cerium. Japanese published patent application H10-57813 discloses a metal oxide catalyst of molybdenum, vanadium, tellurium and/or antimony and an element selected from niobium, tantalum, tungsten, titanium, aluminum, zirconium, chromium, manganese, iron, ruthenium, cobalt, rhodium, nickel, palladium, platinum, bismuth, boron, indium, phosphorus, rare earth elements, alkali metals, alkali-earth metals. Japanese published patent application H10-45664 discloses a catalyst of oxides of molybdenum, vanadium, antimony and an element selected from niobium, tantalum, tungsten, titanium, zirconium, chromium, iron, manganese, ruthenium, cobalt, rhodium, nickel, palladium, platinum, boron, indium, alkali metals, alkali-earth metals, and rare earth elements. European published patent application 0 962 253 discloses a catalyst having oxides of molybdenum, tungsten, iron, niobium, tantalum, zirconium, ruthenium and mixtures thereof; vanadium, cerium, chromium and mixtures, thereof; tellurium, bismuth, antimony, selenium, and mixtures thereof; and niobium, tantalum, tungsten, titanium, aluminum, zirconium, chromium, manganese, iron, ruthenium, cobalt, rhenium, nickel, palladium, platinum, antimony, bismuth, boron, indium, cerium and mixtures thereof. Japanese issued patent no. 96-120,617 discloses a supported catalyst having oxides of molybdenum, vanadium, antimony, one of niobium, tantalum, tin, tungsten, titanium, nickel, iron, chromium or cobalt, and at least one of sodium, potassium, rubidium, cesium, phosphorus and arsenic. Japanese patent no. 00-246,108 discloses a catalyst having oxides of molybdenum, vanadium, antimony, at least one of niobium and tantalum and at least one of silver, zinc, tin, lead, arsenic, copper, thallium and selenium. Japanese published patent application H6-128286 disclosed a heteropolyacid catalyst having oxides of phosphorus, molybdenum, vanadium, at least one of arsenic and antimony, and at least one of tin, lead, cerium, cobalt, iron, zirconium, thorium, tungsten, germanium, nickel, rhenium, bismuth, chromium, boron, magnesium, calcium, barium, strontium, selenium, tellurium, silver, aluminum, zinc, copper, titanium, potassium, rubidium, cesium and thallium. U.S. Pat. Nos. 6,160,162 and 6,114,278 disclose a calcined catalyst having molybdenum, vanadium, gallium, palladium, niobium and at least one of lanthanum, tellurium, germanium, zinc, silicon,
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indium and tungsten. U.S. Pat. No. 5,994,580 discloses oxides of molybdenum, vanadium, antimony and at least one of niobium, tantalum, tin, tungsten, titanium, nickel, iron, chromium and cobalt. Japanese patent no. 11114418 discloses a catalyst having oxides of niobium, molybdenum, antimony, at least one of phosphorus, arsenic, boron, silicon and germanium and at least one of potassium, cesium, rubidium, calcium, magnesium, tellurium, chromium, manganese, iron, cobalt, nickel, cooper silver, lead, bismuth, aluminum, gallium, indium, tin, zinc, lanthanum, cerium, yttrium, tungsten, tantalum, ruthenium, rhodium, palladium, platinum, iridium, osmium, rhenium and hafnium. Chinese patent application 1,159,960 discloses bismuth based catalysts with vanadium, niobium, or tantalum and chromium, molybdenum or tungsten, optionally with lithium, sodium, potassium, copper, silver or gold. U.S. Pat. No. 4,339,355 discloses a catalyst having molybdenum, vanadium and niobium with chromium, cooper, manganese or yttrium. German patent application no. 19622331 discloses a catalyst having molybdenum, bismuth and phosphorus with vanadium, niobium, tantalum, chromium, tungsten, gallium, cerium or lanthanum; lithium, sodium, potassium, rubidium, cesium, copper, silver, gold, palladium or platinum; tin lead, antimony, bismuth, tellurium, iron, cobalt or nickel; and silicon, aluminum, titanium or zirconium. U.S. Pat. No. 5,807,531 discloses a catalyst having molybdenum and vanadium with tungsten, niobium, titanium, zirconium, hafnium, tantalum, chromium, silicon or germanium. Japanese patent application no. 246,108 (2000) discloses a catalyst having molybdenum, vanadium and antimony with niobium or tantalum and silver, zinc, tin, lead, arsenic, copper, thallium or selenium. Catalyst with similar compositions have been used for processes other than those for producing acrylic acid and other unsaturated carboxylic acids from propane and other alkanes in a one step vapor phase catalytic oxidation reaction. U.S. Pat. No. 4,250,346 discloses a catalyst for catalytically oxydehydrogenating ethane to ethylene, said catalyst having molybdenum with chromium, manganese, niobium, tantalum, titanium, vanadium or tungsten or bismuth, cerium, cobalt, copper, iron, potassium, magnesium, nickel, phosphorus, lead, antimony, silicon, tin, thallium or uranium. Japanese patent application no. 98 310,539 discloses a catalyst to form propylene from propane, said catalyst having molybdenum, vanadium and niobium. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Catalyst for use in catalytic oxidation or ammoxidation of propane or isobutane in the gaseous phase Inventor(s): Hinago, Hidenori; (Kurashiki-shi, JP), Komada, Satoru; (Yokosuka-shi, JP), Nagano, Osamu; (Yokohama-shi, JP), Watanabe, Mamoru; (Okayama-ken, JP) Correspondence: BIRCH STEWART KOLASCH & BIRCH; PO BOX 747; FALLS CHURCH; VA; 22040-0747; US Patent Application Number: 20030088118 Date filed: August 30, 2002 Abstract: Disclosed is an oxide catalyst comprising an oxide represented by the formula Mo.sub.1V.sub.aNb.sub.bX.sub.cY.sub.dZ.sub.eQ.sub.fO.sub.n (wherein: X is at least one element selected from the group consisting of Te and Sb; Y is at least one element selected from the group consisting of Al and W; Z is at least one element selected from the group consisting of elements which individually form an oxide having a rutile structure and a Z oxide having a rutile structure is used as a source of Z for producing the catalyst; Q is at least one element selected from the group consisting of titanium, tin,
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germanium, lead, tantalum, ruthenium, rhenium, rhodium, iridium, platinum, chromium, manganese, technetium, osmium, iron, arsenic, cerium, cobalt, magnesium, nickel and zinc, and a Q compound not having a rutile structure is used as a source of Q for producing the catalyst; and a, b, c, d, e, f and n are, respectively, the atomic ratios of V, Nb, X, Y, Z, Q and O, relative to Mo). Also disclosed is a process for producing an unsaturated carboxylic acid or an unsaturated nitrile by using the above-mentioned oxide catalyst. Excerpt(s): This application is a continuation-in-part of PCT Application No. PCT/JP01/05055, filed on Jun. 14, 2001, which designated the United States and on which priority is claimed under 35 U.S.C.sctn.120. wherein X is at least one element selected from the group consisting of tellurium and antimony; Y is at least one element selected from the group consisting of aluminum and tungsten; Z is at least one element selected from the group consisting of elements which individually form an oxide having a rutile structure; Q is at least one element selected from the group consisting of titanium, tin, germanium, lead, tantalum, ruthenium, rhenium, rhodium, iridium, platinum, chromium, manganese, technetium, osmium, iron, arsenic, cerium, cobalt, magnesium, nickel and zinc; and a, b, c, d, e, f and n are, respectively, the atomic ratios of vanadium (V), niobium (Nb), X, Y, Z, Q and oxygen (O), relative to molybdenum (Mo), and wherein: 0.1.ltoreq.a.ltoreq.1.0, 0.01.ltoreq.b.ltoreq.1.0, 0.01.ltoreq.c.ltoreq.1.0, 0.ltoreq.d.ltoreq.0.5, 0.ltoreq.e.ltoreq.3, 0.ltoreq.f.ltoreq.9, with the proviso that 0
Complementary MOS semiconductor device Inventor(s): Hasegawa, Hisashi; (Chiba-shi, JP), Osanai, Jun; (Chiba-shi, JP) Correspondence: ADAMS & WILKS; ATTORNEYS AND COUNSELORS AT LAW; 31st FLOOR; 50 BROADWAY; NEW YORK; NY; 10004; US Patent Application Number: 20030047782 Date filed: September 4, 2002 Abstract: A complementary MOS semiconductor device is provided which is manufactured at low cost and in a short manufacturing period, which enables low voltage operation, and has low power consumption and high driving capability, and which can realizes a power management semiconductor device or an analog
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semiconductor device at high speed operation. A gate electrode of a CMOS is formed of p-type polycrystalline silicon of a singe polarity or a p-type polycide structure. A PMOS is of surface channel type, and thus, enables a shorter channel and a lower threshold voltage. Also, an NMOS of buried channel type has an extremely shallow buried channel since arsenic having a small diffusion coefficient is used as an impurity for threshold control in the NMOS, and thus, enables a shorter channel and a lower threshold voltage. Further, a resistor used in a voltage dividing circuit or a CR circuit is comprised of polycrystalline silicon different from that for the gate electrode, and thus, a voltage dividing circuit with high precision is provided. Accordingly, the high-speed power management semiconductor device or analog semiconductor device is realized. Excerpt(s): The present invention relates to a complementary MOS semiconductor device having a resistor circuit structured on an SOI (silicon on insulator) substrate, in which a low voltage operation, low power consumption, and high driving capability are required, and particularly to a power management semiconductor device such as a voltage detector (hereinafter referred to as VD), a voltage regulator (hereinafter referred to as VR), or a switching regulator (hereinafter referred to as SWR) or an analog semiconductor device such as an operational amplifier or a comparator. In the complementary MOS (CMOS) semiconductor device having a resistor circuit, n+ polycrystalline silicon is often used for a gate electrode in view of the easiness of manufacture and stability. In this case, an NMOS is of surface channel type based on the relationship of a work function between the gate electrode and the semiconductor substrate while in a PMOS, a threshold voltage is about -1 V based on the relationship of a work function between the gate electrode and the semiconductor substrate. Thus, when impurity implantation is conducted in order to reduce the threshold voltage, the PMOS becomes of buried channel type in which a channel is formed in the portion that is little inner from a surface in the substrate. The buried channel type has an advantage that mobility is high since a carrier passes through the interior of the substrate. However, in the buried channel type, when the threshold voltage is lowered, a subthreshold characteristic is extremely deteriorated, which leads to an increase of a leak current. Therefore, it is more difficult to attain a lower voltage and a shorter channel in the PMOS than in the NMOS. Further, in recent years, while reduction in size and reduction in weight are progressed, lower power consumption, higher speed, and higher functions are required in a portable equipment typified by a portable telephone or a PDA. Along with this, electronic components that constitute the portable equipment need to be reduced in size and operated at a higher speed. However, a power management semiconductor device such as a switching regulator needs to have a withstand voltage of about 10 V, and thus, is difficult to be operated at a higher speed resulting from the attainment of higher definition. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Complex oxide catalyst and process for preparation of acrylic acid Inventor(s): Nakamura, Daisuke; (Himeji-shi, JP), Tanimoto, Michio; (Himeji-shi, JP), Yunoki, Hiromi; (Himeji-shi, JP) Correspondence: SHERMAN & SHALLOWAY; 413 North Washington Street; Alexandria; VA; 22314; US Patent Application Number: 20030153786 Date filed: February 25, 2003
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Abstract: A catalyst which is a complex oxide catalyst represented by the following general formula (1):Mo.sub.aV.sub.bW.sub.cCu.sub.dA.sub.eB.sub.fC.sub.gD.sub.hE.sub.iO.sub.x (1)(in which Mo is molybdenum; V is vanadium, W is tungsten, Cu is copper, A is at least an element selected from antimony, niobium and tin; B is at least an element selected from alkaline earth metals; C is at least an element selected from silicon, aluminum, titanium and zirconium; D is at least an element selected from phosphorus, tellurium, cerium, lead, arsenic and zinc; E is at least an element selected from Group IA and Group IIIb elements of the periodic table, boron, iron, bismuth, cobalt, nickel and manganese; and O is oxygen; a, b, c, d, e, f, g, h, i and x denote the atomic ratios of Mo, V, W, Cu, A, B, C, D, E and O, respectively; and where a=12, 2.ltoreq.b.ltoreq.15, 0.ltoreq.c.ltoreq.10, 0
Composition and process for removing arsenic and selenium from aqueous solution Inventor(s): Harck, John F.; (Sun Valley, NV), Wilkis, Stephanie; (Sparks, NV), Winters, Ivan; (Sun Valley, NV) Correspondence: John D. Long; 2941 Sage Ridge Drive; Reno; NV; 89509; US Patent Application Number: 20030155303 Date filed: October 8, 2002 Abstract: The invention is a new composition and process for lanthanum oxide concentrate that is used to significantly reduce arsenic and/or selenium concentration levels in aqueous solutions. The lanthanum oxide concentrate is a mixture of lanthanum oxide and one or more oxides from the following group: neodymium oxide, cerium oxide, parseodymiun oxide, strontium oxide, calcium oxide and sodium oxide. The process of manufacture comprises the steps of sintering the lanthanum oxide
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concentrate, then washing the resultant media. The process of use is the contact of the lanthanum oxide concentrate with an aqueous solution containing arsenic and/or selenium whereby the lanthanum oxide concentrate removes at least a portion of the arsenic and/or selenium from the aqueous solution. Excerpt(s): This application relates back to and claims the filing date of U.S. Provisional Application entitled A COMPOSITION AND PROCESS FOR REMOVING ARSENIC AND SELENIUM FROM AQUEOUS SOLUTION filed on Feb. 2, 2002, assigned Ser. No. 60/357,616 recorded assignment to Clear Water Filtration Systems, REEL/FRAME 012897/0120. Not Applicable. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Compounds derived from la2mo2o9 and their use as ionic conductors Inventor(s): Goutenoire, Francois; (Le Mans, FR), Lacorre, Philippe; (Etival-Les-Le Mans, FR) Correspondence: John A Shedden; Intellectual Property Dept; Rhodia Inc; 259 Prospect Plain Road CN 7500; Cranbury; NJ; 08512-7500; US Patent Application Number: 20030160216 Date filed: March 24, 2003 Abstract: The invention concerns novel compounds derived from La.sub.2Mo.sub.2O.sub.9 and their use as ion conductors.The compounds of the invention have formula (1):A.sub.2-xA'.sub.xB.sub.2-yB'.sub.yO.sub.9-z+.delta.X.sub.zin which A is at least one trivalent element selected from trivalent rare earths, trivalent bismuth, trivalent antimony and trivalent arsenic; A' is at least one monovalent element selected from alkalis; or a divalent element selected from alkaline-earths, tin, lead, samarium, europium, erbium, thulium and ytterbium; or a quadrivalent element selected from thorium, uranium, group IVA elements, cerium, praseodymium and terbium; B is at least one hexavalent element from groups VIA, VIIA, VIII and group VIB with the exception of oxygen; B' is at least one element selected from lithium, sodium, magnesium, calcium, scandium, yttrium, rare earths with atomic numbers 63 to 71, elements from groups IVA to IIB with an oxidation number of less than 6, aluminium III, silicon IV, gallium III, germanium IV, indium III, tin IV, phosphorus V, antimony V and bismuth V; X is selected from sulphur, fluorine and chlorine; where 0.ltoreq.x<2; 0.ltoreq.y<2; 0.ltoreq.z.ltoreq.3; and with the condition that when A is lanthanum and B is tungsten or molybdenum, at least one of x, y or z is different from 0; the compounds having a cationic cubic or pseudo-cubic.beta.-SnWO.sub.4 type lattice. Excerpt(s): The invention relates to novel compounds derived from La.sub.2Mo.sub.2O.sub.9 and to their use as ion conductors. Ion conductors can be used in a number of applications. Fuel cells constitute an area of burgeoning development that can be cited. Thus, there is a need for materials of that type. Further, in the particular case of fuel cells, existing cells function at high temperatures of at least 900.degree. C. At these temperatures, reduction and cationic diffusion phenomena in the different elements of the cell introduce chemical reactions at the interfaces followed by a degradation of electrical performance. Thus, the search is on for conductive materials that can reduce the operational temperatures of said cells and thus for products with sufficient conductivity at lower temperatures. The invention aims to provide compounds that satisfy said needs. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 203
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Device for decontamination of water Inventor(s): Klose, Giselher; (Auerbach, DE) Correspondence: V. Gerald Grafe, esq.; P.O. Box 2689; Corrales; NM; 87048; US Patent Application Number: 20030183516 Date filed: September 12, 2002 Abstract: The invention relates to a device for the decontamination of water, particularly of heavy metals and/or arsenic and/or their compounds, by means of electrolysis, wherein the water to be purified is fed through a receptacle and passes by electrodes of different polarities. According to the invention, a combination of electrodes made from iron, aluminium, and graphite, or from aluminium and graphite, is used. Facing the direction of the receptacle bottom, the undersides of the electrodes are contained in groove-like, electrically insulated recesses that are spaced apart and separated from one another on their opposite side by single electrically insulating spacers, wherein the spacers are attached to the electrodes, and the electrodes, which can be unfolded, are arranged in the groove-like recesses. Excerpt(s): The invention relates to a device for the decontamination of water, particularly removal of heavy metals and/or arsenic and/or their compounds. The elimination of particularly heavy metals and/or arsenic and/or their compounds from water in order to produce drinking water is currently possible only in an unsatisfactory manner. The contamination levels of drinking water with, for example, arsenic-especially in regions with similarly polluted groundwater--generally lie at or above the permitted values. Numerous devices for purifying water are already known; however, they are not effective in removing arsenic DE 33 36 460 A1, for example, describes a method and a device for purifying water by means of electrolysis, wherein the water to be purified is conducted past electrodes made of bivalent or trivalent metals of different polarities. Iron or aluminium is preferably used as the electrode material. Furthermore, an arrangement for treating polluted water by means of electrolysis is known, in which alternating electrodes made from steel and aluminium are combined with one another (DE 43 15 117 A1), or iron and/or aluminium electrodes are used (DE 43 29 272). The use of aluminium electrodes, however, results in a high pH-value, which has an especially negative effect on the removal of arsenic. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Devitrification-resistant chalcogenide glasses Inventor(s): Aitken, Bruce G.; (Corning, NY) Correspondence: CORNING INCORPORATED; SP-TI-3-1; CORNING; NY; 14831 Patent Application Number: 20030104918 Date filed: November 8, 2002 Abstract: The invention resides in a molecular, inorganic glass and a method of making the glass, the glass being vitreous and resistant to devitrification, that is composed, in substantial part at least, of thermally-stable, zero-dimensional clusters or molecules, composed of four atoms of arsenic and three atoms of sulfur, the glass further containing up to 12 atomic percent of germanium, adjoining clusters being bonded to each other primarily by van der Waals forces, and at least 95% of the glass composition consisting of 42-60% arsenic, 37-48% sulfur plus selenium, the selenium being 0-14%.
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Excerpt(s): The present application claims benefit of priority as a continuation-in-part of U.S. patent application Ser. No. 09/894,587, filed on Jun. 28, 2001, which is incorporated herein. The invention relates to molecular, inorganic glasses composed, at least in part, of one species including either thermally stable (i.e., persisting after annealing), zerodimensional molecules or network-forming groups, composed of arsenic and sulfur atoms and associated with germanium atoms. The physical structure of a glass may be characterized by its dimensionality, that is, by the number of directions in which its components extend. Thus, vitreous selenium, which is believed to consist of intertwined chains of selenium atoms, is said to have a one-dimensional structure. Likewise, glassy As.sub.2S.sub.3, which consists of corrugated sheets of As.sub.2S.sub.3 pyramids that share corners, is described as having a two-dimensional structure. Considered in these structural terms, most oxide glasses are said to be three-dimensional. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
FLUID STORAGE AND DELIVERY SYSTEM UTILIZING LOW HEELS CARBON SORBENT MEDIUM Inventor(s): Salsbury, Joseph; (Ithaca, NY), Wang, Luping; (Brookfield, CT) Correspondence: ATMI, INC.; 7 COMMERCE DRIVE; DANBURY; CT; 06810; US Patent Application Number: 20030106429 Date filed: November 12, 2001 Abstract: A fluid storage and dispensing system including a vessel containing a low heel carbon sorbent having fluid adsorbed thereon, with the system arranged to effect desorption of the fluid from the sorbent for dispensing of fluid on demand. The low heel carbon sorbent preferably is characterized by at least one of the following characteristics: (i) Heel, measured for gaseous arsine (AsH.sub.3) at 20.degree. C. at 20 Torr, of not more than 50 grams AsH.sub.3 per liter of bed of the sorbent material; (ii) Heel, measured for gaseous boron trifluoride (BF.sub.3) at 20.degree. C at 20 Torr, of not more than 20 grams boron trifluoride per liter of bed of the sorbent material; (iii) Heel, measured for gaseous germanium tetrafluoride (GeF.sub.4) at 20.degree. C. at 20 Torr, of not more than 250 grams AsH.sub.3 per liter of bed of the sorbent material; (iv) Heel, measured for gaseous arsenic pentafluoride (AsF.sub.5) at 20.degree. C. at 20 Torr, of not more than 700 grams AsF.sub.5 per liter of bed of the sorbent material; (v) Heel, measured for gaseous trimethyl silane (3MS) at 20.degree. C. at 20 Torr, of not more than 160 grams 3MS per liter of bed of the sorbent material; and (vi) Heel, measured for gaseous ethane (C.sub.2H.sub.4) at 21.degree. C. at 25 Torr, of not more than 10 grams ethane per liter of bed of the sorbent material. Excerpt(s): 1. Field of the Invention p This invention relates generally to storage and dispensing systems for the selective dispensing of fluids from a vessel or storage container in which the fluid component(s) are held in sorptive relationship to a solid carbon sorbent medium having low adsorption Heels, and are desorptively released from the carbon sorbent medium in the dispensing operation. In a wide variety of industrial processes and applications, there is a need for a reliable source of process fluid(s). Such process and application areas include semiconductor manufacturing, ion implantation, manufacture of flat panel displays, medical intervention and therapy, water treatment, emergency breathing equipment, welding operations, space-based delivery of liquids and gases, etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Formation of dual work function gate electrode Inventor(s): Kang, Woo-Tang; (Wappingers Falls, NY), Lee, Kilho; (Wappingers Falls, NY), Rengarajan, Rajesh; (Poughkeepsie, NY) Correspondence: Law Office of Jerome J. Norris; Suite 305; 1901 Pennsylvania Avenue, N.W.; Washington; DC; 20006; US Patent Application Number: 20030096471 Date filed: November 19, 2001 Abstract: In a method of making a dual work function gate electrode of a CMOS semiconductor structure, the improvement comprising formation of the dual work function gate electrode so that there is no boron penetration in the channel region and no boron depletion near the gate oxide, comprising:a) forming a gate oxide layer over a channel of a nMOS site and over a channel of a pMOS site;b) forming an undoped polysilicon layer over the gate oxide layer;c) masking the pMOS site, forming an a-Si layer over the nMOS site using a first heavy ion implantation, and implanting arsenic solely into the a-Si layer;d) masking the nMOS site formed by step c), forming an a-Si layer over the pMOS site using a second heavy ion implantation, and implanting boron solely into the a-Si regions;e) laser annealing the nMOS and pMOS sites for a short time and at an energy level sufficient to melt at least a portion of the a-Si but insufficient to melt the polysilicon; andf) affecting cooling after laser annealing to convert a-Si into polysilicon without gate oxide damage. Excerpt(s): The invention relates to a method for forming p-type doped gate electrodes during manufacture of CMOS semiconductor structures without boron penetration into the channel region and without boron depletion near the gate oxide. It is known that, in forming a gate on a substrate during manufacturing of a semiconductor device, large grain poly-silicon is used as the gate material. However, due to the fact that the surface of the layer formed by the large grain poly-silicon is rough because of the size of the grain, UV exposure light is scattered upon patterning the poly-silicon layer to form gates. Unfortunately, when this happens, the critical dimension of the gate is extremely difficult to control and uniformity of the gate cannot be obtained. To resolve this problem in the conventional method of manufacturing semiconductor devices, amorphous silicon (a-Si) is employed as the gate material on a substrate. Because the surface of the layer formed by an a-Si is far smoother than that of large-grain polysilicon, satisfactory critical dimension and uniformity of the gate maybe obtained. Nevertheless, in later thermal processes, the a-Si re-crystallizes at elevated temperatures to form large-grain poly-silicon. The formation of large-grain poly-silicon produces a channeling effect at the interface between the poly-silicon gate and the gate oxide layer. This channeling effect causes penetration of conductive ions i.e. p-type ion dopants, such as the boron ion, through the large-grain poly-silicon into the gate oxide. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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High and low pressure integrated type turbine rotor and process for producing the same Inventor(s): Fujita, Akitsugu; (Nagasaki-shi, JP), Kamada, Masatomo; (Yokohama-shi, JP) Correspondence: OBLON, SPIVAK, MCCLELLAND, MAIER & NEUSTADT, P.C.; 1940 DUKE STREET; ALEXANDRIA; VA; 22314; US Patent Application Number: 20030116240 Date filed: December 4, 2002 Abstract: In CrMoV based heat resistant steels and tungsten-containing CrMoV based heat resistant steels, trace impurities, such as phosphorus, sulfur, copper, aluminum, arsenic, tin, and antimony are reduced lower than a specific level. Furthermore, alloy steels having increased creep strengths in a creep test on an unnotched test piece by addition of trace impurities such as cobalt, niobium, tantalum, nitrogen, boron, or the like is used. The production process therefor includes heating a turbine rotor member having the specific composition at a temperature between 980.degree. C. and 1100.degree. C. at a part corresponding to the high-pressure part thereof and at a temperature between 850.degree. C. and 980.degree. C. at a part corresponding to the low-pressure part thereof, and cooling the turbine rotor member at a cooling rate higher than an air impact cooling rate at the part corresponding to the high-pressure part thereof, and at a cooling rate no lower than an oil quenching rate at the part corresponding to the low-pressure part thereof. The rotor member has a creep rupture time in a creep test on a notched test piece of 10000 hours or longer. Excerpt(s): The present invention relates to turbine rotors and in particular it relates to high pressure and low pressure integrated type turbine rotors used in steam turbines employed in thermal electric power generation. Conventionally, as one type of turbine rotor for steam turbines for thermal electric power generation, high pressure and low pressure integrated turbine rotors utilizing integrated materials from the high pressure part to the low-pressure part have been known. The steam turbine is exposed to hightemperature and high-pressure steam on the side of its steam inlet. As the end portion is being approached, the temperature and pressure of steam decrease, so that the steam turbine is exposed to steam that has a highly expanded volume. Therefore, in the highpressure part, the turbine blades are short in length and the stress applied to the turbine rotor is relatively small, and thus the diameter of the turbine rotor may be small. On the other hand, in the low pressure part, to receive the force exerted by a larger amount of steam, the length of the turbine blades must be large and the diameter of the turbine rotor must be large, resulting in a large stress being applied to the turbine rotor. Therefore, the characteristics required for the high pressure and low pressure integrated type rotors are high temperature strength, in particular excellent creep strength at the high-pressure part, and on the other hand, at the low pressure part, mechanical strength and excellent toughness at ordinary temperature. Conventionally, as examples of heatresistant steels for use in high pressure and low pressure integrated type turbine rotors, CrMoV steels, which belong to low-alloys, and 12Cr steels, which belong to high-Cr steels, have been exclusively used (see Japanese Patent Applications, First Publications (Kokai), Nos. Sho 60-165359 and Sho 62-103345). A process for obtaining a turbine rotor having creep properties and toughness simultaneously has been proposed, in which a CrMoV based steel species is processed into a turbine rotor member and the highpressure and low-pressure parts of a single turbine rotor are separately heat treated under different conditions. For example, Japanese Patent Application, First Publication (Kokai), No. Hei 5-195068 discloses a process for obtaining a high pressure and low
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pressure integrated type turbine rotor having creep strength at high temperatures and toughness simultaneously, in which the high pressure part of a rotor member is quenched after heating at a temperature higher than the low pressure part and then the whole rotor member is tempered at a predetermined temperature. Japanese Patent Application, First Publication (Kokai) No. Hei 8-176671 discloses a process for obtaining a high pressure and low pressure integrated turbine rotor having excellent creep properties at high temperatures and toughness simultaneously, in which a rotor member is normalizing-treated at 1100 to 1150.degree. C. and pearlite-transformed, further normalizing-treated at 920 to 950.degree. C., the high pressure part and low pressure part are quenched at different temperatures, and then the whole rotor member is tempered. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Ink nanotechnology Inventor(s): Kostelecky, Clayton; (Longmont, CO), Yadav, Tapesh; (Longmont, CO) Correspondence: HOGAN & HARTSON LLP; ONE TABOR CENTER, SUITE 1500; 1200 SEVENTEENTH ST; DENVER; CO; 80202; US Patent Application Number: 20030212179 Date filed: May 20, 2003 Abstract: An ink prepared using inorganic nanofillers with modified properties because of the powder size being below 100 nanometers. Both low-loaded and highly-loaded nanocomposites are included. Nanoscale coated, un-coated, whisker type fillers are included. The nanofillers taught comprise of elements from the group actinium, aluminum, antimony, arsenic, barium, beryllium, bismuth, carbon, cadmium, calcium, cerium, cesium, cobalt, copper, dysprosium, erbium, europium, gadolinium, gallium, gold, hafnium, hydrogen, indium, iridium, iron, lanthanum, lithium, magnesium, manganese, mendelevium, mercury, molybdenum, neodymium, neptunium, nickel, niobium, osmium, nitrogen, oxygen, palladium, platinum, potassium, praseodymium, promethium, protactinium, rhenium, rubidium, scandium, silver, sodium, strontium, tantalum, terbium, thallium, thorium, tin, titanium, tungsten, vanadium, ytterbium, yttrium, zinc, and zirconium. Excerpt(s): This application is a divisional of co-pending U.S. patent application Ser. No. 09/790,036 titled "NANOTECHNOLOGY FOR DRUG DELIVERY, CONTRAST AGENTS AND BIOMEDICAL IMPLANTS" filed on Feb. 20, 2001 which is a divisional of U.S. Pat. No. 6,228,904 filed on May 22, 1998, which is incorporated herein by reference and which claims the benefit of U.S. Provisional applications 60/049,077 filed on Jun. 5, 1997, 60/069,936 filed on Dec. 17, 1997, and 60/079,225 filed on Mar. 24, 1998. U.S. Pat. No. 6,228,904 is a continuation-in-part of U.S. patent application Ser. No. 08/739,257, filed Oct. 30, 1996, now U.S. Pat. No. 5,905,000, titled NANOSTRUCTURED ION CONDUCTING SOLID ELECTROLYTES, which is a continuation-in-part of U.S. Ser. No. 08/730,661, filed Oct. 11, 1996, now U.S. Pat. No. 5,952,040 titled "PASSIVE ELECTRONIC COMPONENTS FROM NANOPRECISION ENGINEERED MATERIALS" which is a continuation-in-part of U.S. Ser. No. 08/706,819, filed Sep. 3, 1996, now U.S. Pat. No. 5,851,507 titled "INTEGRATED THERMAL PROCESS FOR THE CONTINUOUS SYNTHESIS OF NANOSCALE POWDERS" and U.S. Ser. No. 08/707,341, filed Sep. 3, 1996, now U.S. Pat. No. 5,788,738 titled "METHOD OF PRODUCING NANOSCALE POWDERS BY QUENCHING OF VAPORS". This application is also a continuation-in-part of co-pending U.S. patent application Ser.
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09/753,806 titled "LOW-COST MULTILAMINATE SENSORS" which is a divisional of U.S. Pat. No. 6,202,471 filed on May 7, 1998 titled "LOW-COST MULTILAMINATE SENSORS". In one aspect, the invention comprises a nanostructured filler, intimately mixed with a matrix to form a nanostructured composite. At least one of the nanostructured filler and the nanostructured composite has a desired material property which differs by at least 20% from the same material property for a micron-scale filler or a micron-scale composite, respectively. The desired material property is selected from the group consisting of refractive index, transparency to light, reflection characteristics, resistivity, permittivity, permeability, coercivity, B-H product, magnetic hysteresis, breakdown voltage, skin depth, curie temperature, dissipation factor, work function, band gap, electromagnetic shielding effectiveness, radiation hardness, chemical reactivity, thermal conductivity, temperature coefficient of an electrical property, voltage coefficient of an electrical property, thermal shock resistance, biocompatibility and wear rate. The nanostructured filler may comprise one or more elements selected from the s, p, d, and f groups of the periodic table, or it may comprise a compound of one or more such elements with one or more suitable anions, such as aluminum, antimony, boron, bromine, carbon, chlorine, fluorine, germanium, hydrogen, indium, iodine, nickel, nitrogen, oxygen, phosphorus, selenium, silicon, sulfur, or tellurium. The matrix may be a polymer (e.g., poly(methyl methacrylate), poly(vinyl alcohol), polycarbonate, polyalkene, or polyaryl), a ceramic (e.g., zinc oxide, indium-tin oxide, hafnium carbide, or ferrite), or a metal (e.g., copper, tin, zinc, or iron). Loadings of the nanofiller may be as high as 95%, although loadings of 80% or less are preferred. The invention also comprises devices which incorporate the nanofiller (e.g., electrical, magnetic, optical, biomedical, and electrochemical devices). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Inorganic colors and related nanotechnology Inventor(s): Yadav, Tapesh; (Longmont, CO) Correspondence: HOGAN & HARTSON LLP; ONE TABOR CENTER, SUITE 1500; 1200 SEVENTEENTH ST; DENVER; CO; 80202; US Patent Application Number: 20030207112 Date filed: May 30, 2003 Abstract: A pigment with modified properties because of the powder size being below 100 nanometers. Blue, yellow and brown pigments are illustrated. Nanoscale coated, uncoated, whisker inorganic fillers are included. Stoichiometric and non-stoichiometric composition are disclosed. The pigment nanopowders taught comprise one or more elements from the group actinium, aluminum, antimony, arsenic, barium, beryllium, bismuth, cadmium, calcium, cerium, cesium, cobalt, copper, chalcogenide, dysprosium, erbium, europium, gadolinium, gallium, gold, hafnium, hydrogen, indium, iridium, iron, lanthanum, lithium, magnesium, manganese, mendelevium, mercury, molybdenum, neodymium, neptunium, nickel, niobium, nitrogen, oxygen, osmium, palladium, platinum, potassium, praseodymium, promethium, protactinium, rhenium, rubidium, scandium, silver, sodium, strontium, tantalum, terbium, thallium, thorium, tin, titanium, tungsten, vanadium, ytterbium, yttrium, zinc, and zirconium. Excerpt(s): The present application is a divisional of copending U.S. patent application Ser. No. 10/150,722 filed on May 17, 2002 entitled "Nanotechnology for Inks and Dopants" which claims the benefit of provisional application No. 60/111,442 filed Dec. 8, 1998 and is a divisional of U.S. patent application Ser. No. 09/274,517 filed on Mar. 23,
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1999 entitled "MATERIALS AND PRODUCTS USING NANOSTRUCTURED NONSTOICHIOMETRIC SUBSTANCES" now U.S. Pat. No. 6,344,271 which claims the benefit of provisional application No. 60/107,318, filed Nov. 6, 1998, entitled "Materials and Products Using Nanostructured Non-stoichiometric Materials," all of which are assigned to the assignee of the present invention and which are incorporated herein by reference. The present application is also a divisional of co-pending U.S. patent application Ser. No. 09/790,036 titled "NANOTECHNOLOGY FOR DRUG DELIVERY, CONTRAST AGENTS AND BIOMEDICAL IMPLANTS" filed on Feb. 20, 2001 which is a divisional of U.S. Pat. No. 6,228,904 filed on May 22, 1998, which is incorporated herein by reference and which claims the benefit of U.S. Provisional applications 60/049,077 filed on Jun. 5, 1997, 60/069,936 filed on Dec. 17, 1997, and 60/079,225 filed on Mar. 24, 1998. U.S. Pat. No. 6,228,904 is a continuation-in-part of U.S. patent application Ser. No. 08/739,257, filed Oct. 30, 1996, now U.S. Pat. No. 5,905,000, titled NANOSTRUCTURED ION CONDUCTING SOLID ELECTROLYTES, which is a continuation-in-part of U.S. Ser. No. 08/730,661, filed Oct. 11, 1996, now U.S. Pat. No. 5,952,040 titled "PASSIVE ELECTRONIC COMPONENTS FROM NANO-PRECISION ENGINEERED MATERIALS" which is a continuation-in-part of U.S. Ser. No. 08/706,819, filed Sep. 3, 1996, now U.S. Pat. No. 5,851,507 titled "INTEGRATED THERMAL PROCESS FOR THE CONTINUOUS SYNTHESIS OF NANOSCALE POWDERS" and U.S. Ser. No. 08/707,341, filed Sep. 3, 1996, now U.S. Pat. No. 5,788,738 titled "METHOD OF PRODUCING NANOSCALE POWDERS BY QUENCHING OF VAPORS". This application is also a continuation-in-part of co-pending U.S. patent application Ser. No. 09/753,806 titled "LOW-COST MULTILAMINATE SENSORS" which is a divisional of U.S. Pat. No. 6,202,471 filed on May 7, 1998 titled "LOW-COST MULTILAMINATE SENSORS". The invention relates to non-stoichiometric substances and more particularly to nanostructured non-stoichiometric substances and products incorporating such substances. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Low base-emitter voltage heterojunction bipolar transistor Inventor(s): Chow, David; (Newbury Park, CA), Elliott, Kenneth; (Thousand Oaks, CA), Nguyen, Chanh; (Calabasas, CA) Correspondence: TOPE-MCKAY & ASSOCIATES; 23852 PACIFIC COAST HIGHWAY #311; MALIBU; CA; 90265; US Patent Application Number: 20030166325 Date filed: December 18, 2002 Abstract: A heterojunction bipolar transistor is presented, comprising a substrate having formed thereon a heterojunction bipolar transistor layer structure, and including an emitter layer. The emitter layer includes a strained, n-doped compound of indium arsenic and phosphorus. The transistor further comprises, between the substrate and emitter layer, a subcollector layer, a collector layer, a base layer, and an optional spacer layer. The emitter layer may include a graded portion. A contact layer is formed on the emitter layer to provide contacts for the device. Excerpt(s): This application claims the benefit of priority to U.S. Provisional Application No. 60/342,340, titled "Low VBE Heterojunction Bipolar Transistor," filed Dec. 18, 2001. The present invention relates to solid-state electronic devices. More specifically, the present invention relates to an improved heterojunction bipolar transistor. The transistor is an important example of an "active" component, a device that can amplify an
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incoming signal to produce an output signal with more power than the input signal. The additional power comes from an external power source. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method and apparatus for measuring ultra-trace amounts of arsenic, selenium and antimony Inventor(s): Simeonsson, Josef B.; (Durham, NC) Correspondence: Gilbreth & Associates, P.C.; P.O. Box 2428; Bellaire; TX; 77402-2428; US Patent Application Number: 20030059950 Date filed: March 11, 2002 Abstract: An analytical apparatus including a hydride generator coupled with a a laserbased detection device, with the generator suitable for generating hydrides from a sample, and the detection device positioned to receive hydrides from the hydride generator, and to provide information regarding quantity, identity, presence and/or species of the hydride. A method of processing a sample includes generating hydrides from the sample, and generating information regarding quantity, identity, presence and/or species of the hydride. Excerpt(s): The present application claims priority of U.S. Provisional Patent Application Serial No. 60/274,570, filed Mar. 9, 2001, which application is also incorporated herein by reference. The present invention relates to detection, speciation, identification, and/or quantification of materials. In another aspect, the present invention relates to methods and apparatus for detection, speciation, identification, and/or quantification of materials. In even another aspect, the present invention relates to methods and apparatus for detection, speciation, identification, and/or quantification of samples containing metaloid elements. In still another aspect, the present invention relates to methods and apparatus for detection, speciation, identification, and/or quantification of samples containing arsenic, selenium, and/or antimony. In yet another aspect, the present invention relates to methods and apparatus for chemically speciating selected arsenic and selenium anion species. In even still another aspect, the present invention relates to apparatus combining laser-induced fluorescence or laser-enhanced ionization with continuous flow-hydride generation for the detection, identification, and/or quantification of samples. There continues to be interest in determination, quantification and/or detection of samples. For example, the trace determination of arsenic (As), selenium (Se) and antimony (Sb) species because of concerns over pollution of the environment and the important roles these elements have in biological systems. In many instances the toxicity and/or essentiality of certain chemicals depends not only on their concentrations, but also on their chemical forms (i.e., "speciation"). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for hydroformylation, xanthene-bridged ligands and catalyst comprising a complex of said ligands Inventor(s): Ahlers, Wolfgang; (Worms, DE), Bartsch, Michael; (Neustadt, DE), Baumann, Robert; (Mannheim, DE), Hewat, Alison; (Eindhoven, NL), Paciello, Rocco; (Bad D?uuml;rkheim, DE), Vogt, Dieter; (Eindhoven, NL), Wiebelhaus, Dag; (Neustadt, DE) Correspondence: KEIL & WEINKAUF; 1350 CONNECTICUT AVENUE, N.W.; WASHINGTON; DC; 20036; US Patent Application Number: 20030195378 Date filed: March 11, 2003 Abstract: In a process for the hydroformylation of ethylenically unsaturated compounds, at least one complex of a metal of transition group VIII. with at least one phosphorus-, arsenic- or antimony-containing compound as ligand is used as hydroformylation catalyst, where the compound used as ligand in each case comprises two groups which comprise a P, As or Sb atom and at least two further hetero atoms and are bound to a xanthene-like molecular framework. New compounds of this type and catalysts which comprise at least one complex of a metal of transition group VIII. with at least one such compound as ligand are also provided. Excerpt(s): The present invention relates to a process for the hydroformylation of ethylenically unsaturated compounds, in which at least one complex of a metal of transition group VIII with at least one phosphorus-, arsenic- or antimony-containing compound as ligand is used as hydroformylation catalyst, where the compound used as ligand in each case comprises at least two groups which comprise a P, As or Sb atom and at least two further hetero atoms and are bound to a xanthene-like molecular framework. The invention also provides new compounds of this type and catalysts which comprise at least one complex of a metal of transition group VIII with at least one such compound as ligand. Hydroformylation or the oxo process is an important industrial process and is employed for preparing aldehydes from olefins, carbon monoxide and hydrogen. If desired, these aldehydes can be hydrogenated by means of hydrogen in the same process step to give the corresponding oxo alcohols. The reaction itself is strongly exothermic and generally proceeds under superatmospheric pressure and at elevated temperatures in the presence of catalysts. Catalysts used are Co, Rh, Ir, Ru, Pd or Pt compounds or complexes which may be modified with N- or P-containing ligands to influence the activity and/or selectivity. The hydroformylation reaction results in formation of mixtures of isomeric aldehydes because of the possible CO addition on to each of the two carbon atoms of a double bond. In addition, double bond isomerization, i.e. shifting of internal double bonds to a terminal position and vice versa, can also occur. Owing to the substantially greater industrial importance of.alpha.aldehydes, optimization of the hydroformylation catalysts to achieve a very high hydroformylation activity together with a very low tendency to form double bonds not in the.alpha. position is sought. In addition, there is a need for hydroformylation catalysts which lead to good yields of.alpha.-aldehydes and in particular n-aldehydes even when internal linear olefins are used as starting materials. Here, the catalyst must make possible both the establishment of equilibrium between internal and terminal double bond isomers and the very selective hydroformylation of the terminal olefins. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for low temperature chemical vapor deposition of low-k films using selected cyclosiloxane and ozone gases for semiconductor applications Inventor(s): Conti, Richard A.; (Katonah, NY), Edelstein, Daniel C.; (White Plains, NY), Lee, Gill Yong; (Wappingers Falls, NY) Correspondence: INTERNATIONAL BUSINESS MACHINES CORPORATION; Intellectual Property Law Department; Bldg 300/Zip 482; 2070 Route 52; Hopewell Junction; NY; 12533; US Patent Application Number: 20030068853 Date filed: November 18, 2002 Abstract: A method is described for forming a low-k dielectric film, in particular, a premetal dielectric (PMD) on a semiconductor wafer which has good gap-filling characteristics. The method uses a thermal sub-atmospheric CVD process that includes a carbon-containing organometallic precusor such as TMCTS or OMCTS, an ozonecontaining gas, and a source of dopants for gettering alkali elements and for lowering the reflow temperature of the dielectric while attaining the desired low-k and gap-filling properties of the dielectric film. Phosphorous is a preferred dopant for gettering alkali elements such as sodium. Additional dopants for lowering the reflow temperature include, but are not limited to boron, germanium, arsenic, fluorine or combinations thereof. Excerpt(s): The present invention relates to semiconductor processing, and more particularly to a process for forming a blanket dielectric layer to fill gaps between device elements. In the manufacturing of semiconductor devices, as the dimensions have shrunk, it has become more challenging to provide dielectric film layers that provide adequate electrical isolation between interconnect features and device components in order to minimize RC delay and crosstalk. One method of doing this is to provide dielectric layers using materials having lower dielectric constants (low-k dielectrics) than conventional dielectric materials such as silicon dioxide (SiO.sub.2) or silicon nitride. Low-k dielectrics typically have dielectric constants below about 4, where air has a dielectric constant of 1. In particular, at the start of the fabrication of a back end of line (BEOL) module which contains the interconnect metal levels, a dielectric layer is typically provided between the devices or features, such as gate conductor stacks, on the substrate, or front end of line (FEOL), and the first layer of metal in the interconnect level or BEOL. This dielectric layer between the device level and the interconnect level is known as the pre-metal dielectric (PMD). The process of forming this PMD is referred to hereinafter as a middle of line process, or MOL process, as opposed to the BEOL processes used to form the intermetal dielectrics (IMD) that separate the metal layers. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for removing toxic substances in water Inventor(s): Santina, Peter F.; (Walnut Creek, CA) Correspondence: Thomas M. Freiburger; 25th Floor; 650 California Street; San Francisco; CA; 94108; US Patent Application Number: 20030196961 Date filed: May 21, 2003
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Abstract: Arsenic and TOC are removed from drinking water or wastewaters by use of finely-divided metallic iron in the presence of powered elemental sulfur or other sulfur compounds such as manganese sulfide, followed by an oxidation step. A premix may be produced for this process, by adding the iron, sulfur and oxidizing agent to water in a predetermined pH range. The iron and sulfur are mixed for a period of time dependent upon the temperature and pH of the water and the presence of complexing or sequestering minerals and organic acids in the water. An oxidizing agent is added to the mixture and agitating is continued. In a preferred embodiment the oxidizing agent is hydrogen peroxide. Water is decanted from the mixture after a sufficient reaction time, to produce a concentrated premix. This premix can be added to water intended for drinking or to industrial effluents containing toxic materials. Use of various gradations and mixtures of this sulfur-modified iron (SMI) premix have been successfully demonstrated to remove the following toxic substances from water: arsenic (arsenite and arsenate); disinfection byproducts and precursors; copper; chrome VI; sulfate; and chlorinated solvents including trichloroethene. Metals removed may be present in the untreated water in either the dissolved state or as a fine particulate. SMI has been fabricated using sulfur in the amount of up to 50% of the weight of the iron. SMI premix has been manufactured using a wetted but non-fluid mix at room temperature and at elevated temperature. SMI has been successfully demonstrated in pressure and gravity contact beds in both upflow and downflow modes. It has been prepared in uniformlygraded media similar in size and gradation to commercially-available filter media. Spent SMI can be recycled as a non-hazardous material as feed material to a steel production facility. Excerpt(s): This is a continuation-in-part of application Ser. No. 09/952,876, filed Sep. 14, 2001, now ______, which was a continuation-in-part of application Ser. No. 09/624,713, filed Jul. 25, 2000, which was a continuation of application Ser. No. 09/241,258, filed Feb. 1, 1999, U.S. Pat. No. 6,093,328, which was a continuation-in-part of application Ser. No. 08/742,652, filed Nov. 4, 1996, U.S. Pat. No. 5,866,014, which was a division of application Ser. No. 08/352,383, filed Dec. 8, 1994, now U.S. Pat. No. 5,575,919. This invention is directed to a method and system which removes several regulated, toxic mineral and organic precursor substances from drinking water or wastewater by causing them to be absorbed and adsorbed onto sulfur-activated sponge iron particles, which may be referred to as "sulfur-modified iron". Specifically, the method and system removes from water trace amounts of (1) dissolved, colloidal, and particulate arsenic, selenium, and lead; and (2) naturally-occurring organic compounds (TOC, total organic carbon in the water), which, when oxidized, form "disinfection byproducts"; and (3) other potentially harmful minerals. The subject matter of this invention is related to some extent to that of U.S. Pat. Nos. 4,940,549 and 5,200,082, which are directed to removal of selenium from agricultural drain water and from refinery effluents and other industrial waste waters. See also U.S. Pat. Nos. 5,575,919, 5,866,014 and 6,093,328. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for the catalytic conversion of gases with a high sulfur dioxide content Inventor(s): Anastasijevic, Nikola; (Altenstadt, DE), Hollnagel, Achim; (Frankfurt/Main, DE), Laibach, Stefan; (Frankfurt/Main, DE), Runkel, Marcus; (Partenheim, DE), Werner, Dietrich; (Messel, DE), Winkler, Egon; (Florsheim, DE) Correspondence: THE FIRM OF KARL F ROSS; 5676 RIVERDALE AVENUE; PO BOX 900; RIVERDALE (BRONX); NY; 10471-0900; US Patent Application Number: 20030157010 Date filed: January 31, 2003 Abstract: A gas mixture comprising molecular oxygen and 15 to 60 vol-% SO.sub.2 flows through a first catalyst layer which contains a catalyst containing vanadium pentoxide, and directly subsequently through a second catalyst layer which contains a catalyst containing iron. With an inlet temperature of 350 to 600.degree. C., the gas mixture is introduced into the first catalyst layer which contains a granular V.sub.2O.sub.5 catalyst and 20 to 80 wt-% catalytically inactive inert material. Directly subsequently, the gas mixture is introduced into the second catalyst layer with a temperature of 500 to 750.degree. C. Preferably, the catalyst of the second catalyst layer contains 3 to 30 wt-% arsenic oxide. There is produced an SO.sub.3-containing product gas with a volume ratio of SO.sub.2: SO.sub.3 of not more than 0.1. Excerpt(s): This invention relates to a process for the catalytic conversion of a gas mixture which contains oxygen and 15 to 60 vol-% SO.sub.2 at temperatures in the range from 350 to 800.degree. C. when flowing through a first catalyst layer which contains a catalyst containing vanadium pentoxide, and directly subsequently through a second catalyst layer which contains a catalyst containing iron, for producing a product gas containing SO.sub.3 with a volume ratio of SO.sub.2 to SO.sub.3 of not more than 0.1. The product gas containing SO.sub.3 can be processed to obtain sulfuric acid in a conventional way. A high SO.sub.2 content in the gas mixture to be converted leads to a high increase in temperature at the catalyst, as the SO.sub.2 oxidation is a strongly exothermal reaction. The conventional vanadium-based catalysts are thermally unstable at the resulting high temperatures, so that usually SO.sub.2 concentrations of only about 10 to 12 vol-% are admitted. To be able to also process gases with a higher SO.sub.2 content, it is proposed in DE-AS 2213580 to perform the conversion first in part on a V.sub.2O.sub.5 catalyst and then pass the gas through a bed of an iron oxide catalyst without intermediate cooling. Upon cooling, the gas should then be passed through at least one further catalyst bed. This process is relatively complex. The process described in DE 198 00 800 A1 employs a special, thermally stable iron catalyst, before which a vanadium-containing ignition layer may be provided. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of fabricating a semiconductor memory device Inventor(s): Chang, Tsai-Fu; (Taichung, TW), Chu, Shih-Lin; (Kaohsiung, TW), Yeh, Ching-Pen; (Hsinchu, TW) Correspondence: BIRCH STEWART KOLASCH & BIRCH; PO BOX 747; FALLS CHURCH; VA; 22040-0747; US Patent Application Number: 20030141278 Date filed: May 31, 2002
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Abstract: A method of fabricating a semiconductor memory device, particularly a mask ROM. A sacrificial oxide layer is formed on a silicon substrate and then a photoresist layer is formed on the sacrificial oxide layer. The photoresist layer is patterned to form a plurality of openings where bit lines are to extend respectively. Taking the patterned photoresist layer as a mask, arsenic ions are implanted into the silicon substrate through the openings and then boron ions are implanted into the silicon substrate through the openings. The implantation depth of boron ions are deeper than arsenic ions. The photoresist layer and the sacrificial oxide layer are removed after implantation. A gate oxide and a field oxide are grown simultaneously on the non-implanted and the implanted regions of the semiconductor layers respectively and a gate conductive layer is deposited on the silicon substrate. Excerpt(s): The present invention relates to a semiconductor memory device, and more particularly to a method of fabricating a mask read-only memory (ROM). Mask ROM (Read Only Memory) is one of the non-volatile memories that retain data even when electric power is off. The MOS transistor array in mask ROM is defined by a photomask during fabrication and the data is programmed according to the photomask pattern. After the data is written in mask ROM, it is neither erasable nor programmable, which makes mask ROM a high capacity, high reliability and low cost memory device applied in various kinds of information, communication or consumption products to store critical data. In the conventional fabrication process describing above, the silicon nitride film 3 is formed as a mask of oxidation to prevent the active areas defined in the silicon substrate 1 from being oxidized. Therefore, an additional step is needed to remove the silicon nitride film 3 after oxidation. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of forming MOS transistor graded junctions using multiple implant of low diffusion specie, and a device formed thereby Inventor(s): Chen, Aikwo Eric; (San Jose, CA) Correspondence: GARY CARY WARE & FREIDENRICH LLP; 1755 EMBARCADERO ROAD; PALO ALTO; CA; 94303-3340; US Patent Application Number: 20030087510 Date filed: November 6, 2001 Abstract: A method of forming a graded junction in silicon includes implanting a first impurity specie into a silicon substrate, annealing the silicon to drive the implanted first specie deeper into the silicon, implanting a second impurity specie into the silicon substrate, and annealing the silicon to drive the second specie deeper into the silicon. Both first and second species, which can be the same or different species, have low silicon diffusion coefficient(s), such as Arsenic or Antimony. At least some of the implanted first specie is driven further into the silicon than any of the implanted second specie. The first specie has a lower dosage and greater implant energy to help form a graded junction, and the second specie has a greater dosage and lower implant energy for creating a high impurity concentration at the surface of the substrate. Excerpt(s): The present invention relates to semiconductor manufacturing, and more particularly to the formation of graded junctions for MOS transistors. Formation of graded P-N junctions in silicon is well known in the art of making MOS transistors. Source and drain regions are typically formed in a silicon substrate (or a well in the substrate), which is doped to have one conductivity type (P or N), by implanting
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impurities to form regions in the substrate (or well) having the other conductivity type. For example, with silicon doped to have P type conductivity, impurities are implanted in select regions of the silicon to cause those regions to have N type conductivity. P-N or N-P junctions are formed at the boundaries of these regions. An ideal junction should have 1) a graded junction doping profile, 2) a high surface doping concentration, and 3) a shallow junction depth with minimal side diffusion. A graded junction means that the dopant profile gradually tails off at the boundary of the source or drain regions, which will sustain higher reverse bias voltages without being damaged (i.e. higher junction breakdown voltage). A high surface doping concentration forms a better ohmic contact at the surface of the substrate. The shallow junction depth with little side diffusion reduces the size of the regions, and thus the overall dimensions of the MOS device. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of manufacturing a dual gate semiconductor device with a poly-metal electrode Inventor(s): Yamamoto, Naoki; (Kawaguchi, JP) Correspondence: ANTONELLI TERRY STOUT AND KRAUS; SUITE 1800; 1300 NORTH SEVENTEENTH STREET; ARLINGTON; VA; 22209 Patent Application Number: 20030057499 Date filed: October 17, 2002 Abstract: In order to realize a dual gate CMOS semiconductor device with little leakage of boron that makes it possible to divisionally doping a p-type impurity and an n-type impurity into a polycrystalline silicon layer with one mask, a gate electrode has a high melting point metal/metallic nitride barrier/polycrystalline silicon structure. The boron is pre-doped in the polycrystalline silicon layer. The phosphorus or arsenic is doped in an n-channel area. Then, the annealing in a hydrogen atmosphere with vapor added therein is performed. As a result, the boron is segregated on the interface of the metallic nitride film and the phosphorus is segregated on the interface of the gate oxide film, for forming an n+ gate. Excerpt(s): The present invention relates to a CMOS (Complementary Metal-oxide Semiconductor) type semiconductor device having as a gate electrode p type and n type conductive polycrystalline silicon and a method of manufacture thereof. The current trend of the semiconductor device has been changed from a CMOS semiconductor device whose gate electrode is composed of only polycrystalline silicon containing an ntype impurity into the so-called dual gate CMOS semiconductor device in which the gate electrode of an n-channel MOS transistor is composed of polycrystalline silicon containing an n-type impurity and the gate electrode of a p-channel MOS transistor is composed of polycrystalline silicon containing a p-type impurity. This dual gate contains a silicon oxide film, a silicon nitride film or resist coated on the surface of the polycrystalline silicon except a target area. A target area (for example, n-type) impurity is implanted in the non-coated area with these films as a mask by means of the ionimplantation technique or the diffusion technique. After removing this mask materials, the surface of the polycrystalline silicon on the area having the above-mentioned impurity is covered with the similar mask materials. The impurity having the opposite conductive type (for example, p type) to the above-mentioned impurity is implanted in the non-covered area by means of the ion-implantation technique. For dividing the polycrystalline area into an n+ and a p+ conductive areas, as mentioned above, a mask material is formed on a specific area in doping a target impurity, which needs two
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associative processes of forming a mask. It is thus necessary to perform each process of forming a mask film, doing photolithography, and dry-etching a mask film twice. It means that the dual gate CMOS semiconductor composed as above has more manufacturing steps than the CMOS semiconductor device composed of polycrystalline silicon containing only one conductive impurity. This brings about the lowering of a manufacturing yield and the rise of a manufacturing cost of the semiconductor device and therefore the rise of a product cost. Further, the slip of fitting the mask patterns may be brought about in dividing the n-type and the p-type areas in the photolithography process. Hence, the fitting allowance is required, which has been an obstacle to finning the element and enhancing the concentration of the semiconductor device. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of manufacturing semiconductor device Inventor(s): Nishida, Yukio; (Tokyo, JP), Shirahata, Masayoshi; (Tokyo, JP) Correspondence: OBLON, SPIVAK, MCCLELLAND, MAIER & NEUSTADT, P.C.; 1940 DUKE STREET; ALEXANDRIA; VA; 22314; US Patent Application Number: 20030100173 Date filed: September 18, 2002 Abstract: A gate structure (4), an LDD region (6) and a sidewall (7) are provided in this order. Arsenic ions (8) are thereafter implanted into the upper surface of a silicon substrate (1) by tilted implantation. The next step is annealing for forming an MDD region (9) in the upper surface of the silicon substrate (1). The MDD region (9) and the gate structure (4) do not overlap one another in plan view. Further, the MDD region (9) formed into a depth shallower than that of the LDD region (6) is higher in concentration than the LDD region (6). Thereafter a source/drain region (11) higher in concentration than the MDD region (9) is provided by vertical implantation into a depth greater than that of the LDD region (6). Excerpt(s): The present invention relates to a method of manufacturing a semiconductor device and more particularly, to a method of manufacturing an MOSFET allowing compensation for degradation of its lifetime caused by hot carriers. In the field of LSI, there has been a growing trend towards microstructure and high degree of integration of an element, thereby allowing reduction in manufacturing cost and increase in operating speed. On the other hand, microstructure of the element will induce high electric field within a semiconductor substrate, causing degradation of characteristic of the element resulting from hot carriers. More particularly, carriers are accelerated by high electric field near drain to have high energy, pass over an energy barrier between the semiconductor substrate and a gate insulating film and get into the gate insulating film. As a result, there arises fluctuation in threshold voltage Vth of an MOSFET. In the present specification and claims, degradation of the element characteristic thereby caused is called as "lifetime degradation caused by Vth shift". The lifetime degradation caused by Vth shift can be compensated for by relaxing high electric field near the drain. For relaxation of high electric field near the drain, an LDD (lightly doped drain) structure has been widely adopted. As described above, the existence of the LDD regions 106 results in compensation for lifetime degradation caused by Vth shift. On the other hand, hot carriers getting into the lower parts of the sidewalls 107 from the LDD regions 106 may be another cause of degradation of element characteristic. More particularly, by repulsive force of carriers accumulated in the lower part of each sidewall 107 (corresponding to electrons when the device is an NMOSFET), carriers
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(electrons) near the upper surface of each LDD region 106 are pressed in a depth direction of the silicon substrate 101. The concentration of carriers in the vicinity of the upper surface of the LDD region 106 is thereby lowered, resulting in increase in parasitic resistance and reduction in drain current. In the present specification and claims, the degradation of the element characteristic thereby caused is called as "lifetime degradation caused by current reduction". Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of manufacturing semiconductor device with offset sidewall structure Inventor(s): Oda, Hidekazu; (Tokyo, JP), Ota, Kazunobu; (Tokyo, JP), Sayama, Hirokazu; (Tokyo, JP) Correspondence: OBLON, SPIVAK, MCCLELLAND, MAIER & NEUSTADT, P.C.; 1940 DUKE STREET; ALEXANDRIA; VA; 22314; US Patent Application Number: 20030059983 Date filed: August 6, 2002 Abstract: A method of manufacturing a semiconductor device with NMOS and PMOS transistors is provided. The semiconductor device can lessen a short channel effect, can reduce gate-drain current leakage, and can reduce parasitic capacitance due to gate overlaps, thereby inhibiting a reduction in the operating speed of circuits. An N-type impurity such as arsenic is ion implanted to a relatively low concentration in the surface of a silicon substrate (1) in a low-voltage NMOS region (LNR) thereby to form extension layers (61). Then, a silicon oxide film (OX2) is formed to cover the whole surface of the silicon substrate (1). The silicon oxide film (OX2) on the side surfaces of gate electrodes (51-54) is used as an offset sidewall. Then, boron is ion implanted to a relatively low concentration in the surface of the silicon substrate (1) in a low-voltage PMOS region (LPR) thereby to form P-type impurity layers (621) later to be extension layers (62). Excerpt(s): The present invention relates to a method of manufacturing a semiconductor device, especially a semiconductor device with an offset sidewall structure. In conventional semiconductor devices, impurity ion implantation is performed with gate electrodes as implant masks thereby to form extension layers in a self-aligned manner. The extension layers here are impurity layers which are formed to produce shallower junctions than main source/drain layers later to be formed. The extension layers are of the same conductivity type as the main source/drain layers and function as source/drain layers; thus, they should be referred to as source/drain extension layers but for convenience's sake, they are referred to herein as the extension layers. In recent semiconductor devices with minimum gate lengths of less than 0.1.mu.m, a short channel effect becomes more prominent and a slight reduction of the gate length from the design value will interfere with transistor operation. That is, the short channel effect has become the leading cause of low manufacturing yield. The gate overlap, which brings about a short channel effect, is thus an undesirable phenomenon. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of molding a glass composition into an optical element Inventor(s): Hashimoto, Kazuaki; (Tokyo, JP), Hirota, Shin-Ichiro; (Tokyo, JP), Oogami, Yu; (Tokyo, JP) Correspondence: SUGHRUE, MION, PLLC; 2100 Pennsylvania Avenue, N.W.; Washington; DC; 20037-3213; US Patent Application Number: 20030200766 Date filed: May 16, 2003 Abstract: A mold has a moling surface of a material containing silicon carbide and/or silicon nitride as a main component and a carbon thin film formed on the molding surface to prevent fusion sticking. A glass substance which has a sag point not higher than 565.degree. C. and a predetermined composition free from arsenic oxide is introduced into the mold. The glass substance is press-formed in a heated and softened condition into a glass optical element of high precision. Excerpt(s): This invention relates to a method of producing a glass optical element with a high precision and to a glass substance processed by the method into the glass optical element. A wide variety of development and research have been made about the technique of press-forming or press-molding a glass substance within a mold to produce a glass optical element of high precision. For example, one attempt has been directed to a mold which has a molding surface of silicon carbide, silicon nitride, and the like. Herein, silicon carbide and silicon nitride are excellent in hardness and strength against a high temperature. Such a molding surface of silicon carbide and/or silicon nitride may be deposited by a chemical vapor deposition (CVD) method. In this event, the molding surface has an excellent compactness without occurrence of surface defects, such as pores, and can be polished into a mirror surface. However, the molding surface of such materials is liable to be oxidized to form a silicon oxide surface layer of several tens of angstroms thick. In this case, it has been pointed out that fusion sticking often takes place between the molding surface and the glass substance during a press-forming step when the glass substance is composed of borosilicate glass or silicate glass containing a large amount of modification components, such as alkali or alkaline earth positive ions. Moreover, stress is concentrated in a following cooling step here and there on the molding surface, which causes cracks to occur on the molding surface. This results in a phenomenon such that the molding surface of the mold is scooped or removed in spots. This phenomenon will hereinafter be simply called a "pullout" or a "pullout" phenomenon. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Niobium powder, sintered body thereof, and capacitor using the same Inventor(s): Naito, Kazumi; (Chiba, JP), Omori, Kazuhiro; (Chiba, JP) Correspondence: SUGHRUE MION, PLLC; 2100 Pennsylvania Avenue, NW; Washington; DC; 20037-3213; US Patent Application Number: 20030205106 Date filed: January 13, 2003 Abstract: A niobium powder comprising at least one element selected from the group consisting of chromium, molybdenum, tungsten, boron, aluminum, gallium, indium, thallium, cerium, neodymium, titanium, rhenium, ruthenium, rhodium, palladium,
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silver, zinc, silicon, germanium, tin, phosphorus, arsenic, bismuth, rubidium, cesium, magnesium, strontium, barium, scandium, yttrium, lanthanum, praseodymium, samarium, europium, gadolinium, terbium, dysprosium, holmium, erbium, thulium, ytterbium, lutetium, hafnium, vanadium, osmium, iridium, platinum, gold, cadmium, mercury, lead, selenium and tellurium; a sintered body of the niobium powder; and a capacitor comprising a sintered body as one electrode, a dielectric material formed on the surface of the sintered body, and counter electrode provided on the dielectric material. Excerpt(s): This application is based on the provisions of 35U.S.C. Article 111(a). with claiming the benefit of filing dates of U.S. provisional applications Ser. Nos. 60/240,828 filed on Oct. 17, 2000, 60/269,855 filed on Feb. 21, 2001, 60/275,467 filed on Mar. 14, 2001, 60/297,441 filed on Jun. 13, 2001, under the provisions of 35 U.S.C. 111(b), pursuant to 35 U.S.C. Article 119(e) (1). The present invention relates to a niobium powder with a large capacitance per unit weight and good leakage current characteristics, a sintered body using the above-mentioned niobium powder, and a capacitor using the above-mentioned sintered body. Capacitors for use in electronic apparatus such as portable telephones and personal computers are required to be small in size and large in capacitance. Of those capacitors, a tantalum capacitor is preferably used, because the capacitance is large, not in proportion to the size, and the tantalum capacitor also has good characteristics. The tantalum capacitor usually employs a sintered body of a tantalum powder as an anode. In order to increase the capacitance of the tantalum capacitor, it is necessary to increase the weight of the sintered body, or to use a sintered body having an increased surface area obtained by pulverizing the tantalum powder. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Olefin trimerisation using a catalyst comprising a source of chromium,molybdenum or tungsten and a ligand containing at least one phosphorous, arsenic or antimony atom bound to at least one (hetero)hydrocarbyl group Inventor(s): Wass, Duncan Frank; (Twickenham, GB) Correspondence: FINNEGAN, HENDERSON, FARABOW, GARRETT & DUNNER; LLP; 1300 I STREET, NW; WASHINGTON; DC; 20005; US Patent Application Number: 20030166456 Date filed: January 10, 2003 Abstract: A process for the trimerisation of olefins is disclosed, comprising contacting a monomeric olefin or mixture of olefins under trimerisation conditions with a catalyst which comprises (a) a source of chromium, molybdenum or tungsten (b) a ligand containing at least one phosphorus, arsenic or antimony atom bound to at least one hydrocarbyl or heterohydrocarbyl group having a polar substituent, but excluding the case where all such polar substituents are phosphane, arsane or stibana groups; and optionally (c) an activator. Excerpt(s): This invention relates to the trimerisation of olefins, such as the preparation of 1-hexene by the trimerisation of ethylene. U.S. Pat. No. 5,198,563 and related patents by Phillips describe chromium-containing catalysts containing monodentate amide ligands useful for trimerising olefins. U.S. Pat. No. 5,968,866 discloses an ethylene oligomerisation/trimerisation process which uses a catalyst comprising a chromium complex which contains a coordinating asymmetric tridentate phosphane, arsane or
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stibane ligand (referred to therein as phosphine, arsine or stibine, and representing a phosphorus, arsenic or antimony atom attached to three hydrocarbyl groups) and an aluminoxane to produce alpha-olefins which are enriched in 1-hexene. There is no suggestion that it is possible to replace any of the phosphane, arsane or stibane groups: indeed, it is impossible to predict what the effect of such a replacement would be. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Phospor, arsenic and antimony compounds based upon diaryl-anellated diarylanellated bicyclo'2.2.n! parent substances and catalysts containing same Inventor(s): Ahlers, Wolfgang; (Worms, DE), Hofmann, Peter; (Heidelberg, DE), Paciello, Rocco; (Bad Durkheim, DE), Roper, Michael; (Wachenheim, DE), Warth, Daniel C.M.; (Heidelberg, DE) Correspondence: KEIL & WEINKAUF; 1350 CONNECTICUT AVENUE, N.W.; WASHINGTON; DC; 20036; US Patent Application Number: 20030055253 Date filed: August 8, 2002 Abstract: Novel compounds of phosphorus, of arsenic and of antimony can be used as ligands to form complexes of metals of transition group VIII which can be used in catalysts for hydroformylation, hydrocyanation, carbonylation, hydrogenations, oligomerization and polymerization of olefins and for metathesis. Excerpt(s): The present invention relates to compounds of phosphorus, of arsenic and of antimony, to a process for preparing them and to a catalyst comprising at least one complex of a metal of transition group VIII with such a compound as ligand. The invention further relates to the use of these catalysts for hydroformylation, hydrocyanation, carbonylation, hydrogenation, olefin oligomerization and olefin polymerization and for metathesis. Hydroformylation or the oxo process is an important industrial process employed for preparing aldehydes from olefins, carbon monoxide and hydrogen. These aldehydes can, if desired in the same process step, be hydrogenated by means of hydrogen to form the corresponding oxo alcohols. The reaction itself is strongly exothermic and generally proceeds under superatmospheric pressure at elevated temperatures in the presence of catalysts. Catalysts used are Co, Rh, Ir, Ru, Pd or Pt compounds or complexes which may be modified by N- or P-containing ligands to influence the activity and/or selectivity. The hydroformylation reaction results in formation of mixtures of isomeric aldehydes because CO can add onto either of the two carbon atoms of a double bond. In addition, double bond isomerization can also occur. In these isomeric mixtures, the n-aldehyde frequently predominates over the isoaldehyde and, owing to the significantly greater industrial importance of the naldehydes, optimization of the hydroformylation catalysts to achieve a greater nselectivity is sought. It is known that phosphorus-costaining ligands can be used in the low-pressure rhodium-catalyzed hydroformylation to stabilize and/or activate the catalyst metal. Examples of suitable phosphorus-containing ligands are phosphines, phosphinites, phosphonites, phosphites, phosphoramidites, phospholes and phosphabenzenes. The most widespread ligands at present are triarylphosphines, e.g. triphenylphosphine and sulfonated triphenylphosphine, since these have sufficient stability under the reaction conditions. However, these ligands have the disadvantage that, in general, only very high ligand excesses give satisfactory yields, in particular of linear aldehydes. On the other hand, chelating phosphites give high yields of linear aldehydes even at generally very low ligand excesses, but these ligands have the
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disadvantage of a low stability which, combined with their relatively high acquisition costs, has an adverse effect on the economics of the hydroformylation process. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Process for forming a storage electrode Inventor(s): Manabe, Kazutaka; (Tokyo, JP) Correspondence: Patent Group; Choate, Hall & Stewart; Exchange Place; 53 State Street; Boston; MA; 02109-2804; US Patent Application Number: 20030157743 Date filed: December 3, 2002 Abstract: In a process for forming a storage electrode having a number of hemi-spherical grains formed on a surface thereof, after a number of hemi-spherical grains are formed on a surface of the storage electrode, phosphorus or arsenic is ion-implanted to the hemi-spherical grains under an ion implantation energy of 20 keV to 50 keV. Excerpt(s): The present invention relates to a process for forming a storage electrode, and more specifically to a process for forming a storage electrode having a number of fine convexities formed on a surface thereof. In a semiconductor memory such as a DRAM (dynamic random access memory), the elevation of the integration density is always demanded. Namely, the target is how to increase the capacitance per an occupying area. One means for achieving this target is a so called HSG (Hemi-SphericalGrain) technology. This HSG technology is to form a number of fine convexities in the form of a mushroom or a hemi-sphere on a surface of a storage electrode so as to increase a surface area of the storage electrode thereby to increase a capacitance. Referring to FIGS. 1A to 1C, there are shown diagrammatic sectional views for illustrating one example of a prior art process for forming a number of hemi-spherical grains on a surface of a storage electrode (capacitor lower plate). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Process for preparing an arsenic-doped single crystal silicon using a submersed dopant feeder Inventor(s): Banan, Mohsen; (Grover, MO), Kulkarni, Milind; (St. Louis, MO), Luers, Christopher V.; (O'Fallon, MO) Correspondence: SENNIGER POWERS LEAVITT AND ROEDEL; ONE METROPOLITAN SQUARE; 16TH FLOOR; ST LOUIS; MO; 63102; US Patent Application Number: 20030061985 Date filed: September 27, 2002 Abstract: A single crystal silicon ingot having a constant diameter portion that contains arsenic dopant atoms at a concentration which results in the silicon having a resistivity that is less than about 0.0025.OMEGA.multidot.cm, and wafers sliced therefrom. The present invention is also directed to a method of doping a silicon melt so that the foregoing ingot may be produced. Specifically, the method entails introducing arsenic dopant below the surface of a silicon melt, rather than on the surface, using a dopant feeder that is at least partially submersed in the silicon melt.
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Excerpt(s): This application claims the benefit of U.S. Provisional Application Nos. 60/325,622 and 60/325,660, filed Sep. 28, 2001. The present invention generally relates to the preparation of semiconductor grade single crystal silicon, which is used in the manufacture of electronic components. More particularly, the present invention relates to a process for the controlled arsenic doping of single crystal silicon, prepared in accordance with the Czochralski method, in order to achieve low resistivity therein. Single crystal silicon, which is the starting material for most processes for the fabrication of semiconductor electronic components, is commonly prepared by the so-called Czochralski ("Cz") method. In this method, polycrystalline silicon ("polysilicon") is charged to a crucible and melted, a seed crystal is brought into contact with the molten silicon, and a single crystal is grown by slow extraction. After formation of a neck is complete, the diameter of the crystal is enlarged by decreasing the pulling rate and/or the temperature field in the melt until the desired or target diameter is reached. The cylindrical main body of the crystal which has an approximately constant diameter is then grown by controlling the pull rate and the melt temperature while compensating for the decreasing melt level. Near the end of the growth process but before the crucible is emptied of molten silicon, the crystal diameter may be reduced gradually to form a conical opposite end. Typically, the opposite end is formed by increasing the crystal pull rate and heat supplied to the crucible. When the diameter becomes small enough, the crystal is then separated from the melt. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Process for producing arsenic trioxide formulations and methods for treating cancer using arsenic trioxide or melarsoprol Inventor(s): Ellison, Ralph; (Palm Beach, FL), Gabrilove, Janice L.; (New York, NY), Pandolfi, Pier P.; (New York, NY), Soignet, Steven; (New York, NY), Warrell, Raymond P. JR.; (Westfield, NJ) Correspondence: Stephen A. Bent; Foley & Lardner, Washington Harbour; Suite 500; 3000 K Street, N.W.; Washington; DC; 20007-5143; US Patent Application Number: 20030099719 Date filed: September 30, 2002 Abstract: The invention relates to the use of arsenic compounds to treat a variety of leukemia, lymphoma and solid tumors. Further, the arsenic compounds may be used in combination with other therapeutic agents, such as a retinoid. The invention also provides a process for producing arsenic trioxide formulations. Excerpt(s): The present invention relates to methods and compositions for the treatment of leukemia, lymphoma, and certain other cancers. More specifically, the present invention relates to the novel uses of arsenic trioxide and an organic arsenic compound for treating acute leukemia and chronic leukemia. Cancer is characterized primarily by an increase in the number of abnormal cells derived from a given normal tissue, invasion of adjacent tissues by these abnormal cells, and lymphatic or blood-borne spread of malignant cells to regional lymph nodes and to distant sites (metastasis). Clinical data and molecular biologic studies indicate that cancer is a multistep process that begins with minor preneoplastic changes, which may under certain conditions progress to neoplasia. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Process for the preparation of arsenic free water, apparatus therefor, method for the manufacture of porous ceramics for use in pressure filtration to produce arsenic free water Inventor(s): Bandyopadhya, Sibdas; (West Bengal, IN), Ghosh, Bishnupada; (West Bengal, IN), Kundu, Dipali; (West Bengal, IN), Maiti, Himadri Sekhar; (West Bengal, IN), Roy, Somendra Nath; (West Bengal, IN) Correspondence: NIXON & VANDERHYE P.C.; 8th Floor; 1100 North Glebe Road; Arlington; VA; 22201; US Patent Application Number: 20030183579 Date filed: March 29, 2002 Abstract: The present invention relates to a process for the preparation of arsenic free water and an apparatus therefor. The present invention also relates to a porous ceramic useful for pressure filtration in order to produce arsenic free water. The present invention particularly relates to a process for preparing arsenic free (<10 ppb) water from arsenic contaminated ground water and apparatus therefor. Excerpt(s): The present invention relates to a process for the preparation of arsenic free water and an apparatus therefor. The present invention also relates to a porous ceramic useful for pressure filtration in order to produce arsenic free water The present invention particularly relates to a process for preparing arsenic free (<10 ppb) water from arsenic contaminated ground water and an equipment therefor. Ground water drawn from intermediate aquifers of various parts of West Bengal and Bangladesh was found to contain arsenic above the permissible limit of 0.05 ppm. The WHO recommended limit being 0.01 ppm. Thus the water from tube wells and hand pumps is unsuitable for drinking purpose. Arsenic contamination of ground water therefore assumed a serious public health issue as ground water serves more than 80% of the drinking water needs primarily in the rural sector. Various physical and chemical processes are known for removing arsenic from wastewater for recovery and/or as a pollution abatement measure. Separation can be achieved by arsenic adsorption on amorphous aluminium hydroxide By such means, as discussed in the Journal of Colloids and Interface Science, volume 54,No. 3,pages 391-399,1976, a plateau of 0.3 ppm arsenic can be attained but further reduction of arsenic content is difficult. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Process for the treatment or removal of impurities in a hydrometallurgical extraction process Inventor(s): Jones, David L.; (Delta, CA) Correspondence: Elbie R. de Kock; RUSSELL REYNEKE LAW CORPORATION; Suite 700- Two Bentall Centre; 555 Burrard Street; Vancouver; BC; V7X 1M8; CA Patent Application Number: 20030192404 Date filed: April 16, 2002 Abstract: A Process for the treatment or removal of impurities, such as arsenic, antimony or bismuth, generated as by-products during smelting and refining of copper concentrates, comprises subjecting the by-products to pressure oxidation along with a copper concentrate in a hydrometallurgical copper extraction process or the treatment of
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impurities when present in a concentrate by subjecting the concentrate to a hydrometallurgical extraction process. Excerpt(s): This invention relates to a process for the treatment or removal of impurities such as arsenic, antimony and bismuth, such as, for example, generated as by-products during smelting and refining of copper concentrates or when present in an ore or concentrate being treated by a hydrometallurgical metal extraction process. It also relates to the treatment of other impurities, such as fluoride and mercury. Arsenic, antimony and bismuth are often found in naturally occurring copper (sulphide) ores, and therefore each or several of them are often a minor constituent of copper concentrates which are obtained from sulphide ore by means of the well-established floatation processes. These elements have little or no commercial value in copper concentrates, unlike other base metals which may also occur in copper concentrates, such as zinc, nickel or cobalt, but instead constitute deleterious impurities which must be removed during the subsequent refining process on the concentrate, otherwise the product of such refining process, i.e. copper metal, will be impure and lose value. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Reactive compositions for fluid treatment Inventor(s): Hughes, Kenneth D.; (Alpharetta, GA) Correspondence: JOHN S. PRATT, ESQ; KILPATRICK STOCKTON, LLP; 1100 PEACHTREE STREET; SUITE 2800; ATLANTA; GA; 30309; US Patent Application Number: 20030196966 Date filed: April 17, 2002 Abstract: A method and device for the chemical conversion, filtration and/or purification of fluids water or other solutions containing microbiological and chemical contaminants, such as fluids containing arsenic, chlorine, bacteria, viruses, and cysts, where the fluid is passed through a purification material composed of fluid treatment carbon, metal phosphates, metal oxides, reduced metals, metal silicates, metal sulfates, metal carbonates, metal hydroxides, or combinations thereof. The material may be included in a fixed binder matrix. Excerpt(s): This invention relates generally to the field of solution and fluid treatment devices, primarily to aqueous solution and water treatment, devices for gases and industrial fluids and other aqueous liquids, which modify the components of the gas or aqueous liquid solution passed through them. In its more particular aspects, the invention relates to the field of such devices that react with chemical and microbiological contaminants, including toxic metals and hydrocarbons, bacteria and viruses and their components, contained in water or aqueous solutions. Purification or filtration of water or other aqueous solutions is necessary for many applications, from the provision of safe or potable drinking water to biotechnology applications including fermentation processing and separation of components from biological fluids, and to industrial processes that require waste stream treatment and recovery of process chemicals. Similarly, the removal of contaminants from fluids used in medical procedures and semiconductor fabrication processes, where ultrapurified fluids are required, and in environments where the fluids will be recirculated, such as aircraft or spacecraft, is also an important application for filtration and fluid treatment materials. In recent years, the need for water filtration and purification in the home has become more recognized, and the competing concerns of energy efficiency and residential fluid
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quality have lead to numerous filtration products, that purport to remove small particles, allergens, microorganisms, intentionally introduced biotoxins, pesticides, and toxic metals such as lead, mercury, and arsenic. There are many well-known methods currently used for water purification, such as reverse osmosis, distillation, ion-exchange, chemical adsorption, coagulation, and filtering or retention. Particle filtration may be completed through the use of membranes or layers of granular materials. Other fluid purification techniques involve chemical introduction which alters the state or chemical identity of the contaminant. Examples of chemical additives include oxidizing agents, flocculating agents, and precipitation agents. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Remediation of metal contaminants with hydrocarbon-utilizing bacteria Inventor(s): Perriello, Felix Anthony; (Norwood, MA) Correspondence: Alan G. Towner; Pietragallo, Bosick & Gordon; One Oxford Centre, 38th Floor; 301 Grant Street; Pittsburgh; PA; 15219; US Patent Application Number: 20030062306 Date filed: July 26, 2002 Abstract: Methods and apparatus are disclosed for remediating metal contaminants using hydrocarbons which stimulate the growth of hydrocarbon-utilizing bacteria. The metal contaminants may include heavy metals such as arsenic, antimony, beryllium, cadmium, chromium, copper, lead, mercury, iron, manganese, magnesium, radium, nickel, selenium, silver, thallium and zinc. The hydrocarbon may include alkanes, alkenes, alkynes, poly(alkene)s, poly(alkyne)s, aromatic hydrocarbons, aromatic hydrocarbon polymers and aliphatic hydrocarbons. Butane is a particularly suitable hydrocarbon which stimulates the growth of butane-utilizing bacteria. Remediation may occur in-situ or ex-situ, and may occur under aerobic, anaerobic or dual aerobic/anaerobic conditions. Examples of applications include the remediation of heavy metals, the remediation of arsenic impacted surface water, groundwater and/or soil, the remediation of acid mine drainage, and the treatment of spent metal plating solutions. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 09/878,656 filed Jun. 11, 2001, which is a continuation of U.S. patent application Ser. No. 09/293,088, now U.S. Pat. No. 6,244,346, which is a continuation-in-part of U.S. patent application Ser. No. 09/275,320, now U.S. Pat. No. 6,245,235, which is a continuation-inpart of U.S. patent application Ser. No. 08/767,750, now U.S. Pat. No. 5,888,396, which are incorporated herein by reference. This application also claims the benefit of U.S. Provisional Application Serial Nos. 60/308,487, 60/308,210 and 60/308,212 filed Jul. 27, 2001, and U.S. Provisional Application Serial No. 60/344,868 filed Dec. 31, 2001, which are incorporated herein by reference. The present invention relates to the remediation of metal contaminants, and more particularly relates to the remediation of metal contaminants with hydrocarbon-utilizing bacteria. Various types of metal contaminants are present in surface water, groundwater, soil, storage tanks, lagoons, industrial gaseous emissions and other sites, often as wastes or byproducts of industrial processes. Arsenic, antimony, beryllium, cadmium, chromium, copper, lead, mercury, iron, manganese, magnesium, radium, nickel, selenium, silver, thallium and zinc are considered to be priority pollutants by the U.S. Environmental Protection Agency (EPA). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Semiconductor device and manufacturing method thereof Inventor(s): Kumeno, Kazuyuki; (Kawasaki, JP) Correspondence: ARMSTRONG,WESTERMAN & HATTORI, LLP; 1725 K STREET, NW; SUITE 1000; WASHINGTON; DC; 20006; US Patent Application Number: 20030107090 Date filed: March 21, 2002 Abstract: When an arsenic ion (As.sup.+) large in mass is injected, polysilicon films are covered with a fifth resist mask so as to cover an end of the resist mask covering the polysilicon films to form a PMOS forming region. Through this process, a silicide nonforming region is arranged not to overlap with a pn junction to prevent the silicide nonforming region from increasing in resistance. Excerpt(s): This application is based upon and claims priority of Japanese Patent Application No. 2001-377623, filed on Dec. 11, 2001, the contents being incorporated herein by reference. The present invention relates to a semiconductor device and a manufacturing method thereof, and, in particular, the present invention is best suited when applied to a semiconductor device provided with a gate electrode including silicide. In a system LSI of late years, in order to lower the resistance of wiring connecting between polysilicon gate electrode and element, a laminated structure of polysilicon and silicide is adopted, and a dual structure in which a gate of NMOS transistor is an N-type and a gate of PMOS transistor is a P-type is adopted. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Semiconductor device and manufacturing method thereof Inventor(s): Saiki, Takashi; (Kawasaki, JP) Correspondence: ARMSTRONG,WESTERMAN & HATTORI, LLP; 1725 K STREET, NW; SUITE 1000; WASHINGTON; DC; 20006; US Patent Application Number: 20030178685 Date filed: October 21, 2002 Abstract: A dose of arsenic for an extension region in an NMOS transistor is in a range from 5.times.10.sup.14 to 2.times.10.sup.15 ions/cm.sup.2 and preferably in a range from 1.1.times.10.sup.15 to 1.5.times.10.sup.15 ions/cm.sup.2. Also, in addition to arsenic, a low concentration of phosphorus is doped into the extension region by ion implantation. Consequently, with a semiconductor device of the CMOS structure, it is possible to prevent unwanted creeping of silicide that occurs often in the shallow junction region depending on a concentration of an impurity having a low diffusion coefficient as represented by arsenic. Further, not only can the resistance in the shallow junction region be lowered, but also an amount of overlaps can be optimized in each transistor. Excerpt(s): This application is based upon and claims priority of Japanese Patent Application No. 2002-077218, filed on Mar. 19, 2002, the contents being incorporated herein by reference. The present invention relates to a semiconductor device and a manufacturing method thereof, which are particularly suitable for salicide CMOS transistor applications. Advancements in miniaturization and speedups of a semiconductor device in recent years have been increasing the need for a highperformance and low-power-consumption transistor. In order to meet such a need, it is
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crucial to solve a problem of wiring delay by lowering the resistance of various wires. To this end, for example, a so-called silicide structure, and further, a so-called salicide structure are adopted in a CMOS transistor or the like. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Semiconductor device and method of manufacturing same Inventor(s): Kuroyanagi, Akira; (Okazaki-shi, JP), Okabe, Yoshifumi; (Nagoya-shi, JP), Yamaoka, Masami; (Anjo-shi, JP) Correspondence: HARNESS, DICKEY & PIERCE, P.L.C.; P.O. BOX 828; BLOOMFIELD HILLS; MI; 48303; US Patent Application Number: 20030052366 Date filed: October 30, 2002 Abstract: A semiconductor device including an N-type semiconductor substrate which includes arsenic as an impurity, a first electrode formed on a main surface of the N-type semiconductor substrate, a ground surface formed on another surface of the N-type semiconductor substrate, a second electrode formed on the ground surface and ohmically-contacted with the N-type semiconductor substrate, a semiconductor element formed in the N-type semiconductor substrate and flowing current between the first electrode and the second electrode during ON-state thereof. The device has a reduced ON-resistance thereof. Excerpt(s): This invention relates to a semiconductor device which has a low ONresistance, and further, to a method of manufacturing such a semiconductor device. Many kinds of methods of manufacturing for reducing an ON-resistance of a semiconductor device have been known. For example, Japanese Unexamined Patent Publication 1-169970 discloses a method which an N-type impurity layer is formed in a back surface of a drain substrate so as to reduce a contact resistance between the drain substrate and a drain electrode. Japanese Examined Patent Publication 58-45814 discloses a method of manufacturing the semiconductor device which has a good ohmic contact between the drain substrate and the drain electrode. The device has a multilayer metal electrode on a back surface of a drain substrate. The multilayer metal electrode consists of layers having a gold layer as a main layer. wherein, R1 denotes a contact resistance of a drain electrode 50; R2 denotes a contact resistance between the drain electrode 50 and an N-Type impurity layer 52; R3 denotes a resistance of N drain substrate 54; R4, R5 and R6 denote resistances of N drain region 56 respectively; R7 denotes a resistance of P-Type diffusion region 58 for forming a channel; R8 denotes a resistance of N-type source 60; R9 denotes a contact resistance between the N-Type source 60 and a source electrode 62; and R10 denotes a resistance of the source electrode 62. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Silicon wafer and epitaxial silicon wafer Inventor(s): Horai, Masataka; (Tokyo, JP), Ono, Toshiaki; (Tokyo, JP) Correspondence: CLARK & BRODY; Suite 600; 1750 K Street, NW; Washington; DC; 20006; US Patent Application Number: 20030104222 Date filed: September 18, 2002 Abstract: The invention relates to a silicon wafer and an epitaxial silicon wafer, which are doped with arsenic (As) as an n-type dopant and are excellent in gettering characteristics. A first silicon wafer has a resistivity of 10.OMEGA.cm to 0.001.OMEGA.cm as a result of addition of arsenic and has a nitrogen concentration of 1.times.10.sup.13 to 1.times.10.sup.15 atoms/cm.sup.3. A second silicon wafer has a resistivity of 0.1.OMEGA.cm to 0.005.OMEGA.cm and a nitrogen concentration of 1.times.10.sup.14 to 1.times.10.sup.15 atoms/cm.sup.3. A third silicon wafer has a resistivity of 0.005.OMEGA.cm to 0.001.OMEGA.cm and a nitrogen concentration of 1.times.10.sup.13 to 3.times.10.sup.14 atoms/cm.sup.3. An epitaxial silicon wafer derived from any of the first to third silicon wafers by forming an epitaxial layer in the surface layer portion is provided. In producing this epitaxial silicon wafer, epitaxial layer formation is desirably carried out after subjecting the silicon wafer to heat treatment for forming oxygen precipitates under conditions of a temperature not lower than 700.degree. C. but lower than 900.degree. C. and a period of 30 minutes to 4 hours. By these, an oxygen precipitate density can be secured and a sufficient gettering effect can be produced in the device producing process in spite of their being n-type silicon wafers doped with a high concentration of arsenic. Excerpt(s): The present invention relates to a silicon wafer and an epitaxial silicon wafer, which are to be used for the manufacture of semiconductor integrated circuit devices and, more particularly, to a silicon wafer and an epitaxial silicon wafer, which contain arsenic (As) added as an n-type dopant and are excellent in gettering characteristics. In recent years, the tendency toward higher degree of integration of silicon semiconductor integrated circuit devices has been rapidly increasing and, accordingly, silicon wafers on which devices are formed have been subjected to increasingly severe quality standards. Therefore, in manufacturing highly integrated devices, it is necessary to employ the socalled gettering technology which comprises trapping metal impurities at a site (in a sink) remote from the device active region, since the occurrence of crystal defects or metal impurities other than a dopant in the device active region where devices are to be formed leads to deterioration in electric characteristics, for example an increase in leakage current. It is generally well known that, in p-type silicon wafers doped with boron (B) or the like, crystal defects including oxygen precipitates due to supersaturated interstitial oxygen, dislocations, and stacking faults, are induced in the device producing process. Therefore, an effect of gettering heavy metal impurities by oxygen-induced crystal defects which are spontaneously induced upon heat treatment in the device producing process, namely the intrinsic gettering (IG) effect, is produced in p-type silicon wafers. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Silicon-on-insulator SRAM cells with increased stability and yield Inventor(s): Aipperspach, Anthony Gus; (Austin, TX), Christensen, Todd Alan; (Rochester, MN) Correspondence: Robert R. Williams; IBM Corporation, Dept. 917; 3605 Highway 52 North; Rochester; MN; 55901-7829; US Patent Application Number: 20030123279 Date filed: January 3, 2002 Abstract: An SRAM memory cell made with increased stability using SOI technology is provided. Increased stability results from a decreased threshold voltage of the pullup pfets included in the inverter. Preferably the decrease of threshold voltage is achieved using a decreased concentration of phosphorus, antimony, arsenic, or other n-type ions during implantation. Excerpt(s): This application is related to U.S. patent application Ser. No. 09/962,403 filed Sep. 25, 2001 entitled SILICON-ON-INSULATOR SRAM CELLS WITH INCREASED STABILITY AND YIELD, which application is owned by the assignee herein and which is incorporated by reference in its entirety. The present invention relates generally to the field of static random access memory (SRAM) cells and more specifically relates to increasing the stability of semiconductor-on-insulator, especially silicon-on-insulator (SOI), SRAM cells because certain transistors in the cells have a decreased threshold voltage. Metal Oxide Semiconductor Field Effect Transistor (MOSFET) scaling on bulk silicon has been the primary focus of the semiconductor and microelectronic industry for achieving Complementary Metal Oxide Semiconductor (CMOS) chip performance and density objectives. The shrinking of MOSFET dimensions for high density, low power and enhanced performance requires reduced power supply voltages. Because power consumption is a function of capacitance, voltage, and transition frequency, the focus has been on reducing both the capacitance and the voltage as the operating or switching frequency increases. As a result, dielectric thickness and channel length of the transistors are scaled with power supply voltage. Power supply reduction continues to be the trend for future low voltage CMOS; however, transistor performance is severely impacted by both junction capacitance and the MOSFET body effect at these lower voltages. As technologies scale below 0.25.mu.m channel lengths to 0.15.mu.m and 0.1.mu.m and shorter, short channel effects, gate resistance, channel profiling and other barriers become an issue for advanced CMOS technologies. While significant success has been achieved with successive scaling of bulk CMOS technology, the manufacturing control issues and power consumption become increasingly difficult. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Thin semiconductor gainn layer, method for preparing same, light-emitting diode comprising said layer and illumination device Inventor(s): Damilano, Benjamin Gerard Pierre; (Antibes, FR), Grandjean, Nicolas Pierre; (LeCannet, FR), Massies, Jean Claude; (Valbonne, FR) Correspondence: Thelen Reid & Priest; PO Box 640640; San Jose; CA; 95164-0640; US Patent Application Number: 20030092209 Date filed: October 11, 2002
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Abstract: Thin, single semi conducting layer of GaInN, possibly containing a small percentage of arsenic, phosphorus or antimony, the said layer emitting at least two visible lights with determined colours which can be combined, particularly to obtain white light.Method for preparing this layer.Light emitting diode (LED), particularly a LED emitting white light comprising such a thin layer in its active zone, and lighting device comprising such a diode. Excerpt(s): The invention relates to a thin, semi conducting layer of GaInN and its preparation method. The invention also deals with a light emitting diode (LED), and particularly a light emitting diode emitting white light, comprising such a thin layer in its active zone and finally a lighting device comprising such a diode. The technical field of the invention may be defined as being the generation of white light. The white light satisfies the criteria set down by the IEC in 1964. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with arsenic, 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 “arsenic” (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 arsenic. You can also use this procedure to view pending patent applications concerning arsenic. 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. BOOKS ON ARSENIC Overview This chapter provides bibliographic book references relating to arsenic. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on arsenic include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print®). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “arsenic” at online booksellers’ Web sites, you may discover nonmedical books that use the generic term “arsenic” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “arsenic” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
Analytical Chemistry of Arsenic in Drinking Water by Andrew D. Eaton, et al (1998); ISBN: 0898679079; http://www.amazon.com/exec/obidos/ASIN/0898679079/icongroupinterna
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Antimony, Arsenic, Beryllium, Chromium, Cobalt, Copper, Gallium, Germanium, Indium, Nickel, Selenium, Silver, Thallium, Vanadium and Zinc by Electrothermal AAS, 1988 (Methods for the Examination of Waters and Associated Materials); ISBN: 0117520950; http://www.amazon.com/exec/obidos/ASIN/0117520950/icongroupinterna
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Arsenic; ISBN: 0309026040; http://www.amazon.com/exec/obidos/ASIN/0309026040/icongroupinterna
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Arsenic (1160018) (1981); ISBN: 9241540788; http://www.amazon.com/exec/obidos/ASIN/9241540788/icongroupinterna
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Arsenic and Old Lead: A Layman's Guide to Pollution and Conservation by Ray Y. Gildea; ISBN: 0878050655; http://www.amazon.com/exec/obidos/ASIN/0878050655/icongroupinterna
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Arsenic and Old Mustard: Chemical Problems in the Destruction of Old Arsenical and 'Mustard' Munitions by Joseph F. Bunnett (Editor), et al (1998); ISBN: 0792351754; http://www.amazon.com/exec/obidos/ASIN/0792351754/icongroupinterna
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Arsenic and Tin in Foods: Reviews of Commonly Used Methods of Analysis by William Horwitz (1980); ISBN: 9251007276; http://www.amazon.com/exec/obidos/ASIN/9251007276/icongroupinterna
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Arsenic Exposure and Health Effects IV by Willard R. Chappell (Editor), et al; ISBN: 0080440673; http://www.amazon.com/exec/obidos/ASIN/0080440673/icongroupinterna
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Arsenic Exposure and Health Effects V: Proceedings of the Fifth International Conference on Arsenic Exposure and Health Effects, July 14-18, 2002, San Diego, California by W. R. Chappell (Editor), et al (2004); ISBN: 0444514414; http://www.amazon.com/exec/obidos/ASIN/0444514414/icongroupinterna
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Arsenic in Drinking Water by National Research Council (1999); ISBN: 0309063337; http://www.amazon.com/exec/obidos/ASIN/0309063337/icongroupinterna
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Arsenic in Drinking Water by World Health Organization (Editor), World Health Organization; ISBN: 1900222663; http://www.amazon.com/exec/obidos/ASIN/1900222663/icongroupinterna
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Arsenic in Drinking Water: 2001 Update by National Research Council Subcommittee on Arsenic in Drinking W, et al; ISBN: 0309076293; http://www.amazon.com/exec/obidos/ASIN/0309076293/icongroupinterna
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Arsenic in Ground Water by Alan H. Welch (Editor), Kenneth G. Stollenwerk (Editor) (2003); ISBN: 1402073178; http://www.amazon.com/exec/obidos/ASIN/1402073178/icongroupinterna
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Arsenic in potable waters by atomic absorption spectrophotometry (semiautomatic method) 1982; ISBN: 0117516791; http://www.amazon.com/exec/obidos/ASIN/0117516791/icongroupinterna
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Arsenic in the Aquatic Environment; ISBN: 0412475308; http://www.amazon.com/exec/obidos/ASIN/0412475308/icongroupinterna
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Arsenic in the environment and its incidence on health, May 25 to 29, 1992 by Ana María Sancha F.; ISBN: 9561901706; http://www.amazon.com/exec/obidos/ASIN/9561901706/icongroupinterna
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Arsenic in the Environment, Cycling and Characterization by Jerome O. Nriagu (Editor) (1994); ISBN: 0471579297; http://www.amazon.com/exec/obidos/ASIN/0471579297/icongroupinterna
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Arsenic Metallurgy-Fundamentals and Applications by R.G. Reddy, et al; ISBN: 0873390377; http://www.amazon.com/exec/obidos/ASIN/0873390377/icongroupinterna
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Arsenic Removal by Enhanced Coagulation and Membrane Processes by Janet Et Al Hering, Janet G. Hering; ISBN: 089867865X; http://www.amazon.com/exec/obidos/ASIN/089867865X/icongroupinterna
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Arsenic Removal from Drinking Water by Tatiana Bianchelli (Editor) (2004); ISBN: 1590337239; http://www.amazon.com/exec/obidos/ASIN/1590337239/icongroupinterna
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Arsenic Removal from Drinking Water by Coagulation/Filtration and Lime Softening Plants by Keith A. Fields, et al (2000); ISBN: 0756726565; http://www.amazon.com/exec/obidos/ASIN/0756726565/icongroupinterna
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Arsenic Treatability Options and Evaluation of Residuals Management Issues by Gary Amy, et al (2001); ISBN: 1583210032; http://www.amazon.com/exec/obidos/ASIN/1583210032/icongroupinterna
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Arsenic: Answers to Questions Commonly Asked by Drinking Water Professionals by Bryan Black (Editor) (1999); ISBN: 158321058X; http://www.amazon.com/exec/obidos/ASIN/158321058X/icongroupinterna
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Arsenic: Exposure and Health by Willard R. Chappell (Editor), et al; ISBN: 0905927494; http://www.amazon.com/exec/obidos/ASIN/0905927494/icongroupinterna
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Arsenic: Industrial, Biomedical, Environmental Perspectives (Van Nostrand Reinhold Environmental Engineering Series) by Arsenic Symposium, et al; ISBN: 0442214960; http://www.amazon.com/exec/obidos/ASIN/0442214960/icongroupinterna
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Arsenical pesticides : a symposium sponsored by the Division of Pesticide Chemistry at the 168th meeting of the American Chemical Society, Atlantic City, N.J., Sept. 9, 1974; ISBN: 0841202435; http://www.amazon.com/exec/obidos/ASIN/0841202435/icongroupinterna
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Biological and Environmental Effects of Arsenic: Topics in Environmental Health by Bruce A. Fowler (Editor); ISBN: 0444805133; http://www.amazon.com/exec/obidos/ASIN/0444805133/icongroupinterna
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Chemistry & Treatment of Arsenic in Drinking Water by Ramesh Narasimhan, et al (2004); ISBN: 1583212760; http://www.amazon.com/exec/obidos/ASIN/1583212760/icongroupinterna
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Chemistry of Arsenic, Antimony and Bismuth by N. C. Norman (Editor) (1997); ISBN: 075140389X; http://www.amazon.com/exec/obidos/ASIN/075140389X/icongroupinterna
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Comprehensive Organometallic Chemistry II : Silicon Group, Arsenic, Antimony and Bismuth by E. W. Abel, et al; ISBN: 0080423094; http://www.amazon.com/exec/obidos/ASIN/0080423094/icongroupinterna
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DRI Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, vanadi: Um, and Zinc (Dietary Reference Intakes) by National Academy Press (2002); ISBN: 0309072794; http://www.amazon.com/exec/obidos/ASIN/0309072794/icongroupinterna
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Environmental Chemistry of Arsenic by William T., Jr. Frankenberger (Editor); ISBN: 0824706765; http://www.amazon.com/exec/obidos/ASIN/0824706765/icongroupinterna
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Feasibility of New Epidemiologic Studies of Low Level Arsenic by Allan H. Smith (Editor), et al; ISBN: 0898679613; http://www.amazon.com/exec/obidos/ASIN/0898679613/icongroupinterna
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Food Additives and Contaminants Committee report on the review of the arsenic in food regulations; ISBN: 0112426514; http://www.amazon.com/exec/obidos/ASIN/0112426514/icongroupinterna
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Food and Drugs Arsenic in Food (Scotland) Amendment Regulations 1973 (1973); ISBN: 011031039X; http://www.amazon.com/exec/obidos/ASIN/011031039X/icongroupinterna
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From Arsenic to Ddt: A History of Entomology in Western Canada by Paul W Riegert; ISBN: 0802054994; http://www.amazon.com/exec/obidos/ASIN/0802054994/icongroupinterna
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Gmelin: Handbook of Inorganic and Organometallic Chemistry: W - Tungsten: Supplement Vol A: Part 5B: Metal, Chemical Reactions with Nonmetals, Nitrogen to Arsenic; ISBN: 3540936769; http://www.amazon.com/exec/obidos/ASIN/3540936769/icongroupinterna
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Implementation of Arsenic Treatment Systems: Design Considerations, Operations, and by Zaid K. Chowdhury (Editor), et al (2002); ISBN: 158321254X; http://www.amazon.com/exec/obidos/ASIN/158321254X/icongroupinterna
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Innocence and Arsenic: Studies in Crime and Literature by Albert Borowitz (1977); ISBN: 0060104139; http://www.amazon.com/exec/obidos/ASIN/0060104139/icongroupinterna
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Inorganic Arsenic Compounds by R.J. Fielder, et al; ISBN: 0118838482; http://www.amazon.com/exec/obidos/ASIN/0118838482/icongroupinterna
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Inorganic Arsenic Compounds Other Than Arsine: Health and Safety Guide (Health and Safety Guide); ISBN: 9241510706; http://www.amazon.com/exec/obidos/ASIN/9241510706/icongroupinterna
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Lead, Arsenic and Other Metals in Food (Food Surveillance Paper) by W.H.B. Denner, R. Burt; ISBN: 0112430414; http://www.amazon.com/exec/obidos/ASIN/0112430414/icongroupinterna
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Lead, Mercury, Cadmium and Arsenic in the Environment by K.M. Meema (Editor), et al; ISBN: 0471911267; http://www.amazon.com/exec/obidos/ASIN/0471911267/icongroupinterna
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Mariage sous arsenic, ou, L'affaire Lafarge by Pascal Chadenet; ISBN: 2268003531; http://www.amazon.com/exec/obidos/ASIN/2268003531/icongroupinterna
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Mercury and Arsenic Wastes: Removal, Recovery, Treatment, and Disposal (Pollution Technology Review, No. 214) by United State Environmental Protection Ag (1993); ISBN: 0815513267; http://www.amazon.com/exec/obidos/ASIN/0815513267/icongroupinterna
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More Chemistry and Crime: From Marsh Arsenic Test to DNA Profile by Samuel M. Gerber (Editor), Richard Saferstein (Editor) (1997); ISBN: 084123406X; http://www.amazon.com/exec/obidos/ASIN/084123406X/icongroupinterna
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Organometallic Compounds of Arsenic, Antimony and Bismuth by George O. Doak, Leon D. Freedman; ISBN: 047121650X; http://www.amazon.com/exec/obidos/ASIN/047121650X/icongroupinterna
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Poison Widows: A True Story of Witchcraft, Arsenic, and Murder by George Cooper; ISBN: 0312199473; http://www.amazon.com/exec/obidos/ASIN/0312199473/icongroupinterna
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Research Plan for Arsenic in Drinking Water by Lawrence W. Reiter; ISBN: 0756704545; http://www.amazon.com/exec/obidos/ASIN/0756704545/icongroupinterna
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Risk Based Standards for Arsenic, Lead, and Cadmium in Urban Soils by R. L. Chaney, J. A. Ryan (1994); ISBN: 3926959630; http://www.amazon.com/exec/obidos/ASIN/3926959630/icongroupinterna
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Second Supplements to the 2nd Edition of Rodd's Chemistry of Carbon Compounds : Heterocyclic Compounds : Six-Membered Heterocyclic Compounds with (a) a single Nitrogen Atom in the Ring (cont'd): Polycyclic Fused Ring Compounds, (b) an Atom of Phosphorus, Arsenic, Antimony or Bismuth. Alkaloids with a Six-Membered Heterocyclic Ring; Part H: Six-Membered Fused-Ring Heterocyclic Compounds with a Single Nitrogen Atom in the Ring (cont'd). Monocyclic Ring Compounds with Two Hetero-Atoms in th by Malcolm Sainsbury (Editor); ISBN: 0444829792; http://www.amazon.com/exec/obidos/ASIN/0444829792/icongroupinterna
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Selenium in waters, 1984; Selenium and arsenic in sludges, soils, and related materials, 1985; A Note on the use of hydrite generator kits, 1987; ISBN: 0117519332; http://www.amazon.com/exec/obidos/ASIN/0117519332/icongroupinterna
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Speciation of Arsenic in Water and Biological Matrices by X. Chris Le; ISBN: 1583210857; http://www.amazon.com/exec/obidos/ASIN/1583210857/icongroupinterna
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Studies in Ancient Technology: Metallurgy in Antiquity - Copper and Bronze, Tin, Arsenic, Antimony and Iron by R.J. Forbes; ISBN: 9004034870; http://www.amazon.com/exec/obidos/ASIN/9004034870/icongroupinterna
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Survey of arsenic in food : the eighth report of the Steering Group on Food Surveillance, The Working Party on the Monitoring of Foodstuffs for Heavy Metals; ISBN: 0112412122; http://www.amazon.com/exec/obidos/ASIN/0112412122/icongroupinterna
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Synthetic Methods of Organometallic & Inorganic Chemistry: Phosphorus, Arsenic, Antimony, & Bismuth by W. A. Herrmann (Editor) (1997); ISBN: 0865776547; http://www.amazon.com/exec/obidos/ASIN/0865776547/icongroupinterna
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The arsenic papers by M. A. Rychlo; ISBN: 0889541450; http://www.amazon.com/exec/obidos/ASIN/0889541450/icongroupinterna
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The Certification of the Content (Mass Fractions) of Arsenic, Cadmium, Copper, Cobalt, Manganese, Lead, Selenium and Zinc in a Single Cell Protein: c by B. Griepink (Editor); ISBN: 928257427X; http://www.amazon.com/exec/obidos/ASIN/928257427X/icongroupinterna
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The Certification of the Contents Mass Fractions of Arsenic, Cadmium, Copper, Lead, Selenium and Zinc in a Sea Lettuce (B) by B. Griepnik, H. Muntau (1988); ISBN: 9282577716; http://www.amazon.com/exec/obidos/ASIN/9282577716/icongroupinterna
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The Chemistry of Organic Arsenic, Antimony and Bismuth Compounds by Saul Patai (Editor); ISBN: 047193044X; http://www.amazon.com/exec/obidos/ASIN/047193044X/icongroupinterna
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The Heterocyclic Derivatives of Phosphorus, Arsenic, Antimony, and Bismuth by Frederick George Mann; ISBN: 047137489X; http://www.amazon.com/exec/obidos/ASIN/047137489X/icongroupinterna
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Toxic Substances in Surface Waters and Sediments: A Study to Assess the Effects of Arsenic-Contaminated Alluvial Sediment in Whitewood Creek, South Dakota: U.S. Geological Survey Toxics Sic by James S. Kuwabara (Editor) (2003); ISBN: 060793722X; http://www.amazon.com/exec/obidos/ASIN/060793722X/icongroupinterna
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Transition metal complexes of phosphorus, arsenic and antimony ligands by C. A. McAuliffe; ISBN: 0333136284; http://www.amazon.com/exec/obidos/ASIN/0333136284/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 “arsenic” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
A probationary essay on the antidotes to arsenic. Author: Mackenzie, Donald.; Year: 1968; Edinburgh: her majesty's printers, 1839
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A Summary of information gathered on the major issues by the Ministry of Labour after the October 20, 1983 public meeting on the proposed arsenic regulation. Author: Ontario. Occupational Health and Safety Division. Program Development Unit.; Year: 1904; [Ontario?]: Occupational Health and Safety Division, Program Development Unit, 1984
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Arsenic and its compounds. Author: Canada. Environment Canada.; Year: 1970; [Ottawa]: Environment Canada, c1993; ISBN: 0662204883
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Arsenic and its compounds: arsenic, arsenic trioxide, arsenic chloride, copper arsenite, copper aceto arsenite, arsine, cacodylic acid, ethyl arsine, cacodyl. [Comp. with the assistance of the Work Projects Administration]. Author: Ohio. Dept. of Health. Division of Adult Hygiene.; Year: 1975; Columbus, 1940
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Arsenic and lead in water; a bibliography. Author: Water Resources Scientific Information Center.; Year: 1971; Washington, Reproduced by National Technical Information Service, Springfield, Va., 1971
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Arsenic toxicology: January 1977 through October 1981, 354 citations Author: Jackson, Silas.; Year: 1984; [Bethesda, Md.]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, [1981]
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Arsenic. Author: Vallee, Bert L.; Year: 1973; Washington, American Petroleum Institute [1973]
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Arsenical paper-hangings Author: Brown, Francis H. (Francis Henry),; Year: 1976; [Boston?: s.n., 1876?]
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Determination of arsenic in germanium by the combination of isotope dilution and activation analysis [by] F. W. Lima [and] C. M. Silva. Author: Lima, Fausto W. (Fausto Walter); Year: 1977; São Paulo, Instituto de Energia Atômica, 1970
11
In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
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Ecologic role of arsenic in reproductive growth; its potential role as catalyst of germination, high-energy metabolism, and immunoprotein sensitization. Author: Satterlee, Henry Suydam,; Year: 1966; New London, N. H., Country Press [c1965]
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Effects of arsenic in the Canadian environment Author: National Research Council Canada. Subcommittee on Heavy Metals and Certain Other Elements.; Year: 1985; Ottawa: [s.n.], 1978
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Health effects of occupational lead and arsenic exposure: a symposium Author: Society for Occupational and Environmental Health.; Year: 1983; Cincinnati: U. S. Dept. of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health, Division of Surveillance, Hazard Evaluations and Field Studies; Washington: For sale by the Supt. of Docs., U. S. Govt. Print. Off., 1976
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Medical reports of the effects of arsenic, in the cure of agues, remitting fevers, and periodic headaches Author: Fowler, Thomas,; Year: 1981; London: Printed for J. Johnson. and William Brown., 1786
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Method for the determination of arsenic (silver diethyldithiocarbamate procedure). Author: British Standards Institution.; Year: 1968; London, 1968
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Occupational exposure to inorganic arsenic, new criteria, 1975: criteria for a recommended standard. Author: National Institute for Occupational Safety and Health.; Year: 1981; Cincinnati: U. S. Dept. of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health; Washington: for sale by the Supt. of Docs., U. S. Govt. Print. Off., 1975
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Preliminary air pollution survey of arsenic and its compounds: a literature review Author: Sullivan, Ralph J.; Year: 1971; Raleigh, N.C.: U.S. Dept. of Health, Education, and Welfare, National Air Pollution Control Administration, [1969]
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Report on arsenic; revised recommendations for limits for arsenic in foods. Author: Great Britain. Food Standards Committee.; Year: 1955; London, H. M. Stationery Off., 1955
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Study of the influence of various factors on the radiochemical-Gutzeit method of activation analysis of arsenic [by] Fausto W. Lima and Célia M. Silva. Author: Lima, Fausto W. (Fausto Walter); Year: 1968; [São Paulo, Instituto de Energia Atômica] 1968
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Toxicity of arsenic compounds. Author: Buchanan, William Drummond.; Year: 1962; Amsterdam, Elsevier Pub. Co., 1962
Chapters on Arsenic In order to find chapters that specifically relate to arsenic, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and arsenic 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 “arsenic” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on arsenic:
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Drugs and the Liver Source: in Sherlock, S.; Dooley, J. Diseases of the Liver and Biliary System. Malden, MA: Blackwell Science, Inc. 2002. p.335-363. Contact: Available from Blackwell Science, Inc. 350 Main Street, Commerce Place, Malden, MA 02148. (800) 215-1000 or (617) 388-8250. Fax (617) 388-8270. E-mail:
[email protected]. Website: www.blackwell-science.com. PRICE: $178.95. ISBN: 0632055820. Summary: The liver is particularly concerned with drug metabolism, and especially of drugs given orally. Drugs can cause toxic effects that can mimic almost every naturally occurring liver disease in man. This chapter on drugs and the liver is from a textbook that presents a comprehensive and up-to-date account of diseases of the liver and biliary system. The chapter is organized into specific pathologies and their potential causes: hepato-cellular zone 3 necrosis, due to carbon tetrachloride, Amanita mushrooms, paracetamol (acetaminophen), salicylates, hyperthermia, hypothermia, and burns; hepato-cellular zone 1 necrosis, due to ferrous sulfate or phosphorus; mitochondrial cytopathies, due to sodium valproate, tetracyclines, tacrine, antiviral nucleoside analogues, and Bacillus cereus; steatohepatitis, due to perhexiline maleate, amiodarone, synthetic estrogens, and calcium channel blockers; fibrosis, due to methotrexate, other cytotoxic drugs, arsenic, vinyl chloride, vitamin A, and retinoids; vascular changes, due to sinusoidal dilatation, peliosis hepatitis, and veno-occlusive disease (VOD); acute hepatitis, due to isoniazid, methyl dopa, halothane, hydrofluorocarbons, systemic antifungals, oncology drugs, nervous system modifiers, sustained-release nicotinic acid (niacin), sulfonamides and derivatives, nonsteroidal anti-inflammatory drugs, antithyroid drugs, quinidine and quinine, troglitazone, and anti-convulsants; chronic hepatitis, due to herbal remedies and recreational drugs; canalicular cholestasis, due to cyclosporine A and ciprofloxacin; hepato-canalicular cholestasis, due to chlorpromazine, penicillins, sulfonamides, erythromycin, haloperidol, cimetidine and ranitidine, oral hypoglycemic agents, tamoxifen, other causes, and dextropropoxyphene; ductular cholestasis; biliary sludge; sclerosing cholangitis; hepatic nodules and tumors; and hepatocellular carcinoma (HCC, liver cancer). 28 figures. 5 tables. 170 references.
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Trace Element Metabolism in Renal Disease and Renal Failure Source: in Kopple, J.D. and Massry, S.G. Nutritional Management of Renal Disease. Baltimore, MD: Williams and Wilkins. 1997. p. 395-414. Contact: Available from Williams and Wilkins. 351 West Camden Street, Baltimore, MD 21201-2436. (800) 638-0672 or (410) 528-4223. Fax (800) 447-8438 or (410) 528-8550. PRICE: $99.00. ISBN: 068304740X. Summary: This chapter on trace element metabolism is from a medical textbook on nutrition and metabolism of individuals with renal disease or renal failure. It is generally accepted that the term 'trace element' applies to elements that occur in the body at concentrations of less than 50 mg per kg under normal conditions. The definition of 'essential' trace elements is that the element should be present in healthy tissues; deficiency of the element consistently produces functional impairment; the abnormalities induced by the deficiency are always followed by specific biochemical changes; and addition of the element prevents or corrects these changes. Topics include methodology for the measurement of trace elements; trace element concentrations in uremia; the potential contribution of trace elements to the uremic syndrome, including impairment of renal function, susceptibility to cancer, cardiovascular disease, glucose intolerance, bone disease, anemia, enzyme dysfunction, encephalopathy and coma, and
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immune deficiency; factors affecting trace element concentration, including inadequate intake, decreased availability, impaired reabsorption, excessive excretion, and extracorporeal losses; specific examples relating to aluminum, lead, selenium and arsenic, zinc, vanadium, silicon, and chromium; and therapeutic considerations. The authors caution that the treatment of uremia by dialysis strategies may cause changes in trace element handling. Trace elements should be considered in the case of any unexplained toxic event in uremia. 5 tables. 89 references. (AA-M). •
Chapter 79: Epithelial Precancerous Lesions Source: in Freedberg, I.M., et al., eds. Fitzpatrick's Dermatology in General Medicine. 5th ed., Vol. 1. New York, NY: McGraw-Hill. 1999. p. 823-839. Contact: Available from McGraw-Hill Customer Services. P.O. Box 548, Blacklick, OH 43004-0548. (800) 262-4729 or (877) 833-5524. Fax (614) 759-3749 or (614) 759-3641. E-mail:
[email protected]. PRICE: $395.00 plus shipping and handling. ISBN: 0070219435. Summary: This chapter provides health professionals with information on the clinical manifestations, pathology, diagnosis, differential diagnosis, treatment, prevention, course, and prognosis of epithelial precancerous lesions. Precancerous skin lesions of keratinocytes are those that may evolve into invasive cancer. The most common epithelial precancerous lesion among people with light complections is actinic keratosis. The actinic keratosis presents on sun exposed body areas, usually in middle aged or older people, as a skin colored or reddish brown or yellowish black, ill defined macule or papule with a dry, adherent scale. Types of actinic keratoses include hypertrophic actinic keratoses, spreading pigmented actinic keratoses, proliferative actinic keratoses, lichenoid actinic keratoses, and bowenoid actinic keratoses. Studies have shown that actinic keratoses are a cutaneous sign in people who are at markedly increased risk for subsequent development of cutaneous squamous cell carcinoma (SCC) and melanoma. The cutaneous horn is another precancerous skin lesion. This morphologic lesion, a conical, dense hyperkeratotic nodule that resembles the horn of an animal, can be produced by various disorders. Arsenical keratoses are those resulting from arsenic exposure. They develop at sites of friction and trauma as multiple, punctate, hard, yellowish, often symmetric, cornlike papules. Hydrocarbon keratoses are keratotic nodules and plaques that occur on the skin as a result of exposure to certain chemicals other than arsenic. They may appear as small, usually grayish, oval, flat, premalignant papules. Thermal keratoses result from chronic stimulation from infrared radiation. Chronic radiation keratoses are premalignant electromagnetic wave induced cutaneous dysplasis. They appear as discrete keratoses or as hyperkeratotic plaques years after x ray exposure. Chronic cicatrix keratoses are those that develop at sites of chronic scar formation. These keratoses appear as papules or erosions. Bowenoid papulosis, which is caused by human papillomavirus infection, is a genital eruption of papules or plaques showing characteristic bowenoid histology. Bowen's disease causes a cutaneous lesion that appears as a sharply demarcated, scaly, often hyperkeratotic, sometimes fissured, macule, papule, or plaque devoid of hair. Erythroplasia of Queyrat, which occurs in men not circumcised in early childhood, is in situ or invasive SCC of the penile mucosa when the characteristic morphology is a sharply demarcated, velvety, bright reddish plaque. Erythoplasis is a red patch of the mucosal surface that often presents as an in situ or invasive SCC of the oral mucosa. Leukoplakia is a white patch or plaque on the mucosa that cannot be rubbed off. Intraepidermal epithelioma is a rare superficial cutaneous tumor that appears as a sharply demarcated, slowly enlarging, solitary gray to tannish brown, scaly hyperkeratotic plaque with a round to irregular shape. The main options
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for treating these epithelial precancerous lesions are excisional surgery, cryosurgery, electrodesiccation and curettage, and topical chemotherapy. 8 figures, 1 table, and 96 references.
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CHAPTER 8. MULTIMEDIA ON ARSENIC Overview In this chapter, we show you how to keep current on multimedia sources of information on arsenic. 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.
Bibliography: Multimedia on Arsenic 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 arsenic (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 arsenic: •
Arsenic in drinking water [electronic resource]: recent regulatory developments and issues Source: Mary Tiemann; Year: 2001; Format: Electronic resource; Washington, DC: National Council for Science and the Environment, [2001]
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CHAPTER 9. PERIODICALS AND NEWS ON ARSENIC Overview In this chapter, we suggest a number of news sources and present various periodicals that cover arsenic.
News Services and Press Releases One of the simplest ways of tracking press releases on arsenic 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 “arsenic” (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 arsenic. 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 “arsenic” (or synonyms). The following was recently listed in this archive for arsenic: •
Arsenic exposure impairs DNA repair gene expression Source: Reuters Medical News Date: April 11, 2003
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Groups ask for US ban on arsenic in playsets Source: Reuters Health eLine Date: March 17, 2003
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Phase II study supports Trisenox in multiple myeloma Source: Reuters Medical News Date: December 09, 2002
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Study: Arsenic may be tainting Bangladeshi crops Source: Reuters Health eLine Date: December 04, 2002
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Water from shallow wells in Bangladesh is highly contaminated with arsenic Source: Reuters Medical News Date: November 22, 2002
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Arsenic in water tied to bladder cancer mutations Source: Reuters Health eLine Date: November 20, 2002
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Arsenic exposure may lead to more aggressive bladder cancers Source: Reuters Medical News Date: November 20, 2002
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Genetically engineered plants may clean up arsenic Source: Reuters Health eLine Date: October 07, 2002
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Well-switching may ease Bangladesh arsenic problem Source: Reuters Health eLine Date: September 16, 2002
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Global efforts needed to keep water arsenic-free Source: Reuters Health eLine Date: June 20, 2002
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Plan gives US utilities years to meet arsenic rules Source: Reuters Health eLine Date: May 09, 2002
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Arsenic, king of poisons, gets an image makeover Source: Reuters Health eLine Date: April 02, 2002
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Arsenic exposure may accelerate artery hardening Source: Reuters Health eLine Date: March 25, 2002
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Thallium and arsenic poisonings reveal clues Source: Reuters Medical News Date: March 05, 2002
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Study lends clues to mechanisms underlying arsenic's anticancer effects Source: Reuters Medical News Date: December 14, 2001
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Selenium supplements can prevent arsenic toxicity Source: Reuters Medical News Date: November 28, 2001
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EPA to tighten limit on arsenic in drinking water Source: Reuters Health eLine Date: November 01, 2001
Periodicals and News
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Small towns want federal help in arsenic cleanup Source: Reuters Health eLine Date: October 04, 2001
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Report says EPA underestimates arsenic risk Source: Reuters Health eLine Date: September 14, 2001
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New study shows bigger risk from arsenic in water Source: Reuters Medical News Date: September 13, 2001
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Senate backs tougher arsenic limit in tap water Source: Reuters Health eLine Date: August 02, 2001
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US backs tougher rule on arsenic in tap water Source: Reuters Health eLine Date: July 27, 2001
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Three sudden deaths reported in leukemia patients taking arsenic trioxide Source: Reuters Medical News Date: July 24, 2001
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Arsenic leukemia therapy linked to sudden death Source: Reuters Health eLine Date: July 23, 2001
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Green group sues EPA over arsenic limits in water Source: Reuters Health eLine Date: June 28, 2001
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NAS panel begins review of federal water standards for arsenic Source: Reuters Medical News Date: May 21, 2001
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Advisory panel reviews federal arsenic rules Source: Reuters Health eLine Date: May 21, 2001
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Patients with advanced multiple myeloma improve on arsenic trioxide therapy Source: Reuters Medical News Date: May 08, 2001
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Average tap water arsenic level safe in pregnancy Source: Reuters Health eLine Date: April 25, 2001
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Cell Therapeutics warns doctors about cardiac events linked to arsenic trioxide Source: Reuters Medical News Date: March 20, 2001
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"Acceptable" levels of arsenic linked to cancer Source: Reuters Health eLine Date: March 15, 2001
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"Acceptable" levels of arsenic in well water linked to bladder cancer Source: Reuters Medical News Date: March 13, 2001
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Arsenic triggers flood of free radicals Source: Reuters Health eLine Date: February 23, 2001
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Arsenic trioxide may improve effect of retinoic acid in promyelocytic leukemia Source: Reuters Medical News Date: February 05, 2001
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Arsenic-eating plant could clear toxin--study Source: Reuters Health eLine Date: January 31, 2001
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EPA lowers allowable arsenic levels in drinking water Source: Reuters Health eLine Date: January 18, 2001
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Arsenic trioxide associated with cardiac toxicity Source: Reuters Medical News Date: December 07, 2000
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Cell Therapeutics' Trisenox wins orphan drug status in Europe Source: Reuters Medical News Date: October 25, 2000
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Arsenic in tap water: know your risk Source: Reuters Health eLine Date: October 20, 2000
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Toxic arsenic levels present in US tap water Source: Reuters Health eLine Date: October 13, 2000
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FDA approves Cell Therapeutics' Trisenox as second line leukemia therapy Source: Reuters Medical News Date: September 27, 2000
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Arsenic-contaminated ground water a 'public emergency' in Bangladesh Source: Reuters Medical News Date: September 13, 2000
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Arsenic in water may cause millions of deaths in Bangladesh Source: Reuters Health eLine Date: September 12, 2000
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Cell Therapeutics' Arsenic TriOxide gains priority review status Source: Reuters Medical News Date: May 17, 2000
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Orphan drug designation for Cell Therapeutics' Arsenic TriOxide Source: Reuters Medical News Date: May 09, 2000
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Arsenic trioxide efficacious in treatment of lymphomas Source: Reuters Medical News Date: May 06, 1999
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Arsenic compound may treat lymphomas Source: Reuters Health eLine Date: May 04, 1999
Periodicals and News
•
Standards for arsenic in drinking water too lenient Source: Reuters Medical News Date: March 24, 1999
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New arsenic standards for US drinking water Source: Reuters Health eLine Date: March 24, 1999
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Arsenic trioxide induces remission in relapsed acute promyelocytic leukemia Source: Reuters Medical News Date: November 05, 1998
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The NIH Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “arsenic” (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 “arsenic” (or synonyms). If you know the name of a company that is relevant to arsenic, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/.
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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 “arsenic” (or synonyms).
Academic Periodicals covering Arsenic Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to arsenic. In addition to these sources, you can search for articles covering arsenic that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for arsenic. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI® Advice for the Patient® can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with arsenic. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to arsenic: Arsenic Trioxide •
Systemic - U.S. Brands: Trisenox http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500241.html
Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult™ Mosby’s Drug Consult™ database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/. PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee. If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
12
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
•
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “arsenic” (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 8282 204 44 2 1 8533
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.19 Simply search by “arsenic” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
15
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
16
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). 17 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 18 19
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 Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
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/.
20 Adapted 21
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. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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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 arsenic 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 arsenic. 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 arsenic. 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 “arsenic”:
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•
Guides on arsenic Arsenic http://www.nlm.nih.gov/medlineplus/arsenic.html
•
Other guides Bone Marrow Diseases http://www.nlm.nih.gov/medlineplus/bonemarrowdiseases.html Drinking Water http://www.nlm.nih.gov/medlineplus/drinkingwater.html Environmental Health http://www.nlm.nih.gov/medlineplus/environmentalhealth.html Multiple Myeloma http://www.nlm.nih.gov/medlineplus/multiplemyeloma.html
Within the health topic page dedicated to arsenic, the following was listed: •
General/Overview Arsenic Source: Agency for Toxic Substances and Disease Registry http://www.atsdr.cdc.gov/tfacts2.html Public Health Statement for Arsenic Source: Agency for Toxic Substances and Disease Registry http://www.atsdr.cdc.gov/toxprofiles/phs2.html Tox Town Source: National Library of Medicine http://toxtown.nlm.nih.gov/ What is Arsenic? http://www-nehc.med.navy.mil/downloads/ep/Posters/arsensml.pdf
•
Specific Conditions/Aspects Arsenic in Drinking Water Source: Environmental Protection Agency http://www.epa.gov/epahome/hi-arsenic.htm Cancellation of Residential Uses of CCA - Treated Wood Source: Environmental Protection Agency http://www.epa.gov/pesticides/factsheets/chemicals/residential_use_cancellatio n.htm Inorganic Arsenical Pressure-Treated Wood, Including Chromate Copper Arsenate (CCA) Source: Environmental Protection Agency, Office of Prevention, Pesticides and Toxic Substances http://www.epa.gov/pesticides/factsheets/chemicals/cca_consumer_safety.htm
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Manufacturers to Use New Wood Preservatives, Replacing Most Residential Uses of CCA Source: Environmental Protection Agency, Office of Pesticide Programs http://www.epa.gov/pesticides/factsheets/chemicals/cca_transition.htm What You Need to Know About Wood Pressure Treated with Chromated Copper Arsenate (CCA) Source: Environmental Protection Agency, Office of Prevention, Pesticides and Toxic Substances http://www.epa.gov/pesticides/factsheets/chemicals/cca_qa.htm •
Law and Policy Arsenic in Drinking Water Source: Environmental Protection Agency, Office of Water http://www.epa.gov/safewater/arsenic.html
•
Organizations Agency for Toxic Substances and Disease Registry http://www.atsdr.cdc.gov/ Environmental Protection Agency http://www.epa.gov/
•
Pictures/Diagrams Arsenic in Ground Water of the United States Source: U.S. Geological Survey http://co.water.usgs.gov/trace/arsenic/
•
Research Arsenic in Well Water Related to Atherosclerosis Source: American Heart Association http://www.americanheart.org/presenter.jhtml?identifier=3001554
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 arsenic. 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.
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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: •
Skin Cancer Source: Postgraduate Medicine. 107(7): 225-226. June 2000. Summary: This journal article provides the general public and people who have skin cancer with information on this disease. The major types of skin cancer are basal cell carcinoma, squamous cell carcinoma, and melanoma. The basal cell and squamous cell types occur most often on areas of the skin that are regularly exposed to the sun. Melanoma tends to occur on areas of the body that are not regularly exposed to the sun. Signs of skin cancer include any changes in the size, color, shape, or texture of a mole; the development of a new mole; or any other unusual change in the skin. Risk factors include repeated exposure to bright sunlight, sunburn, use of skin creams or lotions that contain tar, exposure to organic arsenic, and exposure to radiation therapy or chemotherapy. The risk of skin cancer can be reduced by minimizing sun exposure; wearing sunglasses and protective clothing; using a sunscreen with both ultraviolet (UV) A and UVB protection; being careful on sand, snow, or water; avoiding artificial tanning devices; and taking special precautions with children. 1 figure. 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 arsenic. 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
•
Family Village: http://www.familyvillage.wisc.edu/specific.htm
•
Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
•
Med Help International: http://www.medhelp.org/HealthTopics/A.html
•
Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
•
Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
•
WebMD®Health: http://my.webmd.com/health_topics
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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to arsenic. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with arsenic. 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 arsenic. 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 “arsenic” (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 “arsenic”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “arsenic” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months.
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The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “arsenic” (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.23
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
23
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)24: •
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/
24
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/
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Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
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Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
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Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
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Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
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Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
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Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
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Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
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Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
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Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
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Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
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Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
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Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
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National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
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National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
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National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
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New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
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New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
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New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
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New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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•
South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
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MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
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Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
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On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
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Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
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MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
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Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
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Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
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ARSENIC 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] Aberrant: Wandering or deviating from the usual or normal course. [EU] Acatalasia: A rare autosomal recessive disorder resulting from the absence of catalase activity. Though usually asymptomatic, a syndrome of oral ulcerations and gangrene may be present. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acne Vulgaris: A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors. [NIH] Acrylonitrile: A highly poisonous compound used widely in the manufacture of plastics, adhesives and synthetic rubber. [NIH] Actin: Essential component of the cell skeleton. [NIH] Actinic keratosis: A precancerous condition of thick, scaly patches of skin. Also called solar or senile keratosis. [NIH] Actinium: A trivalent radioactive element and the prototypical member of the actinide family. It has the atomic symbol Ac, atomic number 89, and atomic weight 227.0278. Its principal isotope is 227 and decays primarily by beta-emission. [NIH] Acute leukemia: A rapidly progressing cancer of the blood-forming tissue (bone marrow). [NIH]
Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic leukemia. [NIH]
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Acute myelogenous leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute nonlymphocytic leukemia. [NIH] Acute myeloid leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myelogenous leukemia or acute nonlymphocytic leukemia. [NIH] Acute nonlymphocytic leukemia: A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute myelogenous leukemia. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenoma: A benign epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adhesives: Substances that cause the adherence of two surfaces. They include glues (properly collagen-derived adhesives), mucilages, sticky pastes, gums, resins, or latex. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerobic Metabolism: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as aerobic respiration, oxidative metabolism, or cell
Dictionary 277
respiration. [NIH] Aerobic Respiration: A chemical process in which oxygen is used to make energy from carbohydrates (sugars). Also known as oxidative metabolism, cell respiration, or aerobic metabolism. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
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] Affinity Chromatography: In affinity chromatography, a ligand attached to a column binds specifically to the molecule to be purified. [NIH] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Agarose: A polysaccharide complex, free of nitrogen and prepared from agar-agar which is produced by certain seaweeds (red algae). It dissolves in warm water to form a viscid solution. [NIH] Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [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] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU]
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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] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allo: A female hormone. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allogeneic bone marrow transplantation: A procedure in which a person receives stem cells, the cells from which all blood cells develop, from a compatible, though not genetically identical, donor. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alpha-helices: One of the secondary element of protein. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amiodarone: An antianginal and antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting Na,K-activated myocardial adenosine triphosphatase. There is a resulting decrease in heart rate and in vascular resistance. [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] Ampulla: A sac-like enlargement of a canal or duct. [NIH]
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Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] 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] Analytes: A component of a test sample the presence of which has to be demonstrated. The term "analyte" includes where appropriate formed from the analyte during the analyses. [NIH]
Anaphase: The third phase of cell division, in which the chromatids separate and migrate to opposite poles of the spindle. [NIH] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anergy: Absence of immune response to particular substances. [NIH] Aneuploidy: The chromosomal constitution of cells which deviate from the normal by the addition or subtraction of chromosomes or chromosome pairs. In a normally diploid cell the loss of a chromosome pair is termed nullisomy (symbol: 2N-2), the loss of a single chromosome is monosomy (symbol: 2N-1), the addition of a chromosome pair is tetrasomy (symbol: 2N+2), the addition of a single chromosome is trisomy (symbol: 2N+1). [NIH] Aneurysm: A sac formed by the dilatation of the wall of an artery, a vein, or the heart. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiogenesis inhibitor: A substance that may prevent the formation of blood vessels. In anticancer therapy, an angiogenesis inhibitor prevents the growth of blood vessels from surrounding tissue to a solid tumor. [NIH] Angiosarcoma: A type of cancer that begins in the lining of blood vessels. [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
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or other tissues are called xenograft models. [NIH] Anionic: Pertaining to or containing an anion. [EU] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Anisomycin: An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system. [NIH]
Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anode: Electrode held at a positive potential with respect to a cathode. [NIH] Anomalies: Birth defects; abnormalities. [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] Anthracycline: A member of a family of anticancer drugs that are also antibiotics. [NIH] Anthropogenic: Of human origin or influence. [NIH] Antianginal: Counteracting angina or anginal conditions. [EU] 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] Antidepressant: A drug used to treat depression. [NIH] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
Antifungals: Drugs that treat infections caused by fungi. [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]
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Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] 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] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Aperture: A natural hole of perforation, especially one in a bone. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Applicability: A list of the commodities to which the candidate method can be applied as presented or with minor modifications. [NIH] Aqueous: Having to do with water. [NIH]
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Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in platelets. EC 1.13.11.31. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [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] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Argon: A noble gas with the atomic symbol Ar, atomic number 18, and atomic weight 39.948. It is used in fluorescent tubes and wherever an inert atmosphere is desired and nitrogen cannot be used. [NIH] Arnica: Genus of composite-flowered plants in the family Asteraceae. The dried flower heads of Arnica montana are used externally as a counterirritant and tincture for sprains and bruises. Arnica contains volatile oils, arnicin, arnisterol, flavonoids, tannins, and resin. [NIH]
Aromatic: Having a spicy odour. [EU] Arrhythmia: Any variation from the normal rhythm or rate of the heart beat. [NIH] Arsenic trioxide: An anticancer drug that induces programmed cell death (apoptosis) in certain cancer cells. [NIH] Arsenicals: Inorganic or organic compounds that contain arsenic. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] 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] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringent: Causing contraction, usually locally after topical application. [EU]
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Astrocytoma: A tumor that begins in the brain or spinal cord in small, star-shaped cells called astrocytes. [NIH] Atherogenic: Causing the formation of plaque in the lining of the arteries. [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] Atrial: Pertaining to an atrium. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Auditory: Pertaining to the sense of hearing. [EU] Autologous: Taken from an individual's own tissues, cells, or DNA. [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] Babesiosis: A group of tick-borne diseases of mammals including zoonoses in humans. They are caused by protozoans of the genus babesia, which parasitize erythrocytes, producing hemolysis. In the U.S., the organism's natural host is mice and transmission is by the deer tick ixodes scapularis. [NIH] Bacteremia: The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Barbiturate: A drug with sedative and hypnotic effects. Barbiturates have been used as sedatives and anesthetics, and they have been used to treat the convulsions associated with epilepsy. [NIH] Barium: An element of the alkaline earth group of metals. It has an atomic symbol Ba, atomic number 56, and atomic weight 138. All of its acid-soluble salts are poisonous. [NIH]
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Basal cell carcinoma: A type of skin cancer that arises from the basal cells, small round cells found in the lower part (or base) of the epidermis, the outer layer of the skin. [NIH] Basal cells: Small, round cells found in the lower part (or base) of the epidermis, the outer layer of the skin. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [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 Sequence: The sequence of purines and pyrimidines in nucleic acids and polynucleotides. It is also called nucleotide or nucleoside sequence. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Berylliosis: A lung disease caused by exposure to metallic beryllium or its soluble salts. [NIH]
Beryllium: An element with the atomic symbol Be, atomic number 4, and atomic weight 9.01218. Short exposure to this element can lead to a type of poisoning known as berylliosis. [NIH]
Beta Rays: A stream of positive or negative electrons ejected with high energy from a disintegrating atomic nucleus; most biomedically used isotopes emit negative particles (electrons or negatrons, rather than positrons). Cathode rays are low-energy negative electrons produced in cathode ray tubes, also called television tubes or oscilloscopes. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Bexarotene: An anticancer drug used to decrease the growth of some types of cancer cells. Also called LGD1069. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile Ducts: Tubes that carry bile from the liver to the gallbladder for storage and to the small intestine for use in digestion. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Bioassay: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU]
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Bioavailable: The ability of a drug or other substance to be absorbed and used by the body. Orally bioavailable means that a drug or other substance that is taken by mouth can be absorbed and used by the body. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biochemical reactions: In living cells, chemical reactions that help sustain life and allow cells to grow. [NIH] Biofilms: Films of bacteria or other microbial organisms, usually embedded in extracellular polymers such as implanted medical devices, which adhere to surfaces submerged in, or subjected to, aquatic environments (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed). Biofilms consist of multilayers of microbial cells glued together to form microbial communities which are highly resistant to both phagocytes and antibiotics. [NIH] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biological Transport: The movement of materials (including biochemical substances and drugs) across cell membranes and epithelial layers, usually by passive diffusion. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biomedical Engineering: Application of principles and practices of engineering science to biomedical research and health care. [NIH] Biomolecular: A scientific field at the interface between advanced computing and biotechnology. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [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] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Biphasic: Having two phases; having both a sporophytic and a gametophytic phase in the life cycle. [EU]
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Bismuth: A metallic element that has the atomic symbol Bi, atomic number 83 and atomic weight 208.98. [NIH] Bivalent: Pertaining to a group of 2 homologous or partly homologous chromosomes during the zygotene stage of prophase to the first metaphase in meiosis. [NIH] Bladder: The organ that stores urine. [NIH] Blast Crisis: Rapid increase in the proportion of blast cells in the blood and bone marrow. [NIH]
Blast phase: The phase of chronic myelogenous leukemia in which the number of immature, abnormal white blood cells in the bone marrow and blood is extremely high. Also called blast crisis. [NIH] Blasts: Immature blood cells. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] Body Burden: The total amount of a chemical, metal or radioactive substance present at any time after absorption in the body of man or animal. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Bone Cements: Adhesives used to fix prosthetic devices to bones and to cement bone to bone in difficult fractures. Synthetic resins are commonly used as cements. A mixture of monocalcium phosphate, monohydrate, alpha-tricalcium phosphate, and calcium carbonate with a sodium phosphate solution is also a useful bone paste. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone Marrow Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [NIH] 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]
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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] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain 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] Breeding: The science or art of changing the constitution of a population of plants or animals through sexual reproduction. [NIH] Bromine: A halogen with the atomic symbol Br, atomic number 36, and atomic weight 79.904. It is a volatile reddish-brown liquid that gives off suffocating vapors, is corrosive to the skin, and may cause severe gastroenteritis if ingested. [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] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cacodylic Acid: An arsenical that has been used as a dermatologic agent and as an herbicide. [NIH] Cadaver: A dead body, usually a human body. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Compounds: Inorganic compounds that contain cadmium as an integral part of the molecule. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the
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alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium channel blocker: A drug used to relax the blood vessel and heart muscle, causing pressure inside blood vessels to drop. It also can regulate heart rhythm. [NIH] Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cell membranes or on the release and binding of calcium in intracellular pools. Since they are inducers of vascular and other smooth muscle relaxation, they are used in the drug therapy of hypertension and cerebrovascular spasms, as myocardial protective agents, and in the relaxation of uterine spasms. [NIH] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [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] Carboxy: Cannabinoid. [NIH] Carboxylic Acids: Organic compounds containing the carboxy group (-COOH). This group of compounds includes amino acids and fatty acids. Carboxylic acids can be saturated, unsaturated, or aromatic. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual
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patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into excreted compounds. [EU] Catalase: An oxidoreductase that catalyzes the conversion of hydrogen peroxide to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in acatalasia. EC 1.11.1.6. [NIH] Cathepsins: A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissue. They function optimally within an acidic pH range. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Causal: Pertaining to a cause; directed against a cause. [EU] Causality: The relating of causes to the effects they produce. Causes are termed necessary when they must always precede an effect and sufficient when they initiate or produce an effect. Any of several factors may be associated with the potential disease causation or outcome, including predisposing factors, enabling factors, precipitating factors, reinforcing factors, and risk factors. [NIH] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] CDC2: It is crucial for entry into mitosis of eukaryotic cells. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell Extracts: Preparations of cell constituents or subcellular materials, isolates, or substances. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell motility: The ability of a cell to move. [NIH] Cell Physiology: Characteristics and physiological processes of cells from cell division to cell death. [NIH] Cell proliferation: An increase in the number of cells as a result of cell growth and cell
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division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [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] Centromere: The clear constricted portion of the chromosome at which the chromatids are joined and by which the chromosome is attached to the spindle during cell division. [NIH] Ceramide: A type of fat produced in the body. It may cause some types of cells to die, and is being studied in cancer treatment. [NIH] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerium: An element of the rare earth family of metals. It has the atomic symbol Ce, atomic number 58, and atomic weight 140.12. Cerium is a malleable metal used in industrial applications. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Cesium: A member of the alkali metals. It has an atomic symbol Cs, atomic number 50, and atomic weight 132.91. Cesium has many industrial applications, including the construction of atomic clocks based on its atomic vibrational frequency. [NIH] Chelating Agents: Organic chemicals that form two or more coordination bonds with a central metal ion. Heterocyclic rings are formed with the central metal atom as part of the ring. Some biological systems form metal chelates, e.g., the iron-binding porphyrin group of hemoglobin and the magnesium-binding chlorophyll of plants. (From Hawley's Condensed Chemical Dictionary, 12th ed) They are used chemically to remove ions from solutions, medicinally against microorganisms, to treat metal poisoning, and in chemotherapy protocols. [NIH] Chelation: Combination with a metal in complexes in which the metal is part of a ring. [EU] Chemical Warfare: Tactical warfare using incendiary mixtures, smokes, or irritant, burning,
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or asphyxiating gases. [NIH] Chemical Warfare Agents: Chemicals that are used to cause the disturbance, disease, or death of humans during war. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chimera: An individual that contains cell populations derived from different zygotes. [NIH] Chlorine: A greenish-yellow, diatomic gas that is a member of the halogen family of elements. It has the atomic symbol Cl, atomic number 17, and atomic weight 70.906. It is a powerful irritant that can cause fatal pulmonary edema. Chlorine is used in manufacturing, as a reagent in synthetic chemistry, for water purification, and in the production of chlorinated lime, which is used in fabric bleaching. [NIH] Chlorine Compounds: Inorganic compounds that contain chlorine as an integral part of the molecule. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking dopamine receptors. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup. [NIH] Chlorpyrifos: An organothiophosphate cholinesterase inhibitor that is used as an insecticide and as an acaricide. [NIH] Cholangitis: Inflammation of a bile duct. [NIH] Cholestasis: Impairment of biliary flow at any level from the hepatocyte to Vater's ampulla. [NIH]
Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic granulocytic leukemia: A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myelogenous leukemia or chronic myeloid leukemia. [NIH] Chronic leukemia: A slowly progressing cancer of the blood-forming tissues. [NIH]
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Chronic lymphocytic leukemia: A slowly progressing disease in which too many white blood cells (called lymphocytes) are found in the body. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic phase: Refers to the early stages of chronic myelogenous leukemia or chronic lymphocytic leukemia. The number of mature and immature abnormal white blood cells in the bone marrow and blood is higher than normal, but lower than in the accelerated or blast phase. [NIH] Chronic phase chronic myelogenous leukemia: A phase of chronic myelogenous leukemia that may last from several months to several years. Although there may be no symptoms of leukemia, there are too many white blood cells. [NIH] Cicatrix: The formation of new tissue in the process of wound healing. [NIH] Cimetidine: A histamine congener, it competitively inhibits histamine binding to H2 receptors. Cimetidine has a range of pharmacological actions. It inhibits gastric acid secretion, as well as pepsin and gastrin output. It also blocks the activity of cytochrome P450. [NIH] Cinchona: A genus of rubiaceous South American trees that yields the toxic cinchona alkaloids from their bark; quinine, quinidine, chinconine, cinchonidine and others are used to treat malaria and cardiac arrhythmias. [NIH] Ciprofloxacin: A carboxyfluoroquinoline antimicrobial agent that is effective against a wide range of microorganisms. It has been successfully and safely used in the treatment of resistant respiratory, skin, bone, joint, gastrointestinal, urinary, and genital infections. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Cisplatin: An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle. [NIH] Citrus: Any tree or shrub of the Rue family or the fruit of these plants. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [NIH] 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]
Clonic: Pertaining to or of the nature of clonus. [EU] 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]
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Clot Retraction: Retraction of a clot resulting from contraction of platelet pseudopods attached to fibrin strands that is dependent on the contractile protein thrombosthenin. Used as a measure of platelet function. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Coal: A natural fuel formed by partial decomposition of vegetable matter under certain environmental conditions. [NIH] Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis. [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] Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Coke: A residue of coal, left after dry (destructive) distillation, used as a fuel. [NIH] Colchicine: A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (periodic disease). [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation
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occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Complete response: The disappearance of all signs of cancer in response to treatment. This does not always mean the cancer has been cured. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU]
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Conduction: The transfer of sound waves, heat, nervous impulses, or electricity. [EU] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Congenita: Displacement, subluxation, or malposition of the crystalline lens. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjugation: 1. The act of joining together or the state of being conjugated. 2. A sexual process seen in bacteria, ciliate protozoa, and certain fungi in which nuclear material is exchanged during the temporary fusion of two cells (conjugants). In bacterial genetics a form of sexual reproduction in which a donor bacterium (male) contributes some, or all, of its DNA (in the form of a replicated set) to a recipient (female) which then incorporates differing genetic information into its own chromosome by recombination and passes the recombined set on to its progeny by replication. In ciliate protozoa, two conjugants of separate mating types exchange micronuclear material and then separate, each now being a fertilized cell. In certain fungi, the process involves fusion of two gametes, resulting in union of their nuclei and formation of a zygote. 3. In chemistry, the joining together of two compounds to produce another compound, such as the combination of a toxic product with some substance in the body to form a detoxified product, which is then eliminated. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consolidation: The healing process of a bone fracture. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contact dermatitis: Inflammation of the skin with varying degrees of erythema, edema and vesinculation resulting from cutaneous contact with a foreign substance or other exposure. [NIH]
Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Convulsants: Substances that act in the brain stem or spinal cord to produce tonic or clonic convulsions, often by removing normal inhibitory tone. They were formerly used to stimulate respiration or as antidotes to barbiturate overdose. They are now most commonly used as experimental tools. [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] Cooperative group: A group of physicians, hospitals, or both formed to treat a large number of persons in the same way so that new treatment can be evaluated quickly. Clinical trials of new cancer treatments often require many more people than a single physician or hospital can care for. [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] Corneum: The superficial layer of the epidermis containing keratinized cells. [NIH]
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Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroids: Hormones that have antitumor activity in lymphomas and lymphoid leukemias; in addition, corticosteroids (steroids) may be used for hormone replacement and for the management of some of the complications of cancer and its treatment. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cotinine: 1-Methyl-5-(3-pyridyl)-2-pyrrolidinone antidepressant. Synonym: Scotine. [NIH]
fumarate.
Stimulant
proposed
as
Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Croton Oil: Viscous, nauseating oil obtained from the shrub Croton tiglium (Euphorbaceae). It is a vesicant and skin irritant used as pharmacologic standard for skin inflammation and allergy and causes skin cancer. It was formerly used as an emetic and cathartic with frequent mortality. [NIH] Cruciferous vegetables: A family of vegetables that includes kale, collard greens, broccoli, cauliflower, cabbage, brussels sprouts, and turnip. These vegetables contain substances that may protect against cancer. [NIH] Cryosurgery: The use of freezing as a special surgical technique to destroy or excise tissue. [NIH]
Crystallization: The formation of crystals; conversion to a crystalline form. [EU] Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as agar or gelatin. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Curettage: Removal of tissue with a curette, a spoon-shaped instrument with a sharp edge.
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[NIH]
Curette: A spoon-shaped instrument with a sharp edge. [NIH] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclin: Molecule that regulates the cell cycle. [NIH] Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cytarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Cytotoxins: Substances elaborated by microorganisms, plants or animals that are specifically toxic to individual cells; they may be involved in immunity or may be contained in venoms. [NIH]
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.
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The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Daunorubicin: Very toxic anthracycline aminoglycoside antibiotic isolated from Streptomyces peucetius and others, used in treatment of leukemias and other neoplasms. [NIH]
De novo: In cancer, the first occurrence of cancer in the body. [NIH] Death Certificates: Official records of individual deaths including the cause of death certified by a physician, and any other required identifying information. [NIH] Decontamination: The removal of contaminating material, such as radioactive materials, biological materials, or chemical warfare agents, from a person or object. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [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] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Dentate Gyrus: Gray matter situated above the gyrus hippocampi. It is composed of three layers. The molecular layer is continuous with the hippocampus in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called granule cells, whose axons pass through the polymorphic layer ending on the dendrites of pyramidal cells in the hippocampus. [NIH] Dentists: Individuals licensed to practice dentistry. [NIH] Depigmentation: Removal or loss of pigment, especially melanin. [EU] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Depressive Disorder: An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent. [NIH] Depsipeptide: Anticancer drugs obtained from microorganisms. [NIH] Dermatitis: Any inflammation of the skin. [NIH] DES: Diethylstilbestrol. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton
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in the nucleus. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnosis, Differential: Determination of which one of two or more diseases or conditions a patient is suffering from by systematically comparing and contrasting results of diagnostic measures. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diarrhoea: Abnormal frequency and liquidity of faecal discharges. [EU] Diastolic: Of or pertaining to the diastole. [EU] Diathermy: The induction of local hyperthermia by either short radio waves or highfrequency sound waves. [NIH] Diazinon: A cholinesterase inhibitor that is used as an organothiophosphorus insecticide. [NIH]
Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dilatation: The act of dilating. [NIH] Dilatation, Pathologic: The condition of an anatomical structure's being dilated beyond normal dimensions. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dilution: A diluted or attenuated medicine; in homeopathy, the diffusion of a given quantity of a medicinal agent in ten or one hundred times the same quantity of water. [NIH] Dimethylnitrosamine: A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties. It causes serious liver damage and is a hepatocarcinogen in rodents. [NIH]
Dioxins: Chlorinated hydrocarbons containing heteroatoms that are present as contaminants of herbicides. Dioxins are carcinogenic, teratogenic, and mutagenic. They have been banned from use by the FDA. [NIH] Diploid: Having two sets of chromosomes. [NIH]
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Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disease-Free Survival: Period after successful treatment in which there is no appearance of the symptoms or effects of the disease. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disinfection: Rendering pathogens harmless through the use of heat, antiseptics, antibacterial agents, etc. [NIH] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Diuresis: Increased excretion of urine. [EU] Dopa: The racemic or DL form of DOPA, an amino acid found in various legumes. The dextro form has little physiologic activity but the levo form (levodopa) is a very important physiologic mediator and precursor and pharmacological agent. [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] Doping: The action of administering a drug to someone before a sports event (originally to a horse before a race); the substance thus administered. [EU] 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] Dose-dependent: Refers to the effects of treatment with a drug. If the effects change when the dose of the drug is changed, the effects are said to be dose dependent. [NIH] Dosimetry: All the methods either of measuring directly, or of measuring indirectly and computing, absorbed dose, absorbed dose rate, exposure, exposure rate, dose equivalent, and the science associated with these methods. [NIH] Doxorubicin: Antineoplastic antibiotic obtained from Streptomyces peucetics. It is a hydroxy derivative of daunorubicin and is used in treatment of both leukemia and solid tumors. [NIH] 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]
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Drug Design: The molecular designing of drugs for specific purposes (such as DNAbinding, enzyme inhibition, anti-cancer efficacy, etc.) based on knowledge of molecular properties such as activity of functional groups, molecular geometry, and electronic structure, and also on information cataloged on analogous molecules. Drug design is generally computer-assisted molecular modeling and does not include pharmacokinetics, dosage analysis, or drug administration analysis. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Drug Toxicity: Manifestations of the adverse effects of drugs administered therapeutically or in the course of diagnostic techniques. It does not include accidental or intentional poisoning for which specific headings are available. [NIH] Duct: A tube through which body fluids pass. [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] Dysprosium: Dysprosium. An element of the rare earth family that has the atomic symbol Dy, atomic number 66, and atomic weight 162.50. Dysprosium is a silvery metal used primarily in the form of various salts. [NIH] Dystrophin: A muscle protein localized in surface membranes which is the product of the Duchenne/Becker muscular dystrophy gene. Individuals with Duchenne muscular dystrophy usually lack dystrophin completely while those with Becker muscular dystrophy have dystrophin of an altered size. It shares features with other cytoskeletal proteins such as spectrin and alpha-actinin but the precise function of dystrophin is not clear. One possible role might be to preserve the integrity and alignment of the plasma membrane to the myofibrils during muscle contraction and relaxation. MW 400 kDa. [NIH] Ecosystem: A dynamic complex of plant, animal and micro-organism communities and their non-living environment interacting as a functional unit. [NIH] Ectoderm: The outer of the three germ layers of the embryo. [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] 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] Eicosanoids: A class of oxygenated, endogenous, unsaturated fatty acids derived from arachidonic acid. They include prostaglandins, leukotrienes, thromboxanes, and
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hydroxyeicosatetraenoic acid compounds (HETE). They are hormone-like substances that act near the site of synthesis without altering functions throughout the body. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [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] Electrodesiccation: The drying of tissue by a high-frequency electric current applied with a needle-shaped electrode. [NIH] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a chemical compound in solution. [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] Electroplating: Coating with a metal or alloy by electrolysis. [NIH] Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] Embolus: Bit of foreign matter which enters the blood stream at one point and is carried until it is lodged or impacted in an artery and obstructs it. It may be a blood clot, an air bubble, fat or other tissue, or clumps of bacteria. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emulsions: Colloids of two immiscible liquids where either phase may be either fatty or aqueous; lipid-in-water emulsions are usually liquid, like milk or lotion and water-in-lipid emulsions tend to be creams. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH]
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Endoscopy: Endoscopic examination, therapy or surgery performed on interior parts of the body. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endothelium: A layer of epithelium that lines the heart, blood vessels (endothelium, vascular), lymph vessels (endothelium, lymphatic), and the serous cavities of the body. [NIH] Endothelium-derived: Small molecule that diffuses to the adjacent muscle layer and relaxes it. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Entorhinal Cortex: Cortex where the signals are combined with those from other sensory systems. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Environmental Pollutants: Substances which pollute the environment. Use environmental pollutants in general or for which there is no specific heading. [NIH]
for
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidermoid carcinoma: A type of cancer in which the cells are flat and look like fish scales. Also called squamous cell carcinoma. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelioma: A neoplasm of epithelial origin, ranging from benign (adenoma and
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papilloma) to malignant (carcinoma). [EU] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Erbium: Erbium. An element of the rare earth family of metals. It has the atomic symbol Er, atomic number 68, and atomic weight 167.26. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Estrogen: One of the two female sex hormones. [NIH] Estrogen receptor: ER. Protein found on some cancer cells to which estrogen will attach. [NIH]
Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethylene Glycol: A colorless, odorless, viscous dihydroxy alcohol. It has a sweet taste, but is poisonous if ingested. Ethylene glycol is the most important glycol commercially available and is manufactured on a large scale in the United States. It is used as an antifreeze and coolant, in hydraulic fluids, and in the manufacture of low-freezing dynamites and resins. [NIH]
Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Europium: An element of the rare earth family of metals. It has the atomic symbol Eu, atomic number 63, and atomic weight 152. Europium is used in the form of its salts as coatings for cathode ray tubes and in the form of its organic derivatives as shift reagents in NMR spectroscopy. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excimer laser: An ultraviolet laser used in refractive surgery to remove corneal tissue. [NIH] Excisional: The surgical procedure of removing a tumor by cutting it out. The biopsy is then examined under a microscope. [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]
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Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] 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] Exons: Coding regions of messenger RNA included in the genetic transcript which survive the processing of RNA in cell nuclei to become part of a spliced messenger of structural RNA in the cytoplasm. They include joining and diversity exons of immunoglobulin genes. [NIH]
Expiration: The act of breathing out, or expelling air from the lungs. [EU] Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] 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] Extracorporeal: Situated or occurring outside the body. [EU] Extraction: The process or act of pulling or drawing out. [EU] Exudate: Material, such as fluid, cells, or cellular debris, which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation. An exudate, in contrast to a transudate, is characterized by a high content of protein, cells, or solid materials derived from cells. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH] Ferritin: An iron-containing protein complex that is formed by a combination of ferric iron with the protein apoferritin. [NIH] Fertilizers: Substances or mixtures that are added to the soil to supply nutrients or to make available nutrients already present in the soil, in order to increase plant growth and productivity. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of
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the blood clot. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Filler: An inactive substance used to make a product bigger or easier to handle. For example, fillers are often used to make pills or capsules because the amount of active drug is too small to be handled conveniently. [NIH] Filtration: The passage of a liquid through a filter, accomplished by gravity, pressure, or vacuum (suction). [EU] Fish Products: Food products manufactured from fish (e.g., fish flour, fish meal). [NIH] Fistula: Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU] Flatus: Gas passed through the rectum. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] 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
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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] Fluorouracil: A pyrimidine analog that acts as an antineoplastic antimetabolite and also has immunosuppressant. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. [NIH] Folate: A B-complex vitamin that is being studied as a cancer prevention agent. Also called folic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Freeze-dried: A method used to dry substances, such as food, to make them last longer. The substance is frozen and then dried in a vacuum. [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] 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] Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallium: A rare, metallic element designated by the symbol, Ga, atomic number 31, and atomic weight 69.72. [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of
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shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] 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]
Gastroenteritis: An acute inflammation of the lining of the stomach and intestines, characterized by anorexia, nausea, diarrhoea, abdominal pain, and weakness, which has various causes, including food poisoning due to infection with such organisms as Escherichia coli, Staphylococcus aureus, and Salmonella species; consumption of irritating food or drink; or psychological factors such as anger, stress, and fear. Called also enterogastritis. [EU] Gastrointestinal: Refers to the stomach and intestines. [NIH] 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] Gemcitabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Pool: The total genetic information possessed by the reproductive members of a population of sexually reproducing organisms. [NIH] Generator: Any system incorporating a fixed parent radionuclide from which is produced a daughter radionuclide which is to be removed by elution or by any other method and used in a radiopharmaceutical. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Techniques: Chromosomal, biochemical, intracellular, and other methods used in the study of genetics. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of
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heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genitourinary: Pertaining to the genital and urinary organs; urogenital; urinosexual. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germanium: A rare metal element with a blue-gray appearance and atomic symbol Ge, atomic number 32, and atomic weight 72.59. [NIH] Germinal Center: The activated center of a lymphoid follicle in secondary lymphoid tissue where B-lymphocytes are stimulated by antigens and helper T cells (T-lymphocytes, helperinducer) are stimulated to generate memory cells. [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] Glioblastoma: A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures. [NIH] Glioblastoma multiforme: A type of brain tumor that forms from glial (supportive) tissue of the brain. It grows very quickly and has cells that look very different from normal cells. Also called grade IV astrocytoma. [NIH] Glioma: A cancer of the brain that comes from glial, or supportive, cells. [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] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucose tolerance: The power of the normal liver to absorb and store large quantities of glucose and the effectiveness of intestinal absorption of glucose. The glucose tolerance test is a metabolic test of carbohydrate tolerance that measures active insulin, a hepatic function based on the ability of the liver to absorb glucose. The test consists of ingesting 100 grams of glucose into a fasting stomach; blood sugar should return to normal in 2 to 21 hours after ingestion. [NIH] Glucose Tolerance Test: Determination of whole blood or plasma sugar in a fasting state before and at prescribed intervals (usually 1/2 hr, 1 hr, 3 hr, 4 hr) after taking a specified amount (usually 100 gm orally) of glucose. [NIH]
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Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
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]
Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] 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] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Gram-Negative Bacteria: Bacteria which lose crystal violet stain but are stained pink when treated by Gram's method. [NIH] Gram-positive: Retaining the stain or resisting decolorization by alcohol in Gram's method of staining, a primary characteristic of bacteria whose cell wall is composed of a thick layer of peptidologlycan with attached teichoic acids. [EU] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Graphite: An allotropic form of carbon that is used in pencils, as a lubricant, and in matches and explosives. It is obtained by mining and its dust can cause lung irritation. [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] 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
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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] Gynecologic oncologist: A doctor who specializes in treating cancers of the female reproductive organs. [NIH] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Haloperidol: Butyrophenone derivative. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Harmine: Alkaloid isolated from seeds of Peganum harmala L., Zygophyllaceae. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic Parkinson disease in the 1920's. [NIH] Hazardous Substances: Substances which, upon release into the atmosphere, water, or soil, or which, in direct contact with the skin, eyes, or mucous membranes, or as additives to food, cause health risks to humans or animals through absorption, inhalation, or ingestion. The concept includes safe handling, transportation, and storage of these substances. [NIH] Hazardous Waste: Waste products which, upon release into the atmosphere, water or soil, cause health risks to humans or animals through skin contact, inhalation or ingestion. Hazardous waste sites which contain hazardous waste substances go here. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heartbeat: One complete contraction of the heart. [NIH] Hematologic malignancies: Cancers of the blood or bone marrow, including leukemia and lymphoma. Also called hematologic cancers. [NIH] Hematology: A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues. [NIH] Hematopoietic growth factors: A group of proteins that cause blood cells to grow and mature. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level
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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] Hemoperfusion: Removal of toxins or metabolites from the circulation by the passing of blood, within a suitable extracorporeal circuit, over semipermeable microcapsules containing adsorbents (e.g., activated charcoal) or enzymes, other enzyme preparations (e.g., gel-entrapped microsomes, membrane-free enzymes bound to artificial carriers), or other adsorbents (e.g., various resins, albumin-conjugated agarose). [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocyte: A liver cell. [NIH] Hepatoma: A liver tumor. [NIH] Herbicide: A chemical that kills plants. [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] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Hiccup: A spasm of the diaphragm that causes a sudden inhalation followed by rapid closure of the glottis which produces a sound. [NIH] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Histone Deacetylase: Hydrolyzes N-acetyl groups on histones. [NIH] Holmium: An element of the rare earth family of metals. It has the atomic symbol Ho, atomic number 67, and atomic weight 164.93. [NIH] Homeopathic remedies: Small doses of medicines, herbs, or both that are believed to stimulate the immune system. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH]
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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] Hormone therapy: Treatment of cancer by removing, blocking, or adding hormones. Also called endocrine therapy. [NIH] Horny layer: The superficial layer of the epidermis containing keratinized cells. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human Activities: Activities performed by humans. [NIH] Human Development: Continuous sequential changes which occur in the physiological and psychological functions during the individual's life. [NIH] Human papillomavirus: HPV. A virus that causes abnormal tissue growth (warts) and is often associated with some types of cancer. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hydrocarbons, Aromatic: Organic compounds containing carbon and hydrogen in the form of an unsaturated, usually hexagonal ring structure. The compounds can be single ring, or double, triple, or multiple fused rings. [NIH] Hydrofluoric Acid: A solution of hydrogen fluoride in water. It is a colorless fuming liquid which can cause painful burns. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxides: Inorganic compounds that contain the OH- group. [NIH] Hyperkeratosis: 1. Hypertrophy of the corneous layer of the skin. 2a. Any of various conditions marked by hyperkeratosis. 2b. A disease of cattle marked by thickening and wringling of the hide and formation of papillary outgrowths on the buccal mucous membranes, often accompanied by watery discharge from eyes and nose, diarrhoea, loss of condition, and abortion of pregnant animals, and now believed to result from ingestion of the chlorinated naphthalene of various lubricating oils. [EU]
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Hyperpigmentation: Excessive pigmentation of the skin, usually as a result of increased melanization of the epidermis rather than as a result of an increased number of melanocytes. Etiology is varied and the condition may arise from exposure to light, chemicals or other substances, or from a primary metabolic imbalance. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypersensitivity, Immediate: Hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigenantibody reaction and causes smooth muscle contraction and increased vascular permeability. [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] Hypnotic: A drug that acts to induce sleep. [EU] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]
Hypoglycemic Agents: Agents which lower the blood glucose level. [NIH] Hypothermia: Lower than normal body temperature, especially in warm-blooded animals; in man usually accidental or unintentional. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idarubicin: An orally administered anthracycline antibiotic. The compound has shown activity against breast cancer, lymphomas and leukemias, together with potential for reduced cardiac toxicity. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] 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] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction. [NIH]
Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct
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elliptical precipitin arc results for each protein detectable by the antisera. [NIH] Immunofluorescence: A technique for identifying molecules present on the surfaces of cells or in tissues using a highly fluorescent substance coupled to a specific antibody. [NIH] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] 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] Incubated: Grown in the laboratory under controlled conditions. (For instance, white blood cells can be grown in special conditions so that they attack specific cancer cells when returned to the body.) [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indolent: A type of cancer that grows slowly. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Induction therapy: Treatment designed to be used as a first step toward shrinking the cancer and in evaluating response to drugs and other agents. Induction therapy is followed by additional therapy to eliminate whatever cancer remains. [NIH] Industrial Waste: Worthless, damaged, defective, superfluous or effluent material from industrial operations. It represents an ecological problem and health hazard. [NIH] Infant, Newborn: An infant during the first month after birth. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the
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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] Information Systems: Integrated set of files, procedures, and equipment for the storage, manipulation, and retrieval of information. [NIH] Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Inhalation Exposure: The exposure to potentially harmful chemical, physical, or biological agents by inhaling them. [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH]
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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] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Iridium: A metallic element with the atomic symbol Ir, atomic number 77, and atomic weight 192.22. [NIH] Irrigation: The washing of a body cavity or surface by flowing solution which is inserted and then removed. Any drug in the irrigation solution may be absorbed. [NIH] Isoniazid: Antibacterial agent used primarily as a tuberculostatic. It remains the treatment of choice for tuberculosis. [NIH] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Keratosis: Any horny growth such as a wart or callus. [NIH] Kidney Cortex: The outer zone of the kidney, beneath the capsule, consisting of kidney glomerulus; kidney tubules, distal; and kidney tubules, proximal. [NIH]
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Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lanthanum: The prototypical element in the rare earth family of metals. It has the atomic symbol La, atomic number 57, and atomic weight 138.91. Lanthanide ion is used in experimental biology as a calcium antagonist; lanthanum oxide improves the optical properties of glass. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Latent period: A seemingly inactive period, as that between exposure of tissue to an injurious agent and the manifestation of response, or that between the instant of stimulation and the beginning of response. [EU] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]
Lead Poisoning: Disease caused by the gradual accumulation of a significant body burden of lead. [NIH] Lesion: An area of abnormal tissue change. [NIH] Leucine: An essential branched-chain amino acid important for hemoglobin formation. [NIH] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leukaemia: An acute or chronic disease of unknown cause in man and other warm-blooded animals that involves the blood-forming organs, is characterized by an abnormal increase in the number of leucocytes in the tissues of the body with or without a corresponding increase of those in the circulating blood, and is classified according of the type leucocyte most prominently involved. [EU] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] 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] Levo: It is an experimental treatment for heroin addiction that was developed by German scientists around 1948 as an analgesic. Like methadone, it binds with opioid receptors, but it is longer acting. [NIH] Levodopa: The naturally occurring form of dopa and the immediate precursor of dopamine. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. It is used for the treatment of parkinsonism and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system. [NIH]
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Library Services: Services offered to the library user. They include reference and circulation. [NIH]
Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligase: An enzyme that repairs single stranded discontinuities in double-stranded DNA molecules in the cell. Purified DNA ligase is used in gene cloning to join DNA molecules together. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipophilic: Having an affinity for fat; pertaining to or characterized by lipophilia. [EU] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liposomal: A drug preparation that contains the active drug in very tiny fat particles. This fat-encapsulated drug is absorbed better, and its distribution to the tumor site is improved. [NIH]
Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]
Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver cancer: A disease in which malignant (cancer) cells are found in the tissues of the liver. [NIH]
Liver Neoplasms: Tumors or cancer of the liver. [NIH] Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] 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] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside
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diameter) and used in transferring microorganisms. [NIH] Lubricants: Oily or slippery substances. [NIH] Luciferase: Any one of several enzymes that catalyze the bioluminescent reaction in certain marine crustaceans, fish, bacteria, and insects. The enzyme is a flavoprotein; it oxidizes luciferins to an electronically excited compound that emits energy in the form of light. The color of light emitted varies with the organism. The firefly enzyme is a valuable reagent for measurement of ATP concentration. (Dorland, 27th ed) EC 1.13.12.-. [NIH] Lutetium: Lutetium. An element of the rare earth family of metals. It has the atomic symbol Lu, atomic number 71, and atomic weight 175. [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). [NIH]
Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphoblastic: One of the most aggressive types of non-Hodgkin lymphoma. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphoproliferative Disorders: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] 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] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH]
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Malignant tumor: A tumor capable of metastasizing. [NIH] Mammary: Pertaining to the mamma, or breast. [EU] Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Man-made: Ionizing radiation emitted by artificial or concentrated natural, radioactive material or resulting from the operation of high voltage apparatus, such as X-ray apparatus or particle accelerators, of nuclear reactors, or from nuclear explosions. [NIH] Mannans: Polysaccharides consisting of mannose units. [NIH] Materia Medica: Materials or substances used in the composition of traditional medical remedies. The use of this term in MeSH was formerly restricted to historical articles or those concerned with traditional medicine, but it can also refer to homeopathic remedies. Nosodes are specific types of homeopathic remedies prepared from causal agents or disease products. [NIH]
Maxillary: Pertaining to the maxilla : the irregularly shaped bone that with its fellow forms the upper jaw. [EU] Maxillary Sinus: One of the paired paranasal sinuses, located in the body of the maxilla, communicating with the middle meatus of the nasal cavity. [NIH] Maximum Tolerated Dose: The highest dose level eliciting signs of toxicity without having major effects on survival relative to the test in which it is used. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]
Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Megaloblastic: A large abnormal red blood cell appearing in the blood in pernicious anaemia. [EU] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Melanosomes: Melanin-containing organelles found in melanocytes and melanophores. [NIH]
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Melarsoprol: Arsenical used in trypanosomiases. It may cause fatal encephalopathy and other undesirable side effects. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Mendelevium: A man-made radioactive element of the actinide family with atomic symbol Md, atomic number 101, and atomic weight 258. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [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] Mercaptopurine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH] Mercuric Chloride: Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous membranes and used as a topical antiseptic and disinfectant. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metallothionein: A low-molecular-weight (approx. 10 kD) protein occurring in the cytoplasm of kidney cortex and liver. It is rich in cysteinyl residues and contains no aromatic amino acids. Metallothionein shows high affinity for bivalent heavy metals. [NIH] Metals, Alkali: Metals that constitute group Ia in the periodic table. They are the most strongly electropositive of the metals. [NIH] Metaphase: The second phase of cell division, in which the chromosomes line up across the equatorial plane of the spindle prior to separation. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methacrylate: A vinyl monomer. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH]
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Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Micronuclei: Nuclei, separate from and additional to the main nucleus of a cell, produced during the telophase of mitosis or meiosis by lagging chromosomes or chromosome fragments derived from spontaneous or experimentally induced chromosomal structural changes. This concept also includes the smaller, reproductive nuclei found in multinucleate protozoans. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Microwaves: That portion of the electromagnetic spectrum lying between UHF (ultrahigh frequency) radio waves and heat (infrared) waves. Microwaves are used to generate heat, especially in some types of diathermy. They may cause heat damage to tissues. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Minority Groups: A subgroup having special characteristics within a larger group, often bound together by special ties which distinguish it from the larger group. [NIH] 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] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitotic: Cell resulting from mitosis. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH]
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Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monosomy: The condition in which one chromosome of a pair is missing. In a normally diploid cell it is represented symbolically as 2N-1. [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] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]
Multidrug resistance: Adaptation of tumor cells to anticancer drugs in ways that make the drugs less effective. [NIH] Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria, and anemia. [NIH] Muscle Proteins: The protein constituents of muscle, the major ones being ACTINS and MYOSIN. More than a dozen accessary proteins exist including troponin, tropomyosin, and dystrophin. [NIH] Musculature: The muscular apparatus of the body, or of any part of it. [EU] Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed). [NIH]
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Mutagen: Any agent, such as X-rays, gamma rays, mustard gas, TCDD, that can cause abnormal mutation in living cells; having the power to cause mutations. [NIH] Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagenic: Inducing genetic mutation. [EU] Myelodysplastic syndrome: Disease in which the bone marrow does not function normally. Also called preleukemia or smoldering leukemia. [NIH] Myelogenous: Produced by, or originating in, the bone marrow. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Myelosuppression: A condition in which bone marrow activity is decreased, resulting in fewer red blood cells, white blood cells, and platelets. Myelosuppression is a side effect of some cancer treatments. [NIH] Myelotoxic: 1. Destructive to bone marrow. 2. Arising from diseased bone marrow. [EU] 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] Myotonia: Prolonged failure of muscle relaxation after contraction. This may occur after voluntary contractions, muscle percussion, or electrical stimulation of the muscle. Myotonia is a characteristic feature of myotonic disorders. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neodymium: Neodymium. An element of the rare earth family of metals. It has the atomic symbol Nd, atomic number 60, and atomic weight 144.24, and is used in industrial applications. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephritis: Inflammation of the kidney; a focal or diffuse proliferative or destructive process which may involve the glomerulus, tubule, or interstitial renal tissue. [EU] Nephrosis: Descriptive histopathologic term for renal disease without an inflammatory component. [NIH]
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Nephrotic: Pertaining to, resembling, or caused by nephrosis. [EU] Nephrotic Syndrome: Clinical association of heavy proteinuria, hypoalbuminemia, and generalized edema. [NIH] Nephrotoxic: Toxic or destructive to kidney cells. [EU] Neptunium: A radioactive element of the actinide metals family. It has the atomic symbol Np, atomic number 93, and atomic weight 237. [NIH] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] 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 Crest: A strip of specialized ectoderm flanking each side of the embryonal neural plate, which after the closure of the neural tube, forms a column of isolated cells along the dorsal aspect of the neural tube. Most of the cranial and all of the spinal sensory ganglion cells arise by differentiation of neural crest cells. [NIH] Neuroblastoma: Cancer that arises in immature nerve cells and affects mostly infants and children. [NIH] Neurodegenerative Diseases: Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures. [NIH] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] 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] Neurotoxicity: The tendency of some treatments to cause damage to the nervous system. [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] Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme urease. [NIH] Nitrates: Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical. [NIH] Nitric acid: A toxic, corrosive, colorless liquid used to make fertilizers, dyes, explosives, and
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other chemicals. [NIH] Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells. It is synthesized from arginine by a complex reaction, catalyzed by nitric oxide synthase. Nitric oxide is endothelium-derived relaxing factor. It is released by the vascular endothelium and mediates the relaxation induced by some vasodilators such as acetylcholine and bradykinin. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic guanylate cyclase and thus elevates intracellular levels of cyclic GMP. [NIH]
Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nitrogen Compounds: Inorganic compounds that contain nitrogen as an integral part of the molecule. [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] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation. [NIH] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU] 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] 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
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environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Oncologist: A doctor who specializes in treating cancer. Some oncologists specialize in a particular type of cancer treatment. For example, a radiation oncologist specializes in treating cancer with radiation. [NIH] Oncology: The study of cancer. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Oroantral Fistula: A fistula between the maxillary sinus and the oral cavity. [NIH] Osmosis: Tendency of fluids (e.g., water) to move from the less concentrated to the more concentrated side of a semipermeable membrane. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overall survival: The percentage of subjects in a study who have survived for a defined period of time. Usually reported as time since diagnosis or treatment. Often called the survival rate. [NIH] Overdose: An accidental or deliberate dose of a medication or street drug that is in excess of what is normally used. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [NIH]
Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative metabolism: A chemical process in which oxygen is used to make energy from
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carbohydrates (sugars). Also known as aerobic respiration, cell respiration, or aerobic metabolism. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxides: Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides. [NIH] 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] P53 gene: A tumor suppressor gene that normally inhibits the growth of tumors. This gene is altered in many types of cancer. [NIH] Paclitaxel: Antineoplastic agent isolated from the bark of the Pacific yew tree, Taxus brevifolia. Paclitaxel stabilizes microtubules in their polymerized form and thus mimics the action of the proto-oncogene proteins c-mos. [NIH] Palladium: A chemical element having an atomic weight of 106.4, atomic number of 46, and the symbol Pd. It is a white, ductile metal resembling platinum, and following it in abundance and importance of applications. It is used in dentistry in the form of gold, silver, and copper alloys. [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] Papillary: Pertaining to or resembling papilla, or nipple. [EU] Papilloma: A benign epithelial neoplasm which may arise from the skin, mucous membranes or glandular ducts. [NIH] Papillomavirus: A genus of Papovaviridae causing proliferation of the epithelium, which may lead to malignancy. A wide range of animals are infected including humans, chimpanzees, cattle, rabbits, dogs, and horses. [NIH] Papule: A small circumscribed, superficial, solid elevation of the skin. [EU] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU] Parenteral Nutrition: The administering of nutrients for assimilation and utilization by a
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patient who cannot maintain adequate nutrition by enteral feeding alone. Nutrients are administered by a route other than the alimentary canal (e.g., intravenously, subcutaneously). [NIH] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Particle: A tiny mass of material. [EU] 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]
Peer Review: An organized procedure carried out by a select committee of professionals in evaluating the performance of other professionals in meeting the standards of their specialty. Review by peers is used by editors in the evaluation of articles and other papers submitted for publication. Peer review is used also in the evaluation of grant applications. It is applied also in evaluating the quality of health care provided to patients. [NIH] Pelvic: Pertaining to the pelvis. [EU] Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peracetic Acid: A liquid that functions as a strong oxidizing agent. It has an acrid odor and is used as a disinfectant. [NIH] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Perhexiline: 2-(2,2-Dicyclohexylethyl)piperidine. Coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis. [NIH] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous
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system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Neuropathy: Nerve damage, usually affecting the feet and legs; causing pain, numbness, or a tingling feeling. Also called "somatic neuropathy" or "distal sensory polyneuropathy." [NIH] Peripheral Vascular Disease: Disease in the large blood vessels of the arms, legs, and feet. People who have had diabetes for a long time may get this because major blood vessels in their arms, legs, and feet are blocked and these limbs do not receive enough blood. The signs of PVD are aching pains in the arms, legs, and feet (especially when walking) and foot sores that heal slowly. Although people with diabetes cannot always avoid PVD, doctors say they have a better chance of avoiding it if they take good care of their feet, do not smoke, and keep both their blood pressure and diabetes under good control. [NIH] Peroxidase: A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 1.11.1.7. [NIH] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Pharmacists: Those persons legally qualified by education and training to engage in the practice of pharmacy. [NIH] Pharmacodynamic: Is concerned with the response of living tissues to chemical stimuli, that is, the action of drugs on the living organism in the absence of disease. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It promotes binding to inhibitory GABA subtype receptors, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations. [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phorbol: Class of chemicals that promotes the development of tumors. [NIH] Phosphates: Inorganic salts of phosphoric acid. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phosphorous: Having to do with or containing the element phosphorus. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and
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teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylates: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] 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] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pilot Projects: Small-scale tests of methods and procedures to be used on a larger scale if the pilot study demonstrates that these methods and procedures can work. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Placentation: Development of a site of fetomaternal union for physiologic exchange, a placenta or placenta-like organ. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH]
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Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Aggregation: The attachment of platelets to one another. This clumping together can be induced by a number of agents (e.g., thrombin, collagen) and is part of the mechanism leading to the formation of a thrombus. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Pneumonitis: A disease caused by inhaling a wide variety of substances such as dusts and molds. Also called "farmer's disease". [NIH] 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] Polonium: A radioactive element that is a member of the chalcogen family. It has the atomic symbol Po, atomic number 84, and the atomic weight of the isotope with the longest half-life (209Po) is 208.98. It decays by alpha-emission. [NIH] Polychlorinated Biphenyls: Industrial products consisting of a mixture of chlorinated biphenyl congeners and isomers. These compounds are highly lipophilic and tend to accumulate in fat stores of animals. Many of these compounds are considered toxic and potential environmental pollutants. [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] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Porosity: Condition of having pores or open spaces. This often refers to bones, bone implants, or bone cements, but can refer to the porous state of any solid substance. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of
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the body. In lower animals, it refers to the caudal end of the body. [EU] Postoperative: After surgery. [NIH] Postoperative Period: The period following a surgical operation. [NIH] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [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] Power Plants: Units that convert some form of energy into electrical energy, such as hydroelectric or steam-generating stations, diesel-electric engines in locomotives, or nuclear power plants. [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] Praseodymium: Praseodymium. An element of the rare earth family of metals. It has the atomic symbol Pr, atomic number 59, and atomic weight 140.91. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Precipitating Factors: Factors associated with the definitive onset of a disease, illness, accident, behavioral response, or course of action. Usually one factor is more important or more obviously recognizable than others, if several are involved, and one may often be regarded as "necessary". Examples include exposure to specific disease; amount or level of an infectious organism, drug, or noxious agent, etc. [NIH] Precipitation: The act or process of precipitating. [EU] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Pregnancy Complications: The co-occurrence of pregnancy and a disease. The disease may precede or follow conception and it may or may not have a deleterious effect on the pregnant woman or fetus. [NIH] Preleukemia: Conditions in which the abnormalities in the peripheral blood or bone marrow represent the early manifestations of acute leukemia, but in which the changes are not of sufficient magnitude or specificity to permit a diagnosis of acute leukemia by the usual clinical criteria. [NIH]
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Premalignant: A term used to describe a condition that may (or is likely to) become cancer. Also called precancerous. [NIH] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Presumptive: A treatment based on an assumed diagnosis, prior to receiving confirmatory laboratory test results. [NIH] 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] Prickle: Several layers of the epidermis where the individual cells are connected by cell bridges. [NIH] Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] 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] Prokaryotic Cells: Cells, such as those of bacteria and the blue green algae, which lack a nuclear membrane so that the nuclear material is either scattered in the cytoplasm or collected in a nucleoid region. [NIH] Promethium: Promethium. A radioactive element of the rare earth family of metals. It has the atomic symbol Pm, atomic number 61, and atomic weight 147. It has been used in the construction of atomic batteries, in the preparation of self-luminous compounds, and as a beta-particle source for thickness gauges. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promotor: In an operon, a nucleotide sequence located at the operator end which contains all the signals for the correct initiation of genetic transcription by the RNA polymerase holoenzyme and determines the maximal rate of RNA synthesis. [NIH] Promyelocytic leukemia: A type of acute myeloid leukemia, a quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. [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] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Propoxur: A carbamate insecticide. [NIH] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to
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indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protactinium: Protactinium. A radioactive element of the actinide group of metals. It has the atomic symbol Pa, atomic number 91, and atomic weight 231. It decays by alpha-emission. [NIH]
Protective Agents: Synthetic or natural substances which are given to prevent a disease or disorder or are used in the process of treating a disease or injury due to a poisonous agent. [NIH]
Protective Clothing: Clothing designed to protect the individual against possible exposure to known hazards. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein Engineering: Procedures by which nonrandom single-site changes are introduced into structural genes (site-specific mutagenesis) in order to produce mutant genes which can be coupled to promoters that direct the synthesis of a specifically altered protein, which is then analyzed for structural and functional properties and then compared with the predicted and sought-after properties. The design of the protein may be assisted by computer graphic technology and other advanced molecular modeling techniques. [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino
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acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] 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] Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. [NIH] Proto-Oncogene Proteins c-mos: Cellular proteins encoded by the c-mos genes. They function in the cell cycle to maintain maturation promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time. [NIH] 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] Protraction: A method of administration of radiation by delivering it continuously over a relatively long period at a low absorbed dose rate. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Purifying: Respiratory equipment whose function is to remove contaminants from
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otherwise wholesome air. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Quadrivalent: Pertaining to a group of 4 homologous or partly homologous chromosomes during the zygotene stage of prophase to the first metaphase in meiosis. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quaternary: 1. Fourth in order. 2. Containing four elements or groups. [EU] Quiescent: Marked by a state of inactivity or repose. [EU] Quinidine: An optical isomer of quinine, extracted from the bark of the Cinchona tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular action potential, and decreases automaticity. Quinidine also blocks muscarinic and alphaadrenergic neurotransmission. [NIH] Quinine: An alkaloid derived from the bark of the cinchona tree. It is used as an antimalarial drug, and is the active ingredient in extracts of the cinchona that have been used for that purpose since before 1633. Quinine is also a mild antipyretic and analgesic and has been used in common cold preparations for that purpose. It was used commonly and as a bitter and flavoring agent, and is still useful for the treatment of babesiosis. Quinine is also useful in some muscular disorders, especially nocturnal leg cramps and myotonia congenita, because of its direct effects on muscle membrane and sodium channels. The mechanisms of its antimalarial effects are not well understood. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation oncologist: A doctor who specializes in using radiation to treat cancer. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radio Waves: That portion of the electromagnetic spectrum beyond the microwaves, with wavelengths as high as 30 KM. They are used in communications, including television. Short Wave or HF (high frequency), UHF (ultrahigh frequency) and VHF (very high frequency) waves are used in citizen's band communication. [NIH] Radioactive: Giving off radiation. [NIH] Radiochemical: The proportion of the total activity of the radionuclide in the sample considered, which is due to the nuclide in the stated chemical form. [NIH] Radioimmunotherapy: Radiotherapy where cytotoxic radionuclides are linked to antibodies in order to deliver toxins directly to tumor targets. Therapy with targeted radiation rather
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than antibody-targeted toxins (immunotoxins) has the advantage that adjacent tumor cells, which lack the appropriate antigenic determinants, can be destroyed by radiation cross-fire. Radioimmunotherapy is sometimes called targeted radiotherapy, but this latter term can also refer to radionuclides linked to non-immune molecules (radiotherapy). [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiopharmaceutical: Any medicinal product which, when ready for use, contains one or more radionuclides (radioactive isotopes) included for a medicinal purpose. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Radium: A radioactive element symbol Ra, atomic number 88, disintegration of uranium and is is used clinically as a source brachytherapy. [NIH]
of the alkaline earth series of metals. It has the atomic and atomic weight 226. Radium is the product of the present in pitchblende and all ores containing uranium. It of beta and gamma-rays in radiotherapy, particularly
Radon: A naturally radioactive element with atomic symbol Rn, atomic number 86, and atomic weight 222. It is a member of the noble gas family and released during the decay of radium and found in soil. There is a link between exposure to radon and lung 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] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Ranitidine: A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers. [NIH] Reabsorption: 1. The act or process of absorbing again, as the selective absorption by the kidneys of substances (glucose, proteins, sodium, etc.) already secreted into the renal tubules, and their return to the circulating blood. 2. Resorption. [EU] Reaction Time: The time from the onset of a stimulus until the organism responds. [NIH] Reactivation: The restoration of activity to something that has been inactivated. [EU] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Cytokine: Cell surface proteins that bind cytokines and trigger intracellular changes influencing the behavior of cells. [NIH]
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Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Reconstitution: 1. A type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. The restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflective: Capable of throwing back light, images, sound waves : reflecting. [EU] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regional lymph node: In oncology, a lymph node that drains lymph from the region around a tumor. [NIH] Registries: The systems and processes involved in the establishment, support, management, and operation of registers, e.g., disease registers. [NIH] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Reliability: Used technically, in a statistical sense, of consistency of a test with itself, i. e. the extent to which we can assume that it will yield the same result if repeated a second time. [NIH]
Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renal pelvis: The area at the center of the kidney. Urine collects here and is funneled into the ureter, the tube that connects the kidney to the bladder. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes,
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which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] 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] Residual disease: Cancer cells that remain after attempts have been made to remove the cancer. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory failure: Inability of the lungs to conduct gas exchange. [NIH] Response Elements: Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promotor and enhancer regions. [NIH]
Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retinoid: Vitamin A or a vitamin A-like compound. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Rhabdomyolysis: Necrosis or disintegration of skeletal muscle often followed by myoglobinuria. [NIH] Rheumatoid: Resembling rheumatism. [EU] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents. [NIH]
Rods: One type of specialized light-sensitive cells (photoreceptors) in the retina that provide side vision and the ability to see objects in dim light (night vision). [NIH] Rotenone: A botanical insecticide that is an inhibitor of mitochondrial electron transport. [NIH]
Rubber: A high-molecular-weight polymeric elastomer derived from the milk juice (latex) of Hevea brasiliensis and other trees. It is a substance that can be stretched at room temperature to atleast twice its original length and after releasing the stress, retractrapidly, and recover its original dimensions fully. Synthetic rubber is made from many different chemicals, including styrene, acrylonitrile, ethylene, propylene, and isoprene. [NIH] Rubidium: An element that is an alkali metal. It has an atomic symbol Rb, atomic number 37, and atomic weight 85.47. It is used as a chemical reagent and in the manufacture of photoelectric cells. [NIH]
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Ruthenium: A hard, brittle, grayish-white rare earth metal with an atomic symbol Ru, atomic number 44, and atomic weight 101.07. It is used as a catalyst and hardener for platinum and palladium. [NIH] Salicylate: Non-steroidal anti-inflammatory drugs. [NIH] Salicylic: A tuberculosis drug. [NIH] Salicylic Acids: Derivatives and salts of salicylic acid. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Salvage Therapy: A therapeutic approach, involving chemotherapy, radiation therapy, or surgery, after initial regimens have failed to lead to improvement in a patient's condition. Salvage therapy is most often used for neoplastic diseases. [NIH] Samarium: An element of the rare earth family of metals. It has the atomic symbol Sm, atomic number 62, and atomic weight 150.36. The oxide is used in the control rods of some nuclear reactors. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Scalpel: A small pointed knife with a convex edge. [NIH] Scandium: Scandium. An element of the rare earth family of metals. It has the atomic symbol Sc, atomic number 21, and atomic weight 45. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to create pictures of areas inside the body. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Seafood: Marine fish and shellfish used as food or suitable for food. (Webster, 3d ed) shellfish and fish products are more specific types of seafood. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and
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cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Sediment: A precipitate, especially one that is formed spontaneously. [EU] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selective estrogen receptor modulator: SERM. A drug that acts like estrogen on some tissues, but blocks the effect of estrogen on other tissues. Tamoxifen and raloxifene are SERMs. [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] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sensitization: 1. Administration of antigen to induce a primary immune response; priming; immunization. 2. Exposure to allergen that results in the development of hypersensitivity. 3. The coating of erythrocytes with antibody so that they are subject to lysis by complement in the presence of homologous antigen, the first stage of a complement fixation test. [EU] Sequester: A portion of dead bone which has become detached from the healthy bone tissue, as occurs in necrosis. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] 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] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] 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] Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [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] Sister Chromatid Exchange: An exchange of segments between the sister chromatids of a chromosome, either between the sister chromatids of a meiotic tetrad or between the sister chromatids of a duplicated somatic chromosome. Its frequency is increased by ultraviolet and ionizing radiation and other mutagenic agents and is particularly high in Bloom syndrome. [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] Skin Manifestations: Dermatologic disorders attendant upon non-dermatologic disease or injury. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Sludge: A clump of agglutinated red blood cells. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smoldering leukemia: Disease in which the bone marrow does not function normally. Also called preleukemia or myelodysplastic syndrome. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
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Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic cells: All the body cells except the reproductive (germ) cells. [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] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrometer: An apparatus for determining spectra; measures quantities such as wavelengths and relative amplitudes of components. [NIH] Spectrophotometry: The art or process of comparing photometrically the relative intensities of the light in different parts of the spectrum. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] 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
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ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spinous: Like a spine or thorn in shape; having spines. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Squamous: Scaly, or platelike. [EU] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cells: Flat cells that look like fish scales under a microscope. These cells cover internal and external surfaces of the body. [NIH] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Staphylococcus: A genus of gram-positive, facultatively anaerobic, coccoid bacteria. Its organisms occur singly, in pairs, and in tetrads and characteristically divide in more than one plane to form irregular clusters. Natural populations of Staphylococcus are membranes of warm-blooded animals. Some species are opportunistic pathogens of humans and animals. [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] Stereotactic: Radiotherapy that treats brain tumors by using a special frame affixed directly to the patient's cranium. By aiming the X-ray source with respect to the rigid frame, technicians can position the beam extremely precisely during each treatment. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on
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muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Strained: A stretched condition of a ligament. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Strontium: An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subiculum: A region of the hippocampus that projects to other areas of the brain. [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] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Sudden death: Cardiac arrest caused by an irregular heartbeat. The term "death" is somewhat misleading, because some patients survive. [NIH] Sulfates: Inorganic salts of sulfuric acid. [NIH] Sulfides: Chemical groups containing the covalent sulfur bonds -S-. The sulfur atom can be bound to inorganic or organic moieties. [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] Sulfur Compounds: Inorganic or organic compounds that contain sulfur as an integral part
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of the molecule. [NIH] Sulfur Dioxide: A highly toxic, colorless, nonflammable gas. It is used as a pharmaceutical aid and antioxidant. It is also an environmental air pollutant. [NIH] Sulfuric acid: A strong acid that, when concentrated is extemely corrosive to the skin and mucous membranes. It is used in making fertilizers, dyes, electroplating, and industrial explosives. [NIH] Sunburn: An injury to the skin causing erythema, tenderness, and sometimes blistering and resulting from excessive exposure to the sun. The reaction is produced by the ultraviolet radiation in sunlight. [NIH] Superoxide: Derivative of molecular oxygen that can damage cells. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Surface Plasmon Resonance: A biosensing technique in which biomolecules capable of binding to specific analytes or ligands are first immobilized on one side of a metallic film. Light is then focused on the opposite side of the film to excite the surface plasmons, that is, the oscillations of free electrons propagating along the film's surface. The refractive index of light reflecting off this surface is measured. When the immobilized biomolecules are bound by their ligands, an alteration in surface plasmons on the opposite side of the film is created which is directly proportional to the change in bound, or adsorbed, mass. Binding is measured by changes in the refractive index. The technique is used to study biomolecular interactions, such as antigen-antibody binding. [NIH] Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] 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] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] 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] Tachypnea: Rapid breathing. [NIH]
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Tacrine: A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders. [NIH] Tamoxifen: A first generation selective estrogen receptor modulator (SERM). It acts as an agonist for bone tissue and cholesterol metabolism but is an estrogen antagonist in mammary and uterine. [NIH] Technetium: The first artificially produced element and a radioactive fission product of uranium. The stablest isotope has a mass number 99 and is used diagnostically as a radioactive imaging agent. Technetium has the atomic symbol Tc, atomic number 43, and atomic weight 98.91. [NIH] Teichoic Acids: Bacterial polysaccharides that are rich in phosphodiester linkages. They are the major components of the cell walls and membranes of many bacteria. [NIH] Tellurium: Tellurium. An element that is a member of the chalcogen family. It has the atomic symbol Te, atomic number 52, and atomic weight 127.60. It has been used as a coloring agent and in the manufacture of electrical equipment. Exposure may cause nausea, vomiting, and CNS depression. [NIH] Telomerase: Essential ribonucleoprotein reverse transcriptase that adds telomeric DNA to the ends of eukaryotic chromosomes. Telomerase appears to be repressed in normal human somatic tissues but reactivated in cancer, and thus may be necessary for malignant transformation. EC 2.7.7.-. [NIH] Telophase: The final phase of cell division, in which two daughter nuclei are formed, the cytoplasm divides, and the chromosomes lose their distinctness and are transformed into chromatin networks. [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] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Terbium: Terbium. An element of the rare earth family of metals. It has the atomic symbol Tb, atomic number 65, and atomic weight 158.92. [NIH] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetradecanoylphorbol Acetate: A phorbol ester found in croton oil with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA. [NIH] Thalidomide: A pharmaceutical agent originally introduced as a non-barbiturate hypnotic, but withdrawn from the market because of its known tetratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor alpha from monocytes, and modulates other cytokine action. [NIH] Theophylline: Alkaloid obtained from Thea sinensis (tea) and others. It stimulates the heart and central nervous system, dilates bronchi and blood vessels, and causes diuresis. The drug is used mainly in bronchial asthma and for myocardial stimulation. Among its more prominent cellular effects are inhibition of cyclic nucleotide phosphodiesterases and antagonism of adenosine receptors. [NIH]
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Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thiamine: 3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2methylthiazolium chloride. [NIH]
hydroxyethyl)-4-
Thioredoxin: A hydrogen-carrying protein that participates in a variety of biochemical reactions including ribonucleotide reduction. Thioredoxin is oxidized from a dithiol to a disulfide during ribonucleotide reduction. The disulfide form is then reduced by NADPH in a reaction catalyzed by thioredoxin reductase. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] 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, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thulium: An element of the rare earth family of metals. It has the atomic symbol Tm, atomic number 69, and atomic weight 168.93. [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] Tilapia: A freshwater fish used as an experimental organism and for food. This genus of the family Cichlidae inhabits Central and South America (one species extends north into Texas), West Indies, Africa, Madagascar, Syria, and coastal India. [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] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tobacco Mosaic Virus: The type species of tobamovirus which causes mosaic disease of tobacco. Transmission occurs by mechanical inoculation. [NIH]
Dictionary 351
Tobamovirus: A genus of plant viruses in which the virion is a rigid filament. Transmission is by mechanical inoculation or seed. The type species is tobacco mosaic virus. [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] Topical: On the surface of the body. [NIH] Topical chemotherapy: Treatment with anticancer drugs in a lotion or cream applied to the skin. [NIH] Torsion: A twisting or rotation of a bodily part or member on its axis. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [NIH] Toxicologic: Pertaining to toxicology. [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] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transferases: Transferases are enzymes transferring a group, for example, the methyl group or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2. [NIH] Transitional cell carcinoma: A type of cancer that develops in the lining of the bladder, ureter, or renal pelvis. [NIH]
352 Arsenic
Translating: Conversion from one language to another language. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Tretinoin: An important regulator of gene expression, particularly during growth and development and in neoplasms. Retinoic acid derived from maternal vitamin A is essential for normal gene expression during embryonic development and either a deficiency or an excess can be teratogenic. It is also a topical dermatologic agent which is used in the treatment of psoriasis, acne vulgaris, and several other skin diseases. It has also been approved for use in promyelocytic leukemia. [NIH] Trisomy: The possession of a third chromosome of any one type in an otherwise diploid cell. [NIH]
Trivalent: Having a valence of three. [EU] Troglitazone: A drug used in diabetes treatment that is being studied for its effect on reducing the risk of cancer cell growth in fat tissue. [NIH] Trophic: Of or pertaining to nutrition. [EU] Tropomyosin: A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by troponin. [NIH] Troponin: One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments. [NIH] Truncal: The bilateral dissection of the abdominal branches of the vagus nerve. [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] Tuberculostatic: Inhibiting the growth of Mycobacterium tuberculosis. [EU] 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] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs
Dictionary 353
from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumor suppressor gene: Genes in the body that can suppress or block the development of cancer. [NIH] Tumorigenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH]
Tungsten: A metallic element with the atomic symbol W, atomic number 74, and atomic weight 183.85. It is used in many manufacturing applications, including increasing the hardness, toughness, and tensile strength of steel; manufacture of filaments for incandescent light bulbs; and in contact points for automotive and electrical apparatus. [NIH] Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ubiquitin: A highly conserved 76 amino acid-protein found in all eukaryotic cells. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Unresectable: Unable to be surgically removed. [NIH] Uranium: A radioactive element of the actinide series of metals. It has an atomic symbol U, atomic number 92, and atomic weight 238.03. U-235 is used as the fissionable fuel in nuclear weapons and as fuel in nuclear power reactors. [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] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureter: One of a pair of thick-walled tubes that transports urine from the kidney pelvis 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] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] 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] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic
354 Arsenic
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] Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. [NIH]
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] Vasodilation: Physiological dilation of the blood vessels without anatomic change. For dilation with anatomic change, dilatation, pathologic or aneurysm (or specific aneurysm) is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Vinblastine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. It is a mitotic inhibitor. [NIH] Vincristine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. [NIH] Vinyl Chloride: A gas that has been used as an aerosol propellant and is the starting material for polyvinyl resins. Toxicity studies have shown various adverse effects, particularly the occurrence of liver neoplasms. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some
Dictionary 355
viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Vulgaris: An affection of the skin, especially of the face, the back and the chest, due to chronic inflammation of the sebaceous glands and the hair follicles. [NIH] Wart: A raised growth on the surface of the skin or other organ. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] 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] Ytterbium: Ytterbium. An element of the rare earth family of metals. It has the atomic symbol Yb, atomic number 70, and atomic weight 173. Ytterbium has been used in lasers and as a portable X-ray source. [NIH] Yttrium: An element of the rare earth family of metals. It has the atomic symbol Y, atomic number 39, and atomic weight 88.91. In conjunction with other rare earths, yttrium is used as a phosphor in television receivers and is a component of the yttrium-aluminum garnet (YAG) lasers. [NIH] Zinc Oxide: A mild astringent and topical protectant with some antiseptic action. It is also used in bandages, pastes, ointments, dental cements, and as a sunblock. [NIH] Zoonoses: Diseases of non-human animals that may be transmitted to man or may be transmitted from man to non-human animals. [NIH] Zygote: The fertilized ovum. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
357
INDEX A Abdomen, 275, 287, 303, 317, 319, 329, 346, 347, 354, 355 Abdominal, 134, 275, 276, 308, 329, 352 Aberrant, 60, 65, 275 Acatalasia, 275, 289 Acceptor, 191, 275, 319, 328, 351 Acetaminophen, 240, 275 Acetylcholine, 275, 327 Acne, 275, 352 Acne Vulgaris, 275, 352 Acrylonitrile, 157, 199, 275, 341 Actin, 40, 41, 275, 352 Actinic keratosis, 241, 275 Actinium, 207, 208, 275 Acute leukemia, 4, 103, 223, 275, 334 Acute lymphoblastic leukemia, 4, 151, 275 Acute lymphocytic leukemia, 275 Acute myelogenous leukemia, 276 Acute myeloid leukemia, 11, 21, 148, 150, 276, 335 Acute nonlymphocytic leukemia, 276 Adaptability, 276, 289, 290 Adaptation, 276, 291, 324 Adenocarcinoma, 146, 148, 152, 276, 312 Adenoma, 276, 303 Adenosine, 276, 278, 332, 349 Adhesives, 275, 276, 286 Adipocytes, 35, 276 Adjustment, 176, 276 Adolescence, 102, 276 Adrenergic, 114, 276, 281, 300, 303, 338 Adsorption, 120, 141, 195, 204, 224, 226, 276 Adsorptive, 276 Adverse Effect, 18, 32, 55, 87, 222, 276, 301, 344, 354 Aerobic, 226, 276, 277, 323, 329 Aerobic Metabolism, 276, 277, 329 Aerobic Respiration, 276, 277, 329 Aerosol, 277, 354 Affinity, 16, 24, 30, 42, 56, 59, 165, 277, 319, 322, 345 Affinity Chromatography, 16, 277 Agar, 28, 277, 296, 314, 332 Agarose, 277, 312, 314 Age Groups, 7, 277 Age of Onset, 277, 353
Aged, 80 and Over, 277 Agonist, 277, 300, 349 Albumin, 277, 312 Aldehydes, 169, 187, 211, 221, 277 Algorithms, 277, 285 Alimentary, 277, 329, 330 Alkaline, 44, 98, 172, 201, 202, 219, 278, 283, 288, 329, 339, 347 Alkaloid, 278, 293, 311, 338, 349 Allergen, 278, 343 Allo, 278, 310 Allogeneic, 89, 96, 278 Allogeneic bone marrow transplantation, 89, 278 Allylamine, 278 Alopecia, 156, 278, 297 Alpha Particles, 278, 338 Alpha-helices, 55, 278 Alternative medicine, 249, 278 Amine, 169, 170, 171, 278, 312 Amino Acid Sequence, 278, 280, 308 Amino Acids, 278, 288, 304, 308, 322, 330, 333, 336, 341, 343, 347, 352, 353 Amiodarone, 240, 278 Ammonia, 157, 170, 181, 278, 353 Ampulla, 278, 291 Amyloid, 41, 279 Anaerobic, 226, 279, 346 Anaesthesia, 279, 315 Anal, 22, 33, 110, 112, 113, 128, 131, 279, 303, 306 Analgesic, 275, 279, 318, 338 Analog, 199, 200, 279, 307 Analogous, 192, 279, 301, 351 Analytes, 196, 279, 348 Anaphase, 8, 279 Anaphylatoxins, 279, 294 Anatomical, 9, 279, 299, 315 Anemia, 240, 279, 287, 293, 307, 324 Anergy, 21, 279 Aneuploidy, 8, 279 Aneurysm, 279, 354 Angina, 279, 280, 330 Angiogenesis, 37, 50, 132, 156, 279 Angiogenesis inhibitor, 132, 279 Angiosarcoma, 5, 279 Animal model, 7, 18, 21, 47, 52, 62, 97, 279 Anionic, 124, 186, 280
358 Arsenic
Anions, 120, 141, 208, 277, 280, 317 Anisomycin, 20, 280 Annealing, 166, 176, 188, 204, 205, 215, 216, 217, 280 Anode, 220, 280 Anomalies, 37, 280, 349 Antagonism, 84, 129, 280, 349 Anthracycline, 280, 298, 314 Anthropogenic, 192, 280 Antianginal, 278, 280 Antiarrhythmic, 278, 280 Antibacterial, 280, 300, 317, 345 Antibiotic, 126, 280, 298, 300, 304, 314, 330, 345 Antibodies, 29, 280, 311, 314, 320, 324, 332, 338 Antibody, 24, 25, 29, 36, 277, 280, 293, 311, 313, 314, 315, 321, 324, 338, 339, 343, 345, 348 Anticoagulant, 280, 336 Antidepressant, 280, 296 Antiemetic, 280, 281, 291 Antifungals, 240, 280 Antigen, 24, 25, 277, 280, 294, 313, 314, 315, 321, 343, 348 Antigen-Antibody Complex, 280, 294 Anti-infective, 281, 313, 317 Anti-inflammatory, 240, 275, 281, 299, 309, 342 Antimetabolite, 281, 307 Antimicrobial, 281, 292 Antineoplastic, 281, 297, 300, 307, 329 Antioxidant, 35, 281, 282, 328, 329, 348 Antipsychotic, 281, 291 Antipyretic, 275, 281, 338 Antiseptic, 281, 322, 355 Antiviral, 240, 281, 316 Anus, 279, 281, 287 Aperture, 175, 281 Applicability, 14, 48, 281 Arachidonate 12-Lipoxygenase, 282, 319 Arachidonate 15-Lipoxygenase, 282, 319 Arachidonate Lipoxygenases, 282, 319 Arachidonic Acid, 282, 301, 318, 335 Arginine, 279, 282, 327 Argon, 100, 282 Arnica, 130, 282 Aromatic, 9, 25, 38, 43, 48, 66, 182, 226, 282, 288, 322, 331 Arrhythmia, 127, 280, 282 Arsenicals, 16, 35, 36, 61, 71, 72, 95, 120, 150, 282
Arterial, 278, 282, 314, 336, 348 Arteries, 282, 283, 286, 296, 322, 350 Arterioles, 282, 286, 288, 354 Artifacts, 95, 113, 282 Ascorbic Acid, 10, 11, 76, 95, 111, 114, 282 Assay, 6, 16, 22, 49, 71, 104, 196, 282 Astringent, 282, 355 Astrocytoma, 283, 309 Atherogenic, 38, 283 Atmospheric Pressure, 158, 176, 283 Atrial, 278, 283 Atrophy, 283, 326 Attenuated, 283, 299 Atypical, 147, 283 Auditory, 103, 115, 283, 354 Autologous, 29, 283 Autonomic, 275, 281, 283, 327, 330 Autonomic Nervous System, 283, 331 B Babesiosis, 283, 338 Bacteremia, 108, 283 Bacteriophage, 283, 332, 351 Bacteriostatic, 283, 304 Bacterium, 60, 283, 295 Barbiturate, 283, 295, 349 Barium, 197, 207, 208, 220, 283 Basal cell carcinoma, 8, 43, 65, 92, 264, 284 Basal cells, 284 Basal Ganglia, 281, 284, 308, 309 Base, 160, 161, 168, 169, 176, 182, 209, 225, 284, 298, 307, 308, 317, 349 Base Sequence, 284, 307, 308 Benign, 276, 284, 303, 308, 325, 329, 339 Berylliosis, 284 Beryllium, 70, 207, 208, 226, 233, 284 Beta Rays, 284, 302 Beta-pleated, 279, 284 Bexarotene, 125, 284 Bilateral, 66, 284, 352 Bile, 13, 284, 291, 307, 319, 346 Bile Acids, 284, 346 Bile Acids and Salts, 284 Bile Ducts, 284 Biliary, 240, 284, 291 Binding Sites, 34, 54, 56, 284 Bioassay, 5, 120, 284 Bioavailability, 14, 27, 48, 284 Bioavailable, 14, 48, 285 Biochemical, 6, 10, 23, 40, 50, 58, 81, 82, 98, 129, 144, 240, 281, 285, 306, 308, 343, 350 Biochemical reactions, 285, 350 Biofilms, 48, 285
Index 359
Biological response modifier, 285, 316 Biological therapy, 285, 311 Biological Transport, 285, 299 Biomarkers, 19, 28, 31, 36, 51, 57, 95, 100, 127, 285 Biomedical Engineering, 5, 285 Biomolecular, 285, 348 Biopsy, 285, 304 Biosynthesis, 42, 156, 282, 285, 343 Biotechnology, 59, 61, 128, 225, 238, 249, 257, 285 Biotransformation, 78, 88, 110, 112, 285 Biphasic, 20, 285 Bismuth, 60, 112, 129, 186, 193, 197, 201, 202, 207, 208, 220, 224, 225, 235, 236, 237, 286 Bivalent, 203, 286, 322 Bladder, 6, 7, 9, 20, 21, 36, 38, 42, 50, 51, 55, 57, 71, 123, 150, 246, 247, 286, 336, 340, 351, 353 Blast Crisis, 4, 286 Blast phase, 286, 292 Blasts, 4, 11, 286 Blood Coagulation, 286, 288, 350 Blood Glucose, 286, 311, 314, 316 Blood pressure, 286, 288, 314, 324, 331, 345 Blood vessel, 34, 156, 279, 286, 288, 290, 303, 305, 309, 319, 320, 331, 332, 344, 345, 347, 349, 350, 354 Blood-Brain Barrier, 286, 318, 349 Body Burden, 286, 318 Body Fluids, 285, 286, 287, 301, 345, 352 Bone Cements, 286, 333 Bone Marrow Cells, 156, 286, 321 Bone Marrow Transplantation, 286 Bone scan, 286, 342 Boron Neutron Capture Therapy, 286, 287 Bowel, 105, 279, 287, 299, 317, 318 Bowel Movement, 287, 299 Brachytherapy, 287, 316, 338, 339 Bradykinin, 287, 327 Brain Stem, 287, 295 Branch, 271, 287, 302, 320, 330, 337, 345, 350 Breakdown, 158, 164, 208, 216, 287, 299, 308 Breeding, 7, 287 Bromine, 163, 175, 208, 287 Bronchi, 287, 303, 349, 351 Bronchial, 36, 287, 312, 349 Buccal, 71, 287, 313 Burns, 240, 287, 313
Burns, Electric, 287 Bypass, 129, 287 C Cacodylic Acid, 238, 287 Cadaver, 39, 287 Cadmium Compounds, 287 Cadmium Poisoning, 17, 287 Calcium, 42, 50, 55, 170, 197, 201, 202, 207, 208, 240, 286, 287, 288, 294, 318, 344, 352 Calcium channel blocker, 240, 288 Calcium Channel Blockers, 240, 288 Callus, 288, 317 Capillary, 54, 287, 288, 354 Capsules, 288, 306, 308 Carbohydrates, 276, 277, 288, 289, 329 Carbon Dioxide, 288, 306, 308, 332, 341 Carboxy, 288 Carboxylic Acids, 196, 197, 288 Carcinogen, 8, 14, 15, 36, 39, 50, 78, 84, 156, 195, 288, 324 Carcinogenesis, 5, 8, 15, 21, 36, 39, 43, 49, 62, 77, 78, 89, 93, 97, 112, 113, 142, 288 Carcinogenic, 5, 8, 13, 15, 22, 25, 27, 36, 38, 43, 67, 170, 190, 288, 299, 316, 328, 335, 346, 353 Carcinoma, 42, 69, 72, 74, 90, 95, 110, 122, 288, 304 Cardiac, 55, 127, 247, 248, 278, 280, 288, 292, 302, 303, 304, 314, 325, 338, 346, 347 Cardiovascular, 6, 34, 38, 74, 100, 114, 240, 288, 318, 343 Cardiovascular disease, 6, 34, 38, 74, 240, 288 Cardiovascular System, 100, 114, 288 Carotene, 86, 288 Case report, 12, 66, 85, 288 Caspase, 12, 45, 96, 289 Catabolism, 94, 113, 289 Catalase, 10, 275, 289 Cathepsins, 25, 289 Cathode, 193, 280, 284, 289, 302, 304 Cations, 289, 317 Causal, 23, 57, 289, 303, 321 Causality, 32, 289 Cause of Death, 289, 298 CDC2, 8, 289 Cell Cycle, 101, 150, 289, 292, 297, 337 Cell Death, 12, 34, 45, 82, 281, 282, 289, 325 Cell Differentiation, 65, 289, 344 Cell Division, 279, 283, 289, 290, 310, 321, 322, 323, 332, 335, 343, 349 Cell Extracts, 112, 289
360 Arsenic
Cell membrane, 285, 288, 289, 298 Cell motility, 46, 289 Cell Physiology, 37, 41, 289 Cell proliferation, 9, 34, 45, 49, 71, 289, 344 Cell Respiration, 277, 290, 323, 329, 341 Cell Size, 290, 306 Cell Survival, 290, 310 Cell Transplantation, 290 Cellulose, 288, 290, 307, 332 Central Nervous System, 81, 275, 283, 290, 308, 309, 310, 318, 331, 343, 349 Centromere, 45, 290 Ceramide, 41, 290 Cerebral, 284, 286, 287, 290, 295, 303, 304, 309 Cerebral hemispheres, 284, 287, 290, 309 Cerebrovascular, 288, 290 Cerium, 197, 199, 201, 202, 207, 208, 219, 290 Cervical, 21, 72, 74, 93, 122, 152, 290 Cervix, 290 Cesium, 157, 196, 197, 207, 208, 220, 290 Chelating Agents, 28, 290 Chelation, 122, 136, 290 Chemical Warfare, 290, 291, 298 Chemical Warfare Agents, 291, 298 Chemotactic Factors, 291, 294 Chimera, 89, 291 Chlorine, 55, 175, 202, 208, 225, 291 Chlorine Compounds, 55, 291 Chlorophyll, 290, 291, 307 Chlorpromazine, 240, 291 Chlorpyrifos, 18, 291 Cholangitis, 240, 291 Cholestasis, 240, 291 Cholesterol, 19, 284, 291, 296, 319, 346, 349 Chromatin, 6, 30, 64, 281, 291, 349 Chromosomal, 8, 26, 59, 61, 67, 111, 279, 291, 308, 323, 332 Chromosome, 5, 43, 45, 146, 151, 279, 290, 291, 295, 311, 323, 324, 343, 344, 352 Chronic Disease, 291, 318 Chronic granulocytic leukemia, 291, 292 Chronic leukemia, 223, 291 Chronic lymphocytic leukemia, 21, 292 Chronic myelogenous leukemia, 82, 146, 151, 286, 291, 292 Chronic phase, 146, 292 Chronic phase chronic myelogenous leukemia, 146, 292 Cicatrix, 241, 292 Cimetidine, 240, 292
Cinchona, 292, 338 Ciprofloxacin, 240, 292 CIS, 186, 292 Cisplatin, 16, 51, 156, 292 Citrus, 282, 292 Clear cell carcinoma, 292, 298 Clinical Medicine, 292, 334 Clinical trial, 4, 10, 11, 19, 46, 52, 53, 145, 150, 152, 257, 292, 295, 297, 324, 337, 339 Clone, 4, 292 Clonic, 292, 295 Cloning, 285, 292, 319 Clot Retraction, 293, 332 Coagulation, 226, 234, 235, 286, 293, 350 Coal, 74, 89, 158, 293 Cobalt, 157, 169, 170, 184, 187, 196, 197, 199, 201, 206, 207, 208, 225, 233, 237, 293 Coenzyme, 282, 293 Cofactor, 293, 326, 336, 350 Cohort Studies, 293, 303 Coke, 15, 293 Colchicine, 293, 352 Collagen, 276, 293, 306, 308, 333 Collapse, 287, 293 Colloidal, 213, 277, 293, 302 Colorectal, 50, 293 Colorectal Cancer, 50, 293 Complement, 42, 279, 293, 294, 343 Complementary and alternative medicine, 119, 137, 294 Complementary medicine, 119, 294 Complete remission, 4, 10, 294, 340 Complete response, 103, 115, 294 Computational Biology, 257, 294 Computed tomography, 294, 342 Computerized axial tomography, 294, 342 Conception, 294, 305, 334, 346 Concomitant, 44, 294 Conduction, 191, 295 Confounding, 7, 51, 91, 295 Confusion, 295, 353 Congenita, 295, 338 Conjugated, 284, 295, 297, 312 Conjugation, 10, 13, 285, 295 Connective Tissue, 282, 286, 293, 295, 306, 308, 320, 347 Consolidation, 29, 295 Contact dermatitis, 92, 295 Contraindications, ii, 295 Convulsants, 240, 295 Convulsions, 283, 295 Cooperative group, 53, 295
Index 361
Coordination, 26, 56, 58, 61, 142, 290, 295 Corneum, 295, 303 Coronary, 38, 288, 296, 322, 330 Coronary heart disease, 288, 296 Coronary Thrombosis, 296, 322 Cortex, 45, 296, 303, 304, 335 Cortical, 45, 296, 343 Corticosteroids, 296, 309 Cortisone, 296, 299 Cotinine, 31, 296 Cranial, 7, 296, 326, 331, 353 Crossing-over, 296, 340 Cross-Sectional Studies, 296, 303 Croton Oil, 296, 349 Cruciferous vegetables, 50, 296 Cryosurgery, 242, 296 Crystallization, 55, 296 Culture Media, 277, 296 Cultured cells, 19, 35, 49, 296 Curative, 30, 296, 326, 350 Curettage, 242, 296 Curette, 296, 297 Cutaneous, 9, 100, 124, 132, 241, 295, 297 Cyclic, 186, 297, 311, 327, 336, 349 Cyclin, 8, 13, 297 Cyclophosphamide, 156, 297 Cyclosporine, 240, 297 Cysteine, 13, 30, 120, 140, 297, 302, 347 Cystine, 297 Cytarabine, 11, 150, 151, 297 Cytochrome, 19, 292, 297 Cytokine, 25, 52, 71, 297, 349 Cytoplasm, 281, 289, 297, 305, 310, 322, 324, 335, 341, 349 Cytoskeleton, 297, 323 Cytotoxic, 16, 126, 130, 240, 297, 338, 339, 344 Cytotoxicity, 16, 69, 110, 122, 129, 156, 278, 292, 297 Cytotoxins, 35, 297 D Databases, Bibliographic, 257, 297 Daunorubicin, 150, 151, 298, 300 De novo, 26, 56, 298 Death Certificates, 18, 298 Decontamination, 203, 298 Degenerative, 298, 312 Deletion, 16, 39, 45, 281, 298 Dendrites, 298, 326 Dendritic, 298, 321, 345 Density, 21, 30, 47, 162, 178, 222, 229, 230, 298, 306, 319, 328, 345
Dental Caries, 298, 307 Dentate Gyrus, 298, 312 Dentists, 88, 298 Depigmentation, 16, 298, 355 Depolarization, 298, 344 Depressive Disorder, 298, 319 Depsipeptide, 29, 298 Dermatitis, 69, 92, 298 DES, 204, 279, 298 Detoxification, 13, 14, 39, 44, 56, 59, 60, 66, 109, 110, 298 Deuterium, 298, 313 Dexamethasone, 145, 299 Diabetes Mellitus, 3, 35, 299, 309, 311 Diagnosis, Differential, 241, 299 Diagnostic procedure, 155, 249, 299 Dialyzer, 299, 311 Diarrhoea, 299, 308, 313 Diastolic, 299, 314 Diathermy, 299, 323 Diazinon, 18, 299 Digestion, 124, 277, 284, 287, 299, 317, 319, 347 Digestive system, 153, 299 Digestive tract, 299, 344, 346 Dihydrotestosterone, 299, 340 Dihydroxy, 299, 304 Dilatation, 240, 279, 299, 354 Dilatation, Pathologic, 299, 354 Dilation, 287, 299, 354 Dilution, 16, 33, 61, 95, 238, 299 Dimethylnitrosamine, 49, 299 Dioxins, 3, 299 Diploid, 8, 279, 299, 324, 332, 352 Direct, iii, 6, 10, 44, 144, 156, 160, 191, 251, 292, 300, 311, 336, 338, 340, 348 Disease-Free Survival, 11, 300 Disinfectant, 300, 304, 322, 330 Disinfection, 213, 300 Dissection, 300, 352 Dissociation, 277, 300, 317 Distal, 300, 302, 317, 331, 337 Diuresis, 300, 349 Dopa, 240, 300, 318 Dopamine, 281, 291, 300, 318, 331 Doping, 140, 158, 160, 166, 169, 176, 181, 188, 190, 216, 222, 223, 300 Dorsal, 300, 326, 333, 345 Dose-dependent, 44, 110, 150, 300 Dosimetry, 5, 300 Doxorubicin, 12, 300 Drive, ii, vi, 10, 107, 110, 112, 201, 215, 300
362 Arsenic
Drug Design, 248, 301 Drug Interactions, 252, 301 Drug Resistance, 52, 55, 64, 301 Drug Tolerance, 301, 351 Drug Toxicity, 51, 301 Duct, 278, 291, 301, 305, 329, 342 Duodenum, 284, 301, 347 Dyes, 279, 301, 306, 326, 348 Dysprosium, 207, 208, 220, 301 Dystrophin, 301, 324 E Ecosystem, 55, 301 Ectoderm, 301, 326 Edema, 295, 301, 324, 326 Effector, 275, 293, 301 Efficacy, 5, 10, 47, 126, 156, 301 Eicosanoids, 38, 301 Electrocoagulation, 293, 302 Electrode, 158, 167, 173, 174, 179, 188, 200, 203, 205, 216, 220, 222, 227, 228, 280, 289, 302 Electrodesiccation, 242, 302 Electrolysis, 203, 280, 289, 302 Electrolyte, 179, 180, 193, 302, 334, 345 Electrons, 217, 281, 284, 289, 302, 317, 328, 338, 339, 348 Electrophoresis, 54, 71, 302, 314 Electrophysiological, 132, 302 Electroplating, 302, 348 Elementary Particles, 302, 326, 337 Embolus, 302, 315 Embryo, 7, 37, 54, 289, 301, 302, 315 Emulsions, 277, 302 Encapsulated, 302, 319 Encephalopathy, 240, 302, 322 Endemic, 35, 72, 82, 302, 346 Endopeptidases, 289, 302 Endoscopy, 98, 303 Endothelial cell, 37, 38, 286, 303, 350 Endothelium, 303, 327, 333 Endothelium-derived, 303, 327 Endotoxin, 303, 352 Enhancer, 303, 341 Entorhinal Cortex, 303, 312 Environmental Exposure, 18, 20, 35, 39, 41, 43, 55, 57, 90, 303, 328 Environmental Pollutants, 17, 32, 40, 303, 333 Enzymatic, 36, 126, 142, 288, 294, 298, 303, 312 Enzyme Inhibitors, 35, 38, 303 Epidemiologic Studies, 55, 58, 235, 303
Epidemiological, 29, 35, 38, 39, 57, 303 Epidermal, 9, 71, 303, 317, 321 Epidermis, 9, 284, 295, 303, 313, 314, 317, 335 Epidermoid carcinoma, 303, 346 Epigastric, 303, 329 Epinephrine, 276, 300, 303, 327, 353 Epithelial, 9, 36, 68, 71, 104, 122, 241, 276, 285, 303, 304, 329 Epithelial Cells, 68, 71, 104, 122, 303, 304 Epithelioma, 241, 303 Epithelium, 303, 304, 329 Erbium, 202, 207, 208, 220, 304 Erythema, 295, 304, 348 Erythrocytes, 25, 279, 283, 286, 304, 340, 343 Erythromycin, 240, 304 Esophageal, 90, 146, 304 Esophagus, 146, 299, 304, 347 Estrogen, 77, 304, 343, 349 Estrogen receptor, 77, 304 Ethanol, 304, 305 Ether, 180, 304 Ethylene Glycol, 183, 304 Eukaryotic Cells, 289, 304, 328, 353 Europium, 202, 207, 208, 220, 304 Evoke, 304, 347 Excimer laser, 163, 304 Excisional, 242, 304 Excitability, 304, 338 Excitation, 141, 161, 305, 306 Exhaustion, 280, 305 Exocrine, 305, 329 Exogenous, 276, 285, 305, 353 Exons, 26, 305 Expiration, 305, 341 Extensor, 305, 337, 355 External-beam radiation, 305, 338 Extracellular, 279, 285, 295, 305, 306, 345 Extracellular Matrix, 295, 305, 306 Extracorporeal, 241, 305, 312 Extraction, 48, 104, 112, 114, 127, 128, 131, 133, 223, 224, 225, 305 Exudate, 48, 305 F Family Planning, 257, 305 Fat, 276, 282, 284, 286, 288, 290, 296, 302, 305, 319, 333, 345, 352 Fatigue, 108, 305 Fatty acids, 277, 288, 301, 305, 319, 335, 350 Femur, 71, 305
Index 363
Fermentation, 225, 305 Ferritin, 95, 305 Fertilizers, 305, 326, 348 Fetus, 55, 305, 332, 334, 335, 353 Fibrin, 286, 293, 305, 332, 350 Fibroblasts, 8, 94, 306 Fibrosis, 123, 240, 278, 306 Filler, 195, 208, 306 Filtration, 202, 224, 225, 235, 306 Fish Products, 306, 342 Fistula, 306, 328 Fixation, 306, 343 Flatus, 306, 308 Flow Cytometry, 25, 306 Fluorescence, 54, 131, 210, 306 Fluorescent Dyes, 306 Fluoridation, 47, 306 Fluorine, 139, 175, 202, 208, 212, 306, 307 Fluorouracil, 156, 307 Folate, 7, 144, 307 Fold, 47, 56, 150, 307 Folic Acid, 50, 307 Fractionation, 179, 307 Frameshift, 44, 307 Frameshift Mutation, 44, 307 Freeze-dried, 127, 307 Friction, 241, 307 Fungi, 280, 295, 307, 310, 322, 323, 355 Fungus, 114, 307 G Gadolinium, 207, 208, 220, 307 Gallbladder, 275, 284, 299, 307 Gamma Rays, 307, 325, 338, 339 Ganglia, 275, 308, 326, 331 Ganglion, 308, 326 Gas, 158, 159, 163, 169, 171, 179, 180, 184, 212, 214, 225, 278, 282, 288, 291, 299, 306, 307, 308, 313, 324, 327, 339, 341, 347, 348, 354 Gas exchange, 308, 341 Gastric, 93, 98, 129, 292, 308, 312, 330, 339 Gastric Acid, 292, 308 Gastrin, 292, 308, 313 Gastroenteritis, 287, 308 Gastrointestinal, 287, 292, 303, 304, 308, 318, 339, 343, 347, 352 Gelatin, 296, 308, 310, 350 Gemcitabine, 148, 308 Gene, 4, 6, 7, 11, 13, 16, 21, 22, 23, 24, 26, 28, 34, 37, 41, 43, 44, 52, 54, 60, 69, 72, 73, 78, 94, 97, 122, 123, 127, 140, 150,
238, 245, 285, 301, 308, 319, 327, 328, 329, 341, 343, 352 Gene Expression, 7, 11, 16, 21, 23, 26, 43, 60, 69, 73, 78, 94, 97, 122, 123, 140, 245, 308, 352 Gene Pool, 28, 308 Generator, 158, 160, 210, 237, 308 Genetic Code, 308, 327 Genetic Techniques, 6, 308 Genetics, 13, 16, 295, 308 Genital, 241, 292, 309, 353 Genitourinary, 108, 121, 309, 353 Genotype, 7, 23, 309, 331 Germ Cells, 309, 321, 328, 345, 349 Germinal Center, 24, 309 Gland, 296, 309, 320, 329, 336, 342, 343, 347, 350 Glioblastoma, 47, 152, 309 Glioblastoma multiforme, 152, 309 Glioma, 82, 152, 309 Glomerular, 41, 309, 340 Glomerulus, 309, 317, 325 Glucocorticoid, 6, 299, 309 Glucose, 35, 240, 282, 286, 290, 291, 299, 309, 311, 316, 339, 342 Glucose Intolerance, 240, 299, 309 Glucose tolerance, 309 Glucose Tolerance Test, 309 Glutamate, 310, 331 Glutamic Acid, 307, 310 Glutathione Peroxidase, 10, 310, 343 Glycine, 284, 310, 343 Glycoprotein, 55, 94, 310, 350, 352 Gonad, 310 Gonadal, 20, 310, 346 Governing Board, 310, 334 Government Agencies, 17, 310, 334 Grade, 223, 309, 310 Grading, 80, 161, 310 Graft, 310, 313 Grafting, 310, 315 Gram-negative, 33, 59, 310 Gram-Negative Bacteria, 33, 59, 310 Gram-positive, 33, 310, 346 Granulocytes, 310, 318, 325, 344, 355 Graphite, 73, 203, 310 Grasses, 307, 310 Growth factors, 11, 38, 52, 310 Guanylate Cyclase, 311, 327 Gynecologic oncologist, 46, 311 H Hair follicles, 311, 355
364 Arsenic
Half-Life, 311, 333 Haloperidol, 240, 311 Haploid, 311, 332 Haptens, 277, 311 Harmine, 18, 311 Hazardous Substances, 27, 55, 70, 73, 76, 79, 85, 91, 100, 119, 123, 311 Hazardous Waste, 49, 311 Heart attack, 288, 311 Heartbeat, 311, 347 Hematologic malignancies, 29, 103, 108, 115, 311 Hematology, 46, 82, 103, 111, 115, 311 Hematopoietic growth factors, 11, 311 Heme, 81, 297, 311, 329 Hemodialysis, 131, 299, 311 Hemoglobin, 279, 290, 304, 311, 312, 318 Hemoglobin A, 290, 312 Hemoperfusion, 131, 312 Hemorrhage, 302, 312, 347 Hepatic, 5, 35, 49, 80, 240, 277, 309, 312 Hepatitis, 240, 312, 330 Hepatocellular, 125, 147, 240, 312 Hepatocellular carcinoma, 125, 147, 240, 312 Hepatocyte, 6, 291, 312 Hepatoma, 101, 312 Herbicide, 287, 312 Hereditary, 312, 326, 331 Heredity, 275, 308, 309, 312 Heterodimers, 46, 312 Heterogeneity, 14, 80, 277, 312 Hiccup, 291, 312 Hippocampus, 45, 298, 312, 347 Histamine, 279, 281, 292, 312, 314, 339 Histology, 241, 312 Histone Deacetylase, 29, 312 Holmium, 220, 312 Homeopathic remedies, 312, 321 Homeostasis, 42, 58, 312 Homogeneous, 187, 313 Homologous, 34, 45, 286, 296, 313, 338, 343, 348 Hormonal, 50, 283, 313 Hormone, 6, 18, 50, 149, 278, 284, 296, 298, 302, 303, 308, 313, 316, 317, 335, 344, 349, 350 Hormone therapy, 149, 313 Horny layer, 303, 313 Host, 23, 37, 43, 283, 313, 314, 318, 354 Human Activities, 38, 313 Human Development, 7, 256, 313
Human papillomavirus, 72, 130, 241, 313 Hybrid, 292, 313 Hybridization, 26, 313 Hydrocarbons, Aromatic, 226, 313 Hydrofluoric Acid, 313, 344 Hydrogen, 10, 169, 170, 175, 179, 181, 186, 188, 207, 208, 211, 213, 216, 221, 275, 278, 284, 288, 289, 298, 310, 313, 319, 324, 326, 327, 328, 337, 350 Hydrogen Peroxide, 10, 186, 213, 289, 310, 313, 319 Hydrolysis, 34, 285, 292, 313, 331, 333, 337 Hydrophobic, 47, 313, 319 Hydroxides, 141, 195, 225, 313 Hyperkeratosis, 9, 72, 130, 313 Hyperpigmentation, 9, 314 Hypersensitivity, 69, 278, 314, 318, 343 Hypersensitivity, Immediate, 314 Hypertension, 40, 81, 123, 288, 314 Hyperthermia, 240, 299, 314 Hypnotic, 283, 314, 349 Hypoglycemic, 240, 314 Hypoglycemic Agents, 240, 314 Hypothermia, 240, 314 I Id, 116, 133, 264, 270, 272, 314 Idarubicin, 11, 29, 314 Idiopathic, 123, 314 Imidazole, 183, 312, 314, 339 Immune response, 279, 280, 296, 311, 314, 315, 343, 347, 355 Immune system, 25, 285, 312, 314, 315, 318, 320, 331, 353, 355 Immunity, 297, 314 Immunization, 314, 343 Immunodeficiency, 47, 314 Immunodiffusion, 277, 314 Immunoelectrophoresis, 277, 314 Immunofluorescence, 25, 315 Immunoglobulin, 280, 305, 315, 324 Immunologic, 291, 314, 315, 339 Immunology, 9, 24, 32, 73, 109, 111, 277, 306, 315 Immunosuppressant, 307, 315 Immunosuppressive, 32, 297, 309, 315 Impairment, 168, 240, 291, 315, 322 Implant radiation, 315, 316, 338 In situ, 9, 48, 170, 186, 241, 315 In vitro, 4, 9, 10, 12, 25, 26, 29, 36, 37, 40, 41, 45, 49, 51, 52, 74, 82, 112, 122, 128, 129, 315, 350
Index 365
In vivo, 5, 11, 12, 13, 19, 26, 34, 37, 40, 41, 45, 47, 49, 51, 52, 74, 129, 130, 315, 328, 350 Incision, 31, 315, 317 Incubated, 25, 315 Indicative, 233, 315, 330, 354 Indolent, 12, 315 Induction therapy, 4, 81, 315 Industrial Waste, 213, 315 Infant, Newborn, 277, 315 Infarction, 81, 296, 315, 322 Infection, 135, 136, 241, 285, 291, 308, 314, 315, 320, 326, 330, 347, 355 Information Systems, 57, 58, 316 Infusion, 12, 316 Ingestion, 14, 38, 65, 92, 131, 132, 287, 309, 311, 313, 316, 333 Inhalation, 28, 38, 79, 277, 311, 312, 316, 333 Inhalation Exposure, 79, 316 Initiation, 20, 49, 316, 335, 351 Insecticides, 316, 331 Insight, 20, 39, 56, 316 Insulator, 158, 166, 200, 230, 316 Insulin, 35, 86, 309, 316, 353 Insulin-dependent diabetes mellitus, 86, 316 Interferon, 15, 316, 320 Interferon-alpha, 316 Internal Medicine, 67, 96, 311, 316 Internal radiation, 316, 338 Interstitial, 41, 45, 127, 166, 229, 287, 316, 325, 340 Intestinal, 156, 288, 309, 316 Intestine, 284, 287, 293, 317, 318 Intoxication, 67, 88, 93, 120, 121, 123, 127, 132, 317, 354, 355 Intramuscular, 317, 329 Intravenous, 5, 12, 94, 150, 316, 317, 329 Intrinsic, 52, 229, 277, 317 Invasive, 9, 241, 314, 317, 320 Iodine, 70, 117, 140, 175, 208, 235, 317 Ionization, 158, 210, 317 Ionizing, 43, 278, 303, 317, 321, 339, 344 Iridium, 184, 198, 199, 207, 208, 220, 317 Irrigation, 98, 105, 160, 317 Isoniazid, 240, 317 J Joint, 15, 292, 317, 348 K Kb, 41, 256, 317 Keratin, 317
Keratinocytes, 9, 13, 71, 73, 78, 114, 123, 127, 133, 241, 317 Keratosis, 108, 121, 130, 241, 275, 317 Kidney Cortex, 317, 322 Kinetic, 25, 36, 56, 317, 318 L Labile, 293, 318 Lanthanum, 197, 201, 202, 207, 208, 220, 318 Large Intestine, 293, 299, 317, 318, 340, 344 Latent, 9, 58, 318 Latent period, 58, 318 Laxative, 277, 318 Lead Poisoning, 17, 318 Lesion, 241, 318 Leucine, 46, 318, 330 Leucocyte, 318, 320 Leukaemia, 68, 72, 80, 111, 318 Leukocytes, 286, 291, 310, 316, 318, 324, 331, 352 Leukotrienes, 282, 301, 318 Levo, 300, 318 Levodopa, 300, 318 Library Services, 270, 319 Life cycle, 285, 307, 319 Life Expectancy, 18, 319 Ligament, 319, 336, 347 Ligands, 140, 170, 211, 220, 221, 238, 319, 348 Ligase, 30, 319 Ligation, 26, 319 Lipid, 302, 316, 319, 329 Lipid Peroxidation, 319, 329 Lipophilic, 319, 333 Lipopolysaccharide, 310, 319 Lipoprotein, 310, 319 Liposomal, 26, 319 Lipoxygenase, 38, 282, 318, 319 Lithium, 99, 113, 143, 175, 179, 180, 193, 196, 198, 202, 207, 208, 281, 319 Liver cancer, 6, 147, 240, 319 Liver Neoplasms, 319, 354 Liver scan, 319, 342 Localized, 50, 85, 147, 298, 301, 302, 306, 315, 319, 332 Locomotion, 319, 332 Loop, 170, 319 Lubricants, 320, 331 Luciferase, 20, 43, 320 Lutetium, 220, 320 Lycopene, 50, 320 Lymph, 290, 303, 320, 340
366 Arsenic
Lymph node, 290, 320, 340 Lymphatic, 223, 303, 316, 320, 345, 346, 350 Lymphatic system, 320, 345, 346, 350 Lymphoblastic, 151, 320 Lymphoblasts, 275, 320 Lymphocyte, 32, 81, 87, 280, 320, 321 Lymphocytic, 148, 320 Lymphoid, 32, 150, 280, 296, 309, 318, 320 Lymphoma, 12, 64, 68, 89, 98, 102, 115, 120, 121, 122, 148, 149, 150, 223, 311, 320 Lymphoproliferative, 12, 320 Lymphoproliferative Disorders, 12, 320 M Macrophage, 25, 320 Magnetic Resonance Imaging, 320, 342 Malignancy, 43, 320, 329 Malignant tumor, 321, 324 Mammary, 321, 349 Manic, 281, 319, 321 Manifest, 156, 321 Man-made, 321, 322 Mannans, 307, 321 Materia Medica, 133, 136, 321 Maxillary, 321, 328 Maxillary Sinus, 321, 328 Maximum Tolerated Dose, 11, 150, 301, 321 Meat, 50, 321 Mediate, 11, 300, 321, 339 Mediator, 32, 300, 321, 343 MEDLINE, 257, 321 Megakaryocytes, 286, 321 Megaloblastic, 307, 321 Meiosis, 46, 286, 321, 323, 338, 348 Melanin, 298, 321, 331, 353 Melanocytes, 9, 16, 314, 321 Melanoma, 16, 43, 140, 241, 264, 287, 321 Melanosomes, 321 Melarsoprol, 223, 322 Memory, 24, 164, 166, 167, 168, 193, 214, 215, 222, 230, 309, 322 Mendelevium, 207, 208, 322 Meninges, 290, 322 Mental Disorders, 153, 322 Mental Health, iv, 4, 153, 256, 258, 322, 337 Mercaptopurine, 150, 151, 322 Mercuric Chloride, 41, 322 Metabolite, 62, 100, 113, 285, 322 Metallothionein, 83, 322 Metals, Alkali, 197, 322
Metaphase, 286, 322, 338 Metastasis, 223, 322 Metastatic, 9, 16, 47, 95, 146, 148, 322, 343 Methacrylate, 208, 322 Methionine, 322, 347 MI, 110, 228, 273, 322 Microbe, 322, 351 Microbiological, 225, 323 Microbiology, 9, 24, 32, 77, 110, 111, 129, 276, 283, 285, 323 Micronuclei, 74, 323 Microorganism, 293, 323, 355 Micro-organism, 298, 301, 323 Microscopy, 30, 323 Microtubules, 46, 122, 129, 323, 329 Microwaves, 159, 323, 338 Migration, 7, 52, 191, 323 Minority Groups, 53, 323 Miscarriage, 37, 323 Miscible, 186, 323 Mitochondria, 20, 36, 41, 90, 114, 129, 323, 328 Mitochondrial Swelling, 323, 325 Mitosis, 8, 46, 109, 281, 289, 323 Mitotic, 8, 45, 122, 323, 354 Mobility, 133, 140, 191, 200, 323 Mobilization, 27, 60, 128, 323 Modeling, 23, 142, 301, 323, 336 Modification, 14, 42, 45, 172, 219, 323, 338 Molecular, 4, 6, 9, 13, 18, 19, 21, 25, 30, 33, 34, 36, 37, 40, 41, 42, 43, 45, 47, 49, 50, 54, 72, 77, 89, 95, 96, 102, 104, 110, 115, 122, 126, 127, 128, 129, 140, 159, 162, 163, 172, 177, 183, 187, 196, 203, 204, 211, 214, 223, 257, 259, 279, 285, 294, 298, 301, 322, 324, 332, 336, 341, 348, 352, 353 Monitor, 36, 158, 159, 324, 327 Monoclonal, 29, 324, 338 Monoclonal antibodies, 29, 324 Monocytes, 318, 324, 325, 349 Mononuclear, 73, 324, 352 Monosomy, 279, 324 Morphogenesis, 7, 37, 45, 324 Morphological, 21, 73, 90, 302, 307, 321, 324 Morphology, 241, 311, 324 Motility, 324, 343 Motion Sickness, 324, 325 Mucosa, 241, 324, 347 Multicenter study, 103, 115, 324
Index 367
Multidrug resistance, 13, 66, 94, 97, 98, 324 Multiple Myeloma, 9, 12, 52, 68, 76, 111, 114, 145, 149, 246, 247, 262, 324 Muscle Proteins, 40, 324 Musculature, 40, 324 Mustard Gas, 324, 325 Mutagen, 72, 325 Mutagenesis, 6, 39, 58, 72, 80, 104, 325, 336 Mutagenic, 13, 38, 299, 325, 344 Myelodysplastic syndrome, 22, 29, 93, 147, 325, 344 Myelogenous, 146, 151, 325 Myeloid Cells, 26, 325 Myeloma, 9, 52, 114, 145, 325 Myelosuppression, 156, 325 Myelotoxic, 22, 325 Myocarditis, 127, 325 Myocardium, 322, 325 Myotonia, 325, 338 N Nausea, 156, 280, 281, 308, 325, 349, 353 NCI, 1, 4, 10, 30, 53, 112, 145, 146, 147, 148, 149, 150, 151, 152, 153, 255, 292, 325 Necrosis, 63, 85, 108, 240, 281, 309, 315, 322, 325, 341, 343 Neodymium, 201, 207, 208, 219, 325 Neoplasia, 49, 223, 325 Neoplasm, 145, 149, 303, 325, 329 Neoplastic, 32, 49, 320, 325, 342 Nephritis, 41, 325 Nephrosis, 325, 326 Nephrotic, 41, 326 Nephrotic Syndrome, 41, 326 Nephrotoxic, 51, 326 Neptunium, 207, 208, 326 Nerve, 42, 276, 298, 308, 321, 326, 331, 334, 346, 347, 352, 353 Nervous System, 18, 37, 102, 240, 283, 290, 321, 326, 330 Networks, 42, 326, 349 Neural, 7, 45, 279, 326 Neural Crest, 7, 326 Neuroblastoma, 147, 326 Neurodegenerative Diseases, 18, 326 Neurologic, 18, 309, 326 Neuronal, 42, 45, 326 Neurons, 45, 298, 308, 318, 326, 348 Neuropathy, 91, 101, 121, 132, 326, 330, 331 Neurotoxicity, 131, 156, 326 Neutrons, 278, 287, 326, 338
Niacin, 240, 326, 352 Nitrates, 58, 326 Nitric acid, 326 Nitric Oxide, 34, 38, 327 Nitrogen Compounds, 194, 327 Norepinephrine, 276, 300, 327 Nuclei, 182, 278, 295, 302, 305, 320, 323, 326, 327, 337, 349 Nucleic acid, 156, 196, 284, 308, 313, 327, 338 Nucleic Acid Hybridization, 313, 327 O Occupational Exposure, 55, 66, 327 Odds Ratio, 327, 340 Odour, 282, 327 Ointments, 327, 355 Oncogene, 72, 94, 109, 113, 327 Oncogenic, 13, 328, 337 Oncologist, 84, 89, 99, 108, 125, 128, 328 Opacity, 298, 328 Operon, 33, 54, 59, 60, 61, 111, 196, 328, 335, 341 Organ Culture, 328, 350 Organelles, 297, 321, 324, 328 Oroantral Fistula, 66, 328 Osmosis, 226, 328 Ovary, 50, 82, 310, 328, 347 Overall survival, 5, 328 Overdose, 83, 295, 328 Overexpress, 12, 328 Oxidants, 23, 34, 35, 177, 328 Oxidation-Reduction, 190, 285, 328 Oxidative metabolism, 36, 276, 277, 318, 328 Oxidative Stress, 9, 19, 23, 26, 35, 36, 42, 44, 75, 329 Oxides, 159, 165, 176, 192, 197, 201, 225, 329 Oxygen Consumption, 329, 341 Oxygenase, 81, 329 Oxygenation, 161, 329 P P53 gene, 43, 329 Paclitaxel, 125, 129, 329 Palladium, 169, 170, 197, 207, 208, 219, 329, 342 Palliative, 329, 350 Pancreas, 35, 50, 71, 148, 275, 285, 299, 316, 329, 352 Pancreatic, 33, 35, 148, 329 Pancreatic cancer, 33, 148, 329 Papillary, 313, 329
368 Arsenic
Papilloma, 304, 329 Papillomavirus, 36, 329 Papule, 241, 329 Parasite, 329 Parasitic, 158, 161, 182, 218, 329 Parenteral, 111, 329 Parenteral Nutrition, 111, 329 Partial remission, 330, 340 Particle, 226, 321, 330, 335, 345, 351 Patch, 241, 330 Pathogenesis, 16, 52, 55, 130, 330 Pathologic, 281, 285, 296, 314, 330, 337 Pathologic Processes, 281, 330 Pathologies, 240, 330 Pathophysiology, 6, 330 Patient Education, 263, 268, 270, 273, 330 Peer Review, 21, 107, 330 Pelvic, 330, 336 Penicillamine, 120, 125, 330 Penicillin, 280, 330, 354 Pepsin, 292, 330 Pepsin A, 292, 330 Peptide, 13, 29, 56, 302, 317, 330, 333, 336, 337 Peracetic Acid, 186, 330 Perforation, 281, 330 Perhexiline, 240, 330 Peripheral blood, 8, 316, 330, 334 Peripheral Nervous System, 18, 326, 330, 347 Peripheral Neuropathy, 97, 331 Peripheral Vascular Disease, 42, 72, 331 Peroxidase, 82, 282, 319, 331 Peroxide, 331 Pesticides, 14, 18, 32, 56, 58, 77, 226, 235, 262, 263, 316, 331 Petroleum, 31, 157, 170, 181, 194, 238, 331 Phagocyte, 328, 331 Pharmacists, 46, 331 Pharmacodynamic, 5, 331 Pharmacokinetic, 5, 19, 150, 331 Pharmacologic, 4, 296, 311, 331, 351 Phenobarbital, 49, 331 Phenotype, 7, 34, 331 Phenylalanine, 330, 331, 353 Phorbol, 331, 349 Phosphates, 225, 331 Phospholipases, 331, 344 Phosphorous, 161, 164, 174, 178, 179, 190, 212, 220, 331 Phosphorus, 140, 142, 143, 157, 164, 165, 169, 170, 173, 175, 176, 184, 187, 188,
189, 193, 196, 197, 201, 202, 206, 208, 209, 211, 216, 220, 221, 222, 227, 230, 231, 237, 238, 240, 288, 331, 332 Phosphorylated, 20, 40, 293, 332 Phosphorylates, 42, 332 Phosphorylation, 13, 40, 41, 42, 156, 332 Photocoagulation, 293, 332 Physiologic, 277, 285, 300, 311, 332, 335, 339 Physiology, 6, 37, 38, 276, 302, 311, 332 Pigment, 208, 298, 320, 321, 332 Pigmentation, 9, 108, 121, 314, 332 Pilot Projects, 30, 332 Pilot study, 12, 56, 77, 332 Placenta, 332, 335 Placentation, 37, 332 Plaque, 241, 283, 332 Plasma cells, 280, 324, 325, 332 Plasmid, 33, 43, 54, 60, 61, 95, 109, 332, 354 Plasmin, 83, 332, 333 Plasminogen, 332, 333 Plasminogen Activators, 332, 333 Platelet Activation, 333, 344 Platelet Aggregation, 74, 279, 327, 333, 350 Platelets, 282, 321, 325, 327, 333, 343, 350 Platinum, 51, 163, 184, 197, 199, 207, 208, 220, 292, 319, 329, 333, 342 Pneumonitis, 287, 333 Policy Making, 310, 333 Polonium, 186, 193, 333 Polychlorinated Biphenyls, 55, 333 Polymers, 226, 285, 333, 336 Polymorphic, 51, 298, 333 Polymorphism, 28, 78, 333 Polypeptide, 278, 293, 313, 330, 332, 333, 336, 355 Polyposis, 293, 333 Polysaccharide, 277, 280, 290, 333 Porosity, 53, 184, 195, 333 Posterior, 279, 300, 329, 333 Postoperative, 62, 334 Postoperative Period, 62, 334 Postsynaptic, 334, 344, 348 Post-translational, 45, 334 Potassium, 143, 157, 196, 197, 207, 208, 334, 338 Potentiates, 10, 20, 66, 334 Potentiating, 39, 334 Potentiation, 131, 334, 344 Power Plants, 160, 334 Practice Guidelines, 258, 334 Praseodymium, 202, 207, 208, 220, 334
Index 369
Precancerous, 241, 275, 334, 335 Precipitating Factors, 289, 334 Precipitation, 6, 177, 197, 226, 334 Preclinical, 52, 150, 334 Pregnancy Complications, 37, 334 Preleukemia, 325, 334, 344 Premalignant, 241, 334, 335 Prenatal, 7, 19, 302, 335 Presumptive, 58, 335 Prevalence, 102, 327, 335 Prickle, 317, 335 Progeny, 15, 295, 335 Progesterone, 335, 346 Progression, 18, 49, 279, 335 Progressive, 289, 301, 310, 325, 326, 333, 335, 340 Prokaryotic Cells, 55, 335 Promethium, 207, 208, 335 Promoter, 43, 113, 335 Promotor, 335, 341 Prophase, 286, 335, 338, 348 Proportional, 335, 348 Propoxur, 18, 335 Prospective Studies, 50, 335 Prostaglandin, 42, 335, 350 Prostaglandins A, 336 Prostate, 50, 56, 68, 122, 149, 285, 336, 352 Protactinium, 207, 208, 336 Protective Agents, 288, 336 Protective Clothing, 264, 336 Protein C, 13, 16, 30, 58, 277, 278, 283, 305, 317, 319, 324, 336, 352, 353 Protein Conformation, 58, 278, 317, 336 Protein Engineering, 30, 336 Protein Kinases, 20, 23, 45, 336 Protein S, 19, 54, 238, 285, 304, 308, 336, 341 Proteinuria, 41, 324, 326, 337 Proteolytic, 25, 144, 294, 332, 333, 337 Protocol, 28, 53, 177, 337 Protons, 141, 278, 313, 317, 337, 338 Proto-Oncogene Proteins, 329, 337 Proto-Oncogene Proteins c-mos, 329, 337 Protozoa, 295, 323, 337 Protraction, 15, 337 Proximal, 51, 300, 317, 337 Psoriasis, 108, 121, 324, 337, 352 Public Health, 14, 17, 27, 31, 43, 50, 55, 57, 76, 79, 80, 97, 110, 112, 224, 238, 239, 258, 262, 337 Public Policy, 257, 337 Publishing, 59, 112, 337
Pulmonary, 39, 286, 291, 295, 318, 337, 354 Pulmonary Edema, 291, 337 Pulse, 32, 324, 337 Purifying, 203, 337 Purines, 284, 338, 343 Q Quadrivalent, 202, 338 Quality of Life, 18, 338 Quaternary, 183, 187, 336, 338 Quiescent, 338, 355 Quinidine, 240, 292, 338 Quinine, 240, 292, 338 R Race, 7, 300, 323, 338 Radiation oncologist, 46, 328, 338 Radiation therapy, 152, 264, 305, 307, 316, 338, 342 Radio Waves, 299, 323, 338 Radiochemical, 239, 338 Radioimmunotherapy, 338, 339 Radiolabeled, 338, 339 Radiopharmaceutical, 308, 339 Radiotherapy, 29, 287, 338, 339, 346 Radium, 143, 226, 339 Radon, 15, 31, 96, 339 Randomized, 21, 130, 151, 301, 339 Randomized clinical trial, 21, 339 Ranitidine, 240, 339 Reabsorption, 241, 339 Reaction Time, 213, 339 Reactivation, 25, 339 Reactive Oxygen Species, 10, 38, 39, 60, 72, 109, 114, 142, 339 Reagent, 24, 291, 320, 339, 341 Receptor, 6, 13, 25, 32, 44, 59, 60, 63, 108, 150, 276, 280, 300, 331, 339, 343, 344 Receptors, Cytokine, 35, 339 Recombinant, 20, 340, 354 Recombination, 44, 295, 340 Reconstitution, 89, 340 Rectum, 50, 281, 287, 293, 299, 306, 308, 318, 336, 340 Red blood cells, 304, 325, 329, 340, 342, 344 Reductase, 35, 54, 340, 350 Refer, 1, 287, 293, 306, 307, 319, 321, 326, 333, 339, 340 Reflective, 22, 340 Refraction, 340, 345 Refractory, 4, 10, 12, 73, 76, 91, 111, 114, 145, 148, 149, 150, 151, 183, 184, 194, 302, 340
370 Arsenic
Regeneration, 340 Regimen, 151, 301, 340 Regional lymph node, 223, 340 Registries, 17, 340 Relapse, 9, 22, 26, 50, 103, 340 Relative risk, 21, 23, 340 Reliability, 161, 178, 215, 340 Remission, 11, 12, 22, 89, 94, 96, 103, 113, 150, 249, 340 Renal failure, 156, 240, 340 Renal pelvis, 340, 351 Repressor, 328, 340 Research Design, 44, 341 Research Support, 24, 26, 27, 341 Residual disease, 22, 29, 341 Respiration, 72, 288, 295, 324, 341 Respiratory failure, 101, 341 Response Elements, 84, 341 Restoration, 339, 340, 341, 355 Retinoid, 223, 341 Retinol, 117, 341 Rhabdomyolysis, 75, 341 Rheumatoid, 328, 341 Ribosome, 280, 341, 352 Rigidity, 30, 332, 341 Risk factor, 8, 18, 22, 43, 50, 51, 74, 264, 289, 303, 340, 341 Rodenticides, 331, 341 Rods, 307, 341, 342 Rotenone, 41, 341 Rubber, 275, 341 Rubidium, 157, 196, 197, 207, 208, 220, 341 Ruthenium, 169, 170, 184, 197, 199, 219, 342 S Salicylate, 342 Salicylic, 342 Salicylic Acids, 342 Salivary, 299, 329, 342 Salivary glands, 299, 342 Salvage Therapy, 122, 342 Samarium, 157, 202, 220, 342 Saponins, 342, 346 Scalpel, 31, 342 Scandium, 202, 207, 208, 220, 342 Scans, 26, 342 Schizoid, 342, 355 Schizophrenia, 342, 355 Schizotypal Personality Disorder, 342, 355 Screening, 16, 28, 30, 48, 292, 342 Seafood, 98, 104, 342 Sebaceous, 342, 355
Secondary tumor, 322, 342 Secretion, 71, 275, 292, 312, 316, 339, 343 Sediment, 26, 63, 237, 343 Segregation, 16, 141, 340, 343 Seizures, 309, 343 Selective estrogen receptor modulator, 343, 349 Semen, 336, 343 Senile, 275, 343 Sensitization, 239, 343 Sequester, 56, 343 Serine, 42, 302, 337, 343 Serotonin, 281, 343, 352 Serum, 10, 39, 86, 140, 277, 279, 293, 340, 343, 352 Sex Characteristics, 276, 343, 349 Shock, 40, 41, 45, 208, 343, 352 Side effect, 150, 160, 251, 276, 281, 285, 297, 322, 325, 344, 351 Signal Transduction, 11, 34, 40, 42, 47, 91, 344 Signs and Symptoms, 340, 344 Silicon Dioxide, 167, 176, 212, 344 Sister Chromatid Exchange, 67, 105, 344 Skeletal, 35, 324, 338, 341, 344, 352 Skeleton, 275, 305, 317, 335, 344 Skin Manifestations, 84, 344 Skull, 344, 349 Sludge, 72, 140, 240, 344 Small intestine, 71, 284, 301, 313, 317, 344 Smoldering leukemia, 325, 344 Smooth muscle, 34, 40, 42, 278, 279, 288, 312, 314, 344, 347 Social Environment, 338, 345 Sodium, 19, 45, 70, 108, 143, 187, 196, 197, 201, 202, 207, 208, 212, 240, 286, 338, 339, 345 Soft tissue, 286, 344, 345 Solid tumor, 47, 147, 223, 279, 300, 345 Solvent, 186, 187, 304, 345 Soma, 345 Somatic, 24, 276, 321, 323, 330, 331, 344, 345, 349, 353 Somatic cells, 321, 323, 345 Sound wave, 295, 299, 340, 345 Specialist, 26, 265, 299, 345 Specificity, 30, 39, 58, 108, 277, 282, 302, 334, 345 Spectrometer, 159, 345 Spectrophotometry, 234, 345 Spectrum, 3, 32, 44, 132, 150, 323, 338, 345 Sperm, 81, 291, 345, 352
Index 371
Spike, 169, 345 Spinal cord, 283, 287, 290, 291, 295, 308, 322, 326, 330, 345, 346 Spinal Nerves, 331, 345 Spinous, 303, 317, 346 Spleen, 24, 320, 346 Sporadic, 326, 346 Squamous, 8, 9, 43, 152, 241, 264, 303, 346 Squamous cell carcinoma, 9, 43, 152, 241, 264, 303, 346 Squamous cells, 346 Staging, 342, 346 Staphylococcus, 61, 108, 308, 346 Steel, 70, 185, 203, 206, 213, 346, 353, 354 Stem cell transplantation, 4, 96, 346 Stem Cells, 278, 346 Stereotactic, 31, 45, 346 Sterility, 297, 346 Steroid, 6, 19, 284, 296, 342, 346 Stimulant, 296, 312, 346, 349, 354 Stimulus, 42, 300, 302, 305, 339, 347, 350 Stomach, 275, 299, 304, 308, 309, 313, 325, 330, 344, 346, 347 Strained, 169, 209, 347 Strand, 74, 77, 347 Stroke, 153, 256, 288, 347 Stromal, 286, 347 Stromal Cells, 286, 347 Strontium, 197, 201, 207, 208, 220, 347 Subacute, 101, 112, 128, 132, 315, 347 Subclinical, 315, 343, 347 Subcutaneous, 276, 301, 329, 347 Subiculum, 312, 347 Subspecies, 345, 347 Substance P, 172, 219, 286, 304, 322, 340, 343, 347 Suction, 306, 347 Sudden death, 247, 347 Sulfates, 225, 347 Sulfides, 171, 347 Sulfur, 139, 141, 143, 177, 178, 179, 180, 184, 193, 194, 203, 204, 206, 208, 213, 214, 322, 347, 348 Sulfur Compounds, 213, 347 Sulfur Dioxide, 180, 214, 348 Sulfuric acid, 192, 214, 347, 348 Sunburn, 264, 348 Superoxide, 34, 348 Supplementation, 130, 348 Suppression, 9, 20, 26, 34, 84, 156, 158, 348 Surface Plasmon Resonance, 196, 348 Survival Rate, 328, 348
Symphysis, 336, 348 Synapses, 345, 348 Synaptic, 344, 348 Synergistic, 5, 22, 45, 48, 101, 348 Systemic, 40, 101, 135, 240, 252, 286, 303, 315, 338, 348, 354 Systolic, 314, 348 T Tachycardia, 96, 283, 348 Tachypnea, 283, 348 Tacrine, 240, 349 Tamoxifen, 125, 240, 343, 349 Technetium, 199, 349 Teichoic Acids, 310, 349 Tellurium, 175, 186, 193, 197, 199, 201, 208, 220, 349 Telomerase, 36, 349 Telophase, 323, 349 Temporal, 7, 78, 312, 349 Teratogenic, 299, 349, 352 Terbium, 202, 207, 208, 220, 349 Testicular, 146, 349 Testis, 20, 349 Testosterone, 340, 349 Tetradecanoylphorbol Acetate, 84, 349 Thalidomide, 52, 349 Theophylline, 21, 338, 349 Therapeutics, 16, 52, 66, 145, 147, 247, 248, 252, 350 Thermal, 15, 80, 160, 166, 181, 185, 190, 205, 206, 208, 212, 241, 287, 300, 326, 350 Thiamine, 131, 350 Thioredoxin, 35, 82, 350 Threonine, 42, 337, 343, 350 Threshold, 84, 162, 167, 200, 217, 230, 304, 314, 350 Thrombin, 305, 333, 336, 350 Thrombomodulin, 336, 350 Thrombosis, 336, 347, 350 Thromboxanes, 282, 301, 350 Thrombus, 74, 296, 315, 333, 350 Thulium, 202, 220, 350 Thymus, 314, 320, 350 Thyroid, 18, 240, 317, 350, 353 Tilapia, 65, 350 Tissue Culture, 12, 350 Tobacco Mosaic Virus, 125, 350, 351 Tobamovirus, 350, 351 Tolerance, 68, 114, 141, 143, 276, 309, 351 Tonic, 295, 351 Topical, 242, 282, 304, 313, 322, 351, 352, 355
372 Arsenic
Topical chemotherapy, 242, 351 Torsion, 315, 351 Toxicokinetics, 39, 351 Toxicologic, 49, 351 Toxins, 3, 15, 41, 280, 312, 315, 324, 338, 351, 354 Trace element, 7, 57, 90, 240, 286, 291, 293, 307, 326, 344, 350, 351 Trachea, 287, 350, 351 Transcriptase, 349, 351 Transcription Factors, 6, 23, 58, 341, 351 Transduction, 13, 344, 351 Transfection, 285, 351 Transferases, 43, 351 Transitional cell carcinoma, 82, 351 Translating, 14, 352 Translation, 20, 304, 352 Translational, 352 Translocation, 10, 304, 352 Transmitter, 275, 300, 321, 327, 348, 352 Trauma, 241, 325, 352 Tretinoin, 150, 352 Trisomy, 279, 352 Trivalent, 35, 71, 72, 150, 202, 203, 275, 352 Troglitazone, 240, 352 Trophic, 45, 352 Tropomyosin, 324, 352 Troponin, 324, 352 Truncal, 92, 352 Tryptophan, 34, 293, 343, 352 Tuberculosis, 295, 317, 342, 352 Tuberculostatic, 317, 352 Tubulin, 46, 125, 323, 352 Tumor marker, 285, 352 Tumor Necrosis Factor, 63, 108, 349, 352 Tumor suppressor gene, 329, 353 Tumorigenic, 36, 353 Tungsten, 139, 157, 184, 197, 199, 201, 202, 206, 207, 208, 219, 220, 236, 289, 353 Type 2 diabetes, 6, 353 Tyrosine, 4, 38, 42, 300, 353 U Ubiquitin, 14, 144, 353 Unconscious, 314, 353 Unresectable, 146, 147, 353 Uranium, 15, 143, 198, 202, 339, 349, 353 Urea, 353 Uremia, 240, 340, 353 Ureter, 340, 351, 353 Urethra, 336, 353 Urinary, 31, 39, 41, 51, 66, 70, 78, 84, 87, 90, 95, 104, 292, 309, 353
Urinary tract, 84, 353 Urine, 13, 35, 51, 70, 81, 82, 91, 92, 100, 286, 300, 337, 340, 353 Urogenital, 309, 353 Uterus, 290, 335, 353 V Vaccine, 29, 337, 353 Vagina, 290, 298, 353 Vagus Nerve, 352, 353 Valine, 330, 354 Vanadium, 55, 70, 71, 111, 157, 182, 183, 197, 199, 201, 207, 208, 214, 220, 233, 241, 354 Vascular, 6, 34, 37, 40, 42, 94, 113, 240, 278, 288, 303, 314, 315, 316, 327, 332, 333, 350, 354 Vascular Resistance, 278, 354 Vasodilation, 34, 354 Vasodilator, 34, 287, 300, 312, 330, 354 Vector, 351, 354 Vein, 279, 317, 327, 354 Venoms, 297, 354 Venous, 336, 354 Ventricle, 312, 337, 348, 354 Ventricular, 96, 278, 354 Venules, 286, 288, 354 Veterinary Medicine, 257, 354 Vinblastine, 352, 354 Vincristine, 352, 354 Vinyl Chloride, 5, 240, 354 Viral, 15, 36, 122, 328, 351, 353, 354 Virulence, 61, 283, 351, 354 Virus, 283, 303, 313, 316, 332, 351, 354 Viscera, 345, 355 Vitiligo, 16, 355 Vitro, 4, 11, 12, 26, 40, 41, 52, 355 Vivo, 5, 11, 12, 13, 26, 41, 45, 47, 49, 52, 355 Vulgaris, 89, 355 W Wart, 317, 355 White blood cell, 151, 275, 280, 286, 291, 292, 315, 318, 320, 325, 332, 355 Windpipe, 350, 355 Withdrawal, 45, 355 Wound Healing, 292, 355 X Xenograft, 280, 355 X-ray, 54, 58, 152, 289, 294, 306, 308, 321, 325, 327, 338, 339, 342, 346, 355 Y Yeasts, 307, 331, 355 Ytterbium, 202, 207, 208, 220, 355
Index 373
Yttrium, 198, 202, 207, 208, 220, 355 Z Zinc Oxide, 191, 208, 355 Zoonoses, 108, 283, 355
Zygote, 294, 295, 355 Zymogen, 336, 355
374 Arsenic
Index 375
376 Arsenic
